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安倍正博

徳島大学

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2024年11月15日更新

職名: 名誉教授 (2023.4)
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学歴: 1984/3: 徳島大学医学部医学科卒業
学位: 博士(医学) (徳島大学) (1994年10月)
職歴・経歴: 〜: 徳島大学講師, 病院 (-2006.9.)
2006/10: 徳島大学助教授, 大学院ヘルスバイオサイエンス研究部 (-2007.3.)
2007/4: 徳島大学准教授, 大学院ヘルスバイオサイエンス研究部 (-2014.12.)
2015/1: 徳島大学教授, 大学院ヘルスバイオサイエンス研究部 (-2015.3.)
2015/4: 徳島大学教授, 大学院医歯薬学研究部 (-2023.3.)

専門分野・研究分野: 医学 (Medicine)
血液学 (Hematology)
腫瘍学 (Oncology)

研究者総覧で最新データを確認する

2024年11月15日更新

専門分野・研究分野: 医学 (Medicine)
血液学 (Hematology)
腫瘍学 (Oncology)
担当経験のある授業科目: 研究者総覧に該当データはありませんでした。
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研究者総覧で最新データを確認する

2024年11月15日更新

専門分野・研究分野: 医学 (Medicine)
血液学 (Hematology)
腫瘍学 (Oncology)

研究テーマ: 血液腫瘍の病態と治療 (骨髄腫 (myeloma), 免疫療法 (immunotherapy), 造血 (hematopoiesis), 造血器腫瘍 (hematological malignancy))

著書

原田武志, 安倍正博 :
くすぶり型多発性骨髄腫別冊日本臨牀領域別症候群シリーズ No.30 血液症候群(第3版)-その他の血液疾患を含めて V,
2024年. 原田武志, 安倍正博 :
最新の骨粗鬆症学(第2版), --- 多発性骨髄腫 ---,
日本臨牀社, 東京, 2023年1月. 原田武志, 安倍正博 :
VII. 骨粗鬆症の類縁疾患の診断と治療. 多発性骨髄腫. 最新の骨粗鬆症学 (第2版) -骨粗鬆症の最新知見-,
2023年. 原田武志, 安倍正博 :
I章近年承認された抗がん薬-13．ダラツムマブ・ボルヒアルロニダーゼアルファ配合(ダラキューロ). 最新のがん薬物療法 2023-2024,
2023年. 原田武志, 安倍正博 :
専門医のための血液病学, --- 多発性骨髄腫 ---,
株式会社医学書院, 2022年3月. 原田武志, 安倍正博 :
多発性骨髄腫,
2022年. 吉田守美子, 原倫世, 山口佑樹, 近藤剛史, 遠藤ふうり, 筒井康継, 桝田志保, 倉橋清衛, 明比祐子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 中島公平, 安倍正博 :
急速に腫瘍が増大し悪性転化が疑われたCushing病の1例,
2019年6月. 賀川久美子, 前田悠作, 大浦雅博, 曽我部公子, 藤野ひかる, 髙橋真美子, 丸橋朋子, 岩佐昌美, 宇高憲吾, 原田武志, 伊勢孝之, 藤井志朗, 中村信元, 三木浩和, 八木秀介, 竹内恭子, 尾崎修治, 安倍正博, 藤野ひかる :
治療後長期生存が得られた心不全合併ALアミロイドーシス症例の検討,
臨床血液, 2017年10月.

(要約): ALアミロイドーシスは，多発性骨髄腫やMGUS(monoclonal gammopathy of undetermined significance)などのモノクローナルな形質細胞が産生する免疫グロブリン軽鎖および重鎖が，アミロイド線維として組織に沈着し，臓器障害を惹起する難治性疾患である．なかでも心アミロイドーシス(以下CA)は，心不全症状が出現してからは，無治療の場合極めて予後不良であるため，その管理・治療が重要である1)．ALアミロイドーシスに対しては，自家末梢血幹細胞移植併用メルファラン大量療法(以下ASCT)の有効性が報告されているが，CAにおいては治療関連毒性が強く，その適応を慎重に検討する必要がある2, 3)．近年，多発性骨髄腫において，ボルテゾミブ(Bor)や，免疫調節薬であるサリドマイド(Thal)やレナリドミド(Len)などの新規薬を用いた治療により，治療成績が向上している．ALアミロイドーシス症例においてもこれらの新規薬の有効性が示され，CAに対しても，重篤な有害事象の発生率が低く，有効であったとの報告がある4∼6)．しかしながら，その長期の治療成績や予後については，十分な情報がない．そこで我々は，当科において治療し，長期生存が得られた心不全合併CA例について，後方視的に検討した．
(キーワード): Cardiac AL amyloidosis / Autologous hematopoietic stem cell transplantation / Long-term survival
(出版サイトへのリンク): ● Publication site (DOI): 10.11406/rinketsu.58.2197
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390282680011466240; ● Search Scopus @ Elsevier (DOI): 10.11406/rinketsu.58.2197

(DOI: 10.11406/rinketsu.58.2197, CiNii: 1390282680011466240) 寺町順平, 安倍正博 :
TAK-1を標的とした骨髄腫骨破壊病変治療薬開発,
日本臨牀社, 2016年7月. 安倍正博 :
「臨床血液学—最新情報と今後の展望 2016年版」多発性骨髄腫,
臨床血液, 2016年2月. 安倍正博, 三木浩和, 中村信元 :
臨床血液学—最新情報と今後の展望 2016年版,
臨床血液, 2016年. 安倍正博 :
もっと知って欲しい多発性骨髄腫のこと 2015年版,
監修キャンサーネットジャパン制作, 2015年11月. 安倍正博 :
多発性骨髄腫における骨病変の発症機構．ブラッシュアップ多発性骨髄腫,
中外医学社, 2015年10月. 安倍正博 :
多発性骨髄腫．Principle and Practice 血液・造血器・リンパ系,
千葉滋集, 2015年10月. 安倍正博 :
話題多発性骨髄腫のPim-2キナーゼの意義,
化学評論社, 2015年8月. 安倍正博 :
多発性骨髄腫．骨ペディア骨疾患・骨代謝キーワード辞典,
羊土社, 2015年5月. 安倍正博 :
多発性骨髄腫,
羊土社, 2015年5月. 安倍正博 :
今日の治療指針 2015年版-私はこう治療している,
医学書院, 2015年1月. 安倍正博, 三木浩和, 中村信元 :
「骨髄腫∼いつ治療するのか?∼初発，再発，そして早期介入」骨髄腫骨病変の管理:ゾレドロン酸かデノスマブか,
臨床血液, 2015年.

(要約): 新規薬が臨床応用され骨髄腫の治療成績が向上しているが，骨破壊病変は依然として生活の質(QoL)の低下の最も多い原因である．初回化学療法を受ける症候性骨髄腫患者すべてに骨病変の有無にかかわらずゾレドロン酸の点滴静注を反復することが骨病変の進行防止と予後の改善の点から推奨されている．デノスマブはゾレドロン酸と同等の治療効果を発揮する．デノスマブは即効性で皮下投与という利便性があり，腎機能にも影響を与えにくいが，低カルシウム血症を来しやすく，ゾレドロン酸と同程度に顎骨壊死の発生がみられる．ゾレドロン酸は骨に長期間蓄積するが，デノスマブは骨への蓄積性がない．したがって，長期投与後の骨質への影響などに両者の違いがある可能性がある．また，治療奏効後の強力な骨吸収抑制薬継続投与の有用性および新規薬との併用下での骨病変治療薬の至適な投与開始時期，投与方法や投与期間，予後に及ぼす影響が今後の検討課題である．
(キーワード): Zoledronic acid / Denosumab / Multiple myeloma / RANKL
(出版サイトへのリンク): ● Publication site (DOI): 10.11406/rinketsu.56.997
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390001205035009152; ● Search Scopus @ Elsevier (DOI): 10.11406/rinketsu.56.997

(DOI: 10.11406/rinketsu.56.997, CiNii: 1390001205035009152) 安倍正博 :
骨髄腫の骨病変:分子機序,
Parma Medica, 2015年. 中村信元, 安倍正博 :
臓器移植．ALアミロイドーシス，多発性骨髄腫の類縁疾患,
医薬ジャーナル社, 2014年8月. 中村信元, 安倍正博 :
アミロイドーシス効果判定基準効果判定基準 2005コンセンサスクライテリア，2011新基準．ALアミロイドーシス，多発性骨髄腫の類縁疾患,
医薬ジャーナル社, 2014年8月. 三木浩和, 安倍正博 :
アミロイド原性light chainの脾臓での産生 ALアミロイドーシス，多発性骨髄腫の類縁疾患,
医薬ジャーナル社, 2014年8月. 安倍正博 :
骨粗鬆症の類縁疾患とその治療,
医薬ジャーナル社, 2013年10月. 安倍正博 :
骨転移の骨病変形成のメカニズム多発性骨髄腫,
メディカルレビュー社, 2013年10月. 安倍正博 :
骨転移の増殖・進展のメカニズム多発性骨髄腫,
メディカルレビュー社, 2013年10月. 安倍正博 :
骨髄腫に伴う骨病変の発症機序,
メディカルレビュー社, 2013年9月. 安倍正博 :
骨痛に対する対策，ビスホスホネートとデノスマブの使い分け,
医薬ジャーナル社, 2013年7月. 安倍正博, 遠藤逸朗 :
高カルシウム血症,
医薬ジャーナル社, 2013年3月. 安倍正博 :
骨病変に対する新規治療薬の開発動向,
医薬ジャーナル社, 2013年3月. 安倍正博 :
骨病変のマネージメント,
医薬ジャーナル社, 2013年3月. 安倍正博 :
骨代謝マーカーの使い方,
医薬ジャーナル社, 2013年3月. 安倍正博 :
骨病変 1) 病態，症状多発性骨髄腫の症候/合併症とその対策,
医薬ジャーナル社, 2013年3月. 遠藤逸朗, 安倍正博, 松本俊夫 :
骨転移の分子標的治療薬,
2012年12月. 安倍正博 :
多発性骨髄腫の骨病変,
2012年12月. 三木浩和, 安倍正博 :
多発性骨髄腫に対する合併症の治療(腎，骨，感染症),
2012年10月. 安倍正博 :
M蛋白がもたらす注意すべき病態，検査値異常,
2012年10月. 安倍正博 :
骨病変の評価(3)バイオマーカー,
2012年10月. 安倍正博 :
骨代謝マーカー:検査値の見方と評価,
2012年10月. 安倍正博 :
骨病変,
2012年10月. 賀川久美子, 安倍正博, 松本俊夫 :
がん骨転移治療―ビスフォスフォネート治療によるBone Management,
株式会社先端医学社, 2012年3月. 中村信元, 安倍正博, 松本俊夫 :
新規治療薬の開発と臨床応用の可能性を探る (抗RANKL抗体などを中心に),
2012年3月. 安倍正博 :
多発性骨髄腫における骨破壊機構とその治療,
中外医学社, 2011年10月. 安倍正博 :
高カルシウム血症,
医薬ジャーナル社, 2011年2月. 三木浩和, 安倍正博 :
Oncology Emergency 過粘稠症候群,
メディカルビュー社, 2011年. 安倍正博, 松本俊夫 :
第2章サイトカインによる生体調節機構 3)代謝, --- 4.Wnt阻害因子sFRP-2と骨芽細胞分化 ---,
株式会社羊土社, 東京, 2005年11月.

(キーワード): 骨芽細胞分化 / canonical Wnt 経路 / Wnt 阻害因子 / sFRP-2 / 多発性骨髄腫

安倍正博, 松本俊夫 :
多発性骨髄腫による骨破壊メカニズム,
メディカルレビュー社, 大阪, 2005年11月.

(キーワード): 骨髄腫 / 破骨細胞 / RANKL / MIP 1 / 骨芽細胞

安倍正博, 松本俊夫 :
癌転移の場としての骨髄,
秀潤社, 東京, 2005年7月.

(キーワード): 骨転移 / 多発性骨髄腫 / 骨髄 / 破骨細胞 / 骨芽細胞

安倍正博 :
骨髄腫細胞は形質細胞とどこが違うのか?, --- 骨髄環境との相互作用 ---,
株式会社先端医学社, 東京, 2005年.

(キーワード): 破骨細胞 / 骨芽細胞 / RANKL / MIP-1 / Wnt

安倍正博, 松本俊夫 :
癌と骨組織との相互作用, --- 多発性骨髄腫 ---,
株式会社中山書店, 東京, 2004年10月.

(キーワード): multiple myeloma / osteoclast / RANKL / MIP-1 / osteoblast

橋本年弘, 安倍正博, 松本俊夫 :
バイオマーカーの意義と問題点, --- 骨転移のバイオマーカー ---,
癌と化学療法社, 東京, 2004年7月.

(要約): Certain types of cancers have a strong propensity to metastasize to bone, which requires combination of multiple factors responsible for the different steps of metastasis. Bone metabolic markers are now widely used in clinical practice and give useful information on the ongoing bone metabolism, reflecting the activity of bone-resorbing osteoclasts and bone-forming osteoblasts. Bone markers have a potential as diagnostic tools for bone metastasis, and are useful in monitoring the response to anticancer as well as antiresorptive therapies. Since bone metabolic markers alone are insufficient for the diagnosis and assessment of bone metastasis, it is important to combine bone markers with tumor-related markers and imaging studies such as scintigraphy and MRI. More recently, soluble receptor activator of nuclear factor-kappaB ligand (RANKL) and osteoprotegerin (OPG) have been implicated as markers for osteoclastogenic activity. Serum levels of these factors and/or their ratios may provide additional information on the severity of bone disease and the prognosis.
(キーワード): 骨転移 (bone metastasis) / Bone markers / Osteoclastogenesis
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15272580; ● Summary page in Scopus @ Elsevier: 2-s2.0-3242671537

(PubMed: 15272580, Elsevier: Scopus) 橋本年弘, 安倍正博, 松本俊夫 :
癌に伴う骨病変の病態と治療,
南江堂, 東京, 2004年4月.

(キーワード): bone metastasis / bone marker / bisphosphonate

安倍正博, 大島隆志 :
骨髄腫細胞と骨芽細胞,
科学評論社, 東京, 2004年3月.

(キーワード): myeloma / osteoblast / BMP-2 / Wnt / osteoclast

橋本年弘, 安倍正博, 井上大輔 :
骨髄腫のビスフォスフォネート療法,
金原出版株式会社, 東京, 2003年1月.

(キーワード): Multiple myelome / Bisphosphonate / Hypercalcemia

安倍正博 :
骨病変に対するbisphosphonateの有効性,
科学評論社, 東京, 2002年11月.

(キーワード): bisphosphonate / myeloma / ATL / osteoclast / hypercalcemia

若槻真吾, 安倍正博, 小阪昌明 :
Ⅳ.検査の実際 6.多発性骨髄腫と関連疾患, --- 2)アミロイドーシスの診断 ---,
株式会社医学書院, 東京, 2002年10月. 安倍正博, 大島隆志, 小阪昌明 :
Ⅳ.検査の実際 6.多発性骨髄腫と関連疾患, --- 1)骨病変の画像評価 ---,
株式会社医学書院, 東京, 2002年10月.

論文

Mamiko Takahashi, Shin Kondo, Kumiko Kagawa, Masafumi Nakamura, Yusaku Maeda, Ryohei Sumitani, Hikaru Yagi, Masahiro Oura, Kimiko Sogabe, Takeshi Harada, Shiroh Fujii, Hirokazu Miki, Itsuro Endo, Masahiro Abe and Shingen Nakamura :
Skeletal muscle mass during chemotherapy for haematological malignancies: a retrospective study.,
BMJ Supportive & Palliative Care, Vol.14, No.2, 195-199, 2024.

(要約): This study investigated whether baseline or alteration in muscle mass affects complications during chemotherapy or overall survival (OS) in haematological malignancies. Skeletal Muscle Index (SMI) was evaluated by bioimpedance analysis before and after chemotherapy in patients with haematological malignancies, and the association between muscle mass and clinical data was retrospectively analysed. Exactly 104 patients were enrolled, with a mean age of 62.2 years. SMI was 7.85 and 6.08 in male and female patients under 65 years and 7.10 and 5.92 over 65 years, before chemotherapy, respectively. Lower baseline SMI was not correlated with worse OS in total patients (p=0.915). After a median measurement interval of 30 days after chemotherapy (n=67), body weight and SMI decreased by 2.73% and 2.87% (mean), respectively. The decrease in body weight correlated with the loss of trunk muscle mass (R=0.2107) but was more strongly associated with the loss of lower limbs muscle mass (R=0.3985). The muscle mass of lower limbs significantly decreased in lymphoma patients who experienced febrile neutropenia (-0.42% vs -6.04%, p=0.040). OS significantly decreased in lymphoma patients with loss of lower limbs muscle ≥2.8% (p=0.0327). Muscle loss occurred following anticancer treatments, significantly contributing to worse outcomes. Body composition assessment and relevant multimodal prevention of muscle loss may be vital for patients receiving chemotherapy for haematological malignancies.
(キーワード): Humans / Male / Female / Retrospective Studies / Middle Aged / Hematologic Neoplasms / Muscle, Skeletal / Aged / Adult / Antineoplastic Agents / Aged, 80 and over / Body Composition / Sarcopenia
(徳島大学機関リポジトリ): ● Metadata: 119635
(出版サイトへのリンク): ● Publication site (DOI): 10.1136/spcare-2024-004870
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38569748; ● Search Scopus @ Elsevier (PMID): 38569748; ● Search Scopus @ Elsevier (DOI): 10.1136/spcare-2024-004870

(徳島大学機関リポジトリ: 119635, DOI: 10.1136/spcare-2024-004870, PubMed: 38569748) Taiki Hori, Taro Shimizu, Hidenori ANDO, Naoto Okada, Hiroki Yamagami, Saya Yasui, Minae Hosoki, Akihiro Tojima, Toshiki Otoda, Tomoyuki Yuasa, Ken-ichi Aihara, Makoto Takishita, Sumiko Yoshida, Masahiro Abe, Tatsuhiro Ishida and Shingen Nakamura :
Humoral immune response against SARS-CoV-2 and polyethylene glycol elicited by anti-SARS-CoV-2 mRNA vaccine, and effect of pre-existing anti-polyethylene glycol antibody in patients with hematological and autoimmune diseases.,
Heliyon, Vol.10, No.10, e31489, 2024.

(要約): The effects of vaccination are modified by hematological and autoimmune diseases and/or treatment. Anti-SARS-CoV-2 mRNA vaccine contains polyethylene glycol (PEG), it is largely unknown whether PEG influences the effects of vaccination or induces a humoral response. This study examined whether anti-PEG antibodies before vaccination (pre-existing) influenced the acquisition of SARS-CoV-2 antibodies and evaluated the relationship between the development of anti-SARS-CoV-2 antibodies and anti-PEG antibodies after SARS-CoV-2 vaccination in hematological and autoimmune diseases. Anti-SARS-CoV-2 antibody IgG, anti-PEG IgG, and IgM titers were evaluated in patients with hematological and autoimmune diseases after the second dose of BNT162B2. Anti-PEG IgG and IgM titers were also measured before vaccination to examine changes after vaccination and the relationship with vaccine efficacy. In patients with hematological (n = 182) and autoimmune diseases (n = 96), anti-SARS-CoV-2 and anti-PEG antibody titers were evaluated after a median of 33 days from 2nd vaccination. The median anti-SARS-CoV-2 antibody titers were 1901 AU/mL and 3832 AU/mL in patients with hematological and autoimmune disease, respectively. Multiple regression analysis showed that age and days from 2nd vaccination were negatively associated with anti-SARS-CoV-2 antibody titers. Anti-CD20 antibody treatment was negatively correlated with anti-SARS-CoV-2 antibody titers in hematological disease, and C-reactive protein (CRP) was positively correlated with anti-SARS-CoV-2 antibody titers in autoimmune disease. Baseline anti-PEG antibody titers were significantly higher in patients with autoimmune disease but were not correlated with anti-SARS-CoV-2 antibody titers. Patients with increased anti-PEG IgG acquired higher anti-SARS-CoV-2 antibody titers in patients with autoimmune disease. Anti-SARS-CoV-2 antibody acquisition was suboptimal in patients with hematological disease, but both anti-SARS-CoV-2 antibody and anti-PEG IgG were acquired in patients with autoimmune disease, reflecting robust humoral immune response. Pre-existing anti-PEG antibody titers did not affect anti-SARS-CoV-2 antibody acquisition.
(徳島大学機関リポジトリ): ● Metadata: 119625
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.heliyon.2024.e31489
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38813140; ● Search Scopus @ Elsevier (PMID): 38813140; ● Search Scopus @ Elsevier (DOI): 10.1016/j.heliyon.2024.e31489

(徳島大学機関リポジトリ: 119625, DOI: 10.1016/j.heliyon.2024.e31489, PubMed: 38813140) Shingen Nakamura, Keijiro Hara, Tomoko Kobayashi, Ryohei Sumitani, Masahiro Oura, Yusaku Maeda, Kimiko Sogabe, Hikaru Yagi, Mamiko Takahashi, Shiroh Fujii, Takeshi Harada, Yoshimi Bando, Masahiro Abe and Hirokazu Miki :
Tl uptake and retention mimicking malignant lymphoma in a patient with human immunodeficiency virus infection.,
Parasitology International, Vol.101, 102895, 2024.

(要約): Various opportunistic infections develop during immunodeficiency due to human immunodeficiency virus (HIV) infection. The treatment options for malignant lymphoma (ML) and toxoplasmic encephalitis (TE) are completely different; therefore, their discrimination is critical. A 25-year-old female of foreign nationality had been experiencing headaches for several weeks and suddenly developed convulsions. Brain computed tomography revealed multiple intracranial lesions; therefore, the patient was referred to the neurosurgery department. Brain magnetic resonance imaging (MRI) revealed multiple masses with surrounding edema, accompanied by enhanced contrast. The largest mass (2 cm) in the left occipital lobe exhibited ringed contrast enhancement. Her blood test results showed a CD4 count of 40/μL, positive HIV Ag/Ab, HIV-RNA level of 56 × 10 copies/mL, positive anti-Toxoplasma IgG (63 IU/mL), and negative anti-Toxoplasma IgM. Tl- single photon emission computed tomography (Tl-SPECT) revealed abnormal accumulation only in the tumor in the left occipital lobe (early T/N ratio, 3.034; delayed T/N ratio, 2.738; retention index, 0.9), which was suspected to be a ML. Both tumors, with or without high accumulation of Tl, were subjected to craniotomy biopsy. Pathological examination revealed infiltration of small lymphocytes with a necrotic background. The patient was diagnosed with TE based on a positive result of a tissue polymerase chain reaction test for Toxoplasma gondii. Two weeks after sulfamethoxazole and trimethoprim combination therapy, MRI imaging showed dramatic improvement in multiple brain tumors. This case is atypical because ML was ruled out despite high Tl-SPECT uptake and retention. Careful diagnosis through pathological examination and DNA testing is important.
(キーワード): Humans / Female / Adult / Toxoplasmosis, Cerebral / Lymphoma / HIV Infections / Magnetic Resonance Imaging / Diagnosis, Differential / Tomography, Emission-Computed, Single-Photon / Toxoplasma
(徳島大学機関リポジトリ): ● Metadata: 119634
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.parint.2024.102895
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38614255; ● Search Scopus @ Elsevier (PMID): 38614255; ● Search Scopus @ Elsevier (DOI): 10.1016/j.parint.2024.102895

(徳島大学機関リポジトリ: 119634, DOI: 10.1016/j.parint.2024.102895, PubMed: 38614255) Shin-ichiro Yanagiya, Takeshi Honda, Hiroki Takanari, Kimiko Sogabe, Shingen Nakamura, Yoshimi Bando, Masahiro Abe and Hirokazu Miki :
Raman Microspectroscopy for Label-Free Diagnosis of Amyloid Light-chain Amyloidosis in Various Organs,
Journal of Raman Spectroscopy, 2024.

(キーワード): ラマン顕微分光法 / 全身性アミロイドーシス / タンパク質 (protein) / 光学顕微鏡法
(徳島大学機関リポジトリ): ● Metadata: 119087
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/jrs.6665
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.1002/jrs.6665

(徳島大学機関リポジトリ: 119087, DOI: 10.1002/jrs.6665) Tomoko Maruhashi, Hirokazu Miki, Kimiko Sogabe, Asuka Oda, Ryohei Sumitani, Masahiro Oura, Mamiko Takahashi, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, Kiyoe Kurahashi, Itsuro Endo and Masahiro Abe :
Acute suppression of translation by hyperthermia enhances anti-myeloma activity of carfilzomib,
International Journal of Hematology, Vol.119, No.3, 291-302, 2024.

(要約): Hyperthermia is a unique treatment option for cancers. Multiple myeloma (MM) remains incurable and innovative therapeutic options are needed. We investigated the efficacy of hyperthermia and carfilzomib in combination against MM cells. Although MM cell lines exhibited different susceptibilities to pulsatile carfilzomib treatment, mild hyperthermia at 43℃ induced MM cell death in all cell lines in a time-dependent manner. Hyperthermia and carfilzomib cooperatively induced MM cell death even under suboptimal conditions. The pro-survival mediators PIM2 and NRF2 accumulated in MM cells due to inhibition of their proteasomal degradation by carfilzomib; however, hyperthermia acutely suppressed translation in parallel with phosphorylation of eIF2α to reduce these proteins in MM cells. Recovery of β5 subunit enzymatic activity from its immediate inhibition by carfilzomib was observed at 24 h in carfilzomib-insusceptible KMS-11, OPM-2, and RPMI8226 cells, but not in carfilzomib-sensitive MM.1S cells. However, heat treatment suppressed the recovery of β5 subunit activity in these carfilzomib-insusceptible cells. Therefore, hyperthermia re-sensitized MM cells to carfilzomib. Our results support the treatment of MM with hyperthermia in combination with carfilzomib. Further research is warranted on hyperthermia for drug-resistant extramedullary plasmacytoma.
(キーワード): Humans / Multiple Myeloma / Oligopeptides / Hyperthermia, Induced
(徳島大学機関リポジトリ): ● Metadata: 119321
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s12185-023-03706-8
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38252236; ● Search Scopus @ Elsevier (PMID): 38252236; ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-023-03706-8

(徳島大学機関リポジトリ: 119321, DOI: 10.1007/s12185-023-03706-8, PubMed: 38252236) Kimiko Sogabe, Shingen Nakamura, Yoshiki Higa, Hirokazu Miki, Asuka Oda, Tomoko Maruhashi, Ryohei Sumitani, Masahiro Oura, Mamiko Takahashi, Masafumi Nakamura, Yusaku Maeda, Tomoyo Hara, Hiroki Yamagami, Shiroh Fujii, Kumiko Kagawa, Shuji Ozaki, Kiyoe Kurahashi, Itsuro Endo, Ken-ichi Aihara, Emiko Nakaue, Masahiro Hiasa, Jumpei Teramachi, Takeshi Harada and Masahiro Abe :
Acute accumulation of PIM2 and NRF2 and recovery of β5 subunit activity mitigate multiple myeloma cell susceptibility to proteasome inhibitors.,
International Journal of Hematology, Vol.119, No.3, 303-315, 2024.

(要約): Resistance to proteasome inhibitors (PIs) has emerged as an important clinical issue. We investigated the mechanisms underlying multiple myeloma (MM) cell resistance to PIs. To mimic their pharmacokinetic/pharmacodynamic (PK/PD) profiles, MM cells were treated with bortezomib and carfilzomib for 1 h at concentrations up to 400 and 1,000 nM, respectively. Susceptibility to these PIs markedly varied among MM cell lines. Pulsatile treatments with PIs suppressed translation, as demonstrated by incorporation of puromycin at 24 h in PI-susceptible MM.1S cells, but not PI-resistant KMS-11 cells. Inhibition of β5 subunit activity decreased at 24 h in KMS-11 cells, even with the irreversible PI carfilzomib, but not under suppression of protein synthesis with cycloheximide. Furthermore, the proteasome-degradable pro-survival factors PIM2 and NRF2 acutely accumulated in MM cells subjected to pulsatile PI treatments. Accumulated NRF2 was trans-localized into the nucleus to induce the expression of its target gene, HMOX1, in MM cells. PIM and Akt inhibition restored the anti-MM effects of PIs, even against PI-resistant KMS-11 cells. Collectively, these results suggest that increased synthesis of β5 proteasome subunit and acute accumulation of PIM2 and NRF2 reduce the anti-MM effects of PIs.
(キーワード): Humans / Proteasome Inhibitors / NF-E2-Related Factor 2 / Multiple Myeloma / Proteasome Endopeptidase Complex / Drug Resistance, Neoplasm / Cell Line, Tumor / Bortezomib / Antineoplastic Agents / Proto-Oncogene Proteins / Protein Serine-Threonine Kinases
(徳島大学機関リポジトリ): ● Metadata: 119384
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s12185-023-03705-9
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38245883; ● Search Scopus @ Elsevier (PMID): 38245883; ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-023-03705-9

(徳島大学機関リポジトリ: 119384, DOI: 10.1007/s12185-023-03705-9, PubMed: 38245883) Hiroki Yamagami, Tomoyo Hara, Saya Yasui, Minae Hosoki, Taiki Hori, Yousuke Kaneko, Yukari Mitsui, Kiyoe Kurahashi, Takeshi Harada, Sumiko Yoshida, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara :
Cross-Sectional and Longitudinal Associations between Skin Autofluorescence and Tubular Injury Defined by Urinary Excretion of Liver-Type Fatty Acid-Binding Protein in People with Type 2 Diabetes.,
Biomedicines, Vol.11, No.11, 3020, 2023.

(要約): = 0.026). In conclusion, SAF is positively correlated with uL-FABP but not with uACR in people with T2D. Thus, there is a possibility that SAF can serve as a novel predictor for the development of diabetic tubular injury.
(キーワード): skin autofluorescence / type 2 diabetes / diabetic kidney disease / albuminuria / tubular injury / L-FABP
(徳島大学機関リポジトリ): ● Metadata: 119108
(出版サイトへのリンク): ● Publication site (DOI): 10.3390/biomedicines11113020
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38002020; ● CiNii @ 国立情報学研究所 (CRID): 1050581224891895040; ● Summary page in Scopus @ Elsevier: 2-s2.0-85178346619

(徳島大学機関リポジトリ: 119108, DOI: 10.3390/biomedicines11113020, PubMed: 38002020, CiNii: 1050581224891895040, Elsevier: Scopus) Masahiro Oura, Takeshi Harada, Asuka Oda, Jumpei Teramachi, Atsushi Nakayama, Ryohei Sumitani, Yusuke Inoue, Yusaku Maeda, Kimiko Sogabe, Maruhashi Tomoko, Mamiko Takahashi, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Shingen Nakamura, Tomoyo Hara, Hiroki Yamagami, Kiyoe Kurahashi, Itsuro Endo, Hiroo Hasegawa, Hiroshi Fujiwara and Masahiro Abe :
Therapeutic efficacy of the resorcylic acid lactone LL-Z1640-2 for adult T-cell leukaemia/lymphoma,
eJHaem, Vol.4, No.3, 667-678, 2023.

(要約): Adult T-cell leukaemia/lymphoma (ATL) remains incurable. The NF-κB and interferon regulatory factor 4 (IRF4) signalling pathways are among the critical survival pathways for the progression of ATL. TGF-β-activated kinase 1 (TAK1), an IκB kinase-activating kinase, triggers the activation of NF-κB. The resorcylic acid lactone LL-Z1640-2 is a potent irreversible inhibitor of TAK1/extracellular signal-regulated kinase 2 (ERK2). We herein examined the therapeutic efficacy of LL-Z1640-2 against ATL. LL-Z1640-2 effectively suppressed the in vivo growth of ATL cells. It induced in vitro apoptosis and inhibited the nuclear translocation of p65/RelA in ATL cells. The knockdown of strongly induced ATL cell death while downregulating MYC. LL-Z1640-2 as well as the NF-κB inhibitor BAY11-7082 decreased the expression of IRF4 and MYC at the protein and mRNA levels, indicating the suppression of the NF-κB-IRF4-MYC axis. The treatment with LL-Z1640-2 also mitigated the phosphorylation of p38 MAPK along with the expression of CC chemokine receptor 4. Furthermore, the inhibition of STAT3/5 potentiated the cytotoxic activity of LL-Z1640-2 against IL-2-responsive ATL cells in the presence of IL-2. Therefore, LL-Z1640-2 appears to be an effective treatment for ATL. Further studies are needed to develop more potent compounds that retain the active motifs of LL-Z1640-2.
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/jha2.758
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37601887; ● Search Scopus @ Elsevier (PMID): 37601887; ● Search Scopus @ Elsevier (DOI): 10.1002/jha2.758

(DOI: 10.1002/jha2.758, PubMed: 37601887) Shotaro Haji, Ryosuke Miyamoto, Hiroyuki Morino, Yusuke Osaki, Seijiro Tsuji, Ichizo Nishino, Masahiro Abe and Yuishin Izumi :
Autosomal Recessive Spinocerebellar Ataxia Type 9 With a Response to Phosphate Repletion: A Case Report.,
Neurology. Genetics, Vol.9, No.3, e200070, 2023.

(要約): This provides Class IV evidence. This is a single observational study without controls.
(出版サイトへのリンク): ● Publication site (DOI): 10.1212/NXG.0000000000200070
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37529414; ● Search Scopus @ Elsevier (PMID): 37529414; ● Search Scopus @ Elsevier (DOI): 10.1212/NXG.0000000000200070

(DOI: 10.1212/NXG.0000000000200070, PubMed: 37529414) Shiho Masuda, Tomoyo Hara, Hiroki Yamagami, Yukari Mitsui, Kiyoe Kurahashi, Sumiko Yoshida, Takeshi Harada, Toshiki Otoda, Tomoyuki Yuasa, Shingen Nakamura, Akio Kuroda, Itsuro Endo, Toshio Matsumoto, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara :
Vascular Endothelial Function Is Associated with eGFR Slope in Female and Non-Smoking Male Individuals with Cardiovascular Risk Factors: A Pilot Study on the Predictive Value of FMD for Renal Prognosis.,
Journal of Atherosclerosis and Thrombosis, 2023.

(要約): In individuals with cardiovascular risk factors, evaluation of vascular endothelial function enables prediction of renal prognosis in females and non-smoking males.
(徳島大学機関リポジトリ): ● Metadata: 118250
(出版サイトへのリンク): ● Publication site (DOI): 10.5551/jat.63987
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37081616; ● Search Scopus @ Elsevier (PMID): 37081616; ● Search Scopus @ Elsevier (DOI): 10.5551/jat.63987

(徳島大学機関リポジトリ: 118250, DOI: 10.5551/jat.63987, PubMed: 37081616) Emiko Nakaue, Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Takeshi Harada, Asuka Oda, Yusuke Inoue, Sou Shimizu, Yoshiki Higa, Kimiko Sogabe, Masahiro Oura, Tomoyo Hara, Ryohei Sumitani, Tomoko Maruhashi, Hiroki Yamagami, Itsuro Endo, Eiji Tanaka and Masahiro Abe :
Mechanisms of preferential bone formation in myeloma bone lesions by proteasome inhibitors.,
International Journal of Hematology, 2023.

(要約): Proteasome inhibitors (PIs) can preferentially restore bone in bone-defective lesions of patients with multiple myeloma (MM) who respond favorably to these drugs. Most prior in vitro studies on PIs used continuous exposure to low PI concentrations, although pharmacokinetic analysis in patients has shown that serum concentrations of PIs change in a pulsatile manner. In the present study, we explored the effects of pulsatile treatment with PIs on bone metabolism to simulate in vivo PI pharmacokinetics. Pulsatile treatment with bortezomib, carfilzomib, or ixazomib induced MM cell death but only marginally affected the viability of osteoclasts (OCs) with F-actin ring formation. Pulsatile PI treatment suppressed osteoclastogenesis in OC precursors and bone resorption by mature OCs. OCs robustly enhanced osteoblastogenesis in cocultures with OCs and MC3T3-E1 pre-osteoblastic cells, indicating OC-mediated coupling to osteoblastogenesis. Importantly, pulsatile PI treatment did not impair robust OC-mediated osteoblastogenesis. These results suggest that PIs might sufficiently reduce MM cell-derived osteoblastogenesis inhibitors to permit OC-driven bone formation coupling while suppressing OC differentiation and activity in good responders to PIs. OC-mediated coupling to osteoblastogenesis appears to be a predominant mechanism for preferential occurrence of bone regeneration at sites of osteoclastic bone destruction in good responders.
(徳島大学機関リポジトリ): ● Metadata: 118380
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s12185-023-03601-2
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37039914; ● Search Scopus @ Elsevier (PMID): 37039914; ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-023-03601-2

(徳島大学機関リポジトリ: 118380, DOI: 10.1007/s12185-023-03601-2, PubMed: 37039914) Takeshi Harada, Hiroto Ohguchi, Asuka Oda, Michiyasu Nakao, Jumpei Teramachi, Masahiro Hiasa, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Tomoko Maruhashi, Mamiko Takahashi, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Shuji Ozaki, Shigeki Sano, Teru Hideshima and Masahiro Abe :
Novel antimyeloma therapeutic option with inhibition of the HDAC1-IRF4 axis and PIM kinase,
Blood Advances, Vol.7, No.6, 1019-1032, 2023.

(要約): Multiple myeloma (MM) preferentially expands and acquires drug resistance in the bone marrow (BM). We herein examined the role of histone deacetylase 1 (HDAC1) in the constitutive activation of the master transcription factor IRF4 and the prosurvival mediator PIM2 kinase in MM cells. The knockdown or inhibition of HDAC1 by the class I HDAC inhibitor MS-275 reduced the basal expression of IRF4 and PIM2 in MM cells. Mechanistically, the inhibition of HDAC1 decreased IRF4 transcription through histone hyperacetylation and inhibiting the recruitment of RNA polymerase II at the IRF4 locus, thereby reducing IRF4-targeting genes, including PIM2. In addition to the transcriptional regulation of PIM2 by the HDAC1-IRF4 axis, PIM2 was markedly upregulated by external stimuli from BM stromal cells and interleukin-6 (IL-6). Upregulated PIM2 contributed to the attenuation of the cytotoxic effects of MS-275. Class I HDAC and PIM kinase inhibitors cooperatively suppressed MM cell growth in the presence of IL-6 and in vivo. Therefore, the present results demonstrate the potential of the simultaneous targeting of the intrinsic HDAC1-IRF4 axis plus externally activated PIM2 as an efficient therapeutic option for MM fostered in the BM.
(キーワード): Histone Deacetylase 1 / Interleukin-6 / Benzamides / Pyridines
(徳島大学機関リポジトリ): ● Metadata: 118211
(出版サイトへのリンク): ● Publication site (DOI): 10.1182/bloodadvances.2022007155
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36129197; ● Search Scopus @ Elsevier (PMID): 36129197; ● Search Scopus @ Elsevier (DOI): 10.1182/bloodadvances.2022007155

(徳島大学機関リポジトリ: 118211, DOI: 10.1182/bloodadvances.2022007155, PubMed: 36129197) Taiki Hori, Shingen Nakamura, Hiroki Yamagami, Saya Yasui, Minae Hosoki, Tomoyo Hara, Yukari Mitsui, Shiho Masuda, Kiyoe Kurahashi, Sumiko Yoshida, Takeshi Harada, Akio Kuroda, Toshiki Otoda, Tomoyuki Yuasa, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara :
Phase angle and extracellular water-to-total body water ratio estimated by bioelectrical impedance analysis are associated with levels of hemoglobin and hematocrit in patients with diabetes.,
Heliyon, Vol.9, No.4, 2023.

(要約): PhA and ECW/TBW but not SMI were associated with levels of Hgb and Hct in patients with diabetes. Therefore, aberrant values of PhA and ECW/TBW suggest a risk of anemia in diabetic patients.
(徳島大学機関リポジトリ): ● Metadata: 118251
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.heliyon.2023.e14724
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37057050; ● Search Scopus @ Elsevier (PMID): 37057050; ● Search Scopus @ Elsevier (DOI): 10.1016/j.heliyon.2023.e14724

(徳島大学機関リポジトリ: 118251, DOI: 10.1016/j.heliyon.2023.e14724, PubMed: 37057050) Jumpei Teramachi, Hirokazu Miki, Shingen Nakamura, Masahiro Hiasa, Takeshi Harada and Masahiro Abe :
Myeloma bone disease: pathogenesis and management in the era of new anti-myeloma agents.,
Journal of Bone and Mineral Metabolism, 1-16, 2023.

(要約): MM cells produce a variety of cytokines to stimulate receptor activator of nuclear factor-κB ligand-mediated osteoclastogenesis and suppress osteoblastic differentiation from bone marrow stromal cells, leading to extensive bone destruction with rapid loss of bone. MM cells alter the microenvironment through bone destruction where they colonize, which in turn favors tumor growth and survival, thereby forming a vicious cycle between tumor progression and bone destruction. Denosumab or zoledronic acid is currently recommended to be administered at the start of treatment in newly diagnosed patients with MM with bone disease. Proteasome inhibitors and the anti-CD38 monoclonal antibody daratumumab have been demonstrated to exert bone-modifying activity in responders. Besides their anti-tumor activity, the effects of new anti-MM agents on bone metabolism should be more precisely analyzed in patients with MM. Because prognosis in patients with MM has been significantly improved owing to the implementation of new agents, the therapeutic impact of bone-modifying agents should be re-estimated in the era of these new agents.
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s00774-023-01403-4
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36856824; ● Search Scopus @ Elsevier (PMID): 36856824; ● Search Scopus @ Elsevier (DOI): 10.1007/s00774-023-01403-4

(DOI: 10.1007/s00774-023-01403-4, PubMed: 36856824) Yoshiki Higa, Masahiro Hiasa, Hirofumi Tenshin, Emiko Nakaue, Mariko Tanaka, Sooha Kim, Motosumi Nakagawa, Sou Shimizu, Kotaro Tanimoto, Jumpei Teramachi, Takeshi Harada, Asuka Oda, Masahiro Oura, Kimiko Sogabe, Tomoyo Hara, Ryohei Sumitani, Tomoko Maruhashi, Hiroki Yamagami, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe :
The Xanthine Oxidase Inhibitor Febuxostat Suppresses Adipogenesis and Activates Nrf2.,
Antioxidants, Vol.12, No.1, 2023.

(要約): Xanthine oxidoreductase (XOR) is a rate-limiting enzyme in purine catabolism that acts as a novel regulator of adipogenesis. In pathological states, xanthine oxidoreductase activity increases to produce excess reactive oxygen species (ROS). The nuclear factor erythroid 2-related factor 2 (Nrf2) is a critical inducer of antioxidants, which is bound and repressed by a kelch-like ECH-associated protein 1 (Keap1) in the cytoplasm. The Keap1-Nrf2 axis appears to be a major mechanism for robust inducible antioxidant defenses. Here, we demonstrate that febuxostat, a xanthine oxidase inhibitor, alleviates the increase in adipose tissue mass in obese mouse models with a high-fat diet or ovariectomy. Febuxostat disrupts in vitro adipocytic differentiation in adipogenic media. Adipocytes appeared at day 7 in absence or presence of febuxostat were 160.8 ± 21.2 vs. 52.5 ± 12.7 (p < 0.01) in 3T3L1 cells, and 126.0 ± 18.7 vs. 55.3 ± 13.4 (p < 0.01) in 10T1/2 cells, respectively. Adipocyte differentiation was further enhanced by the addition of hydrogen peroxide, which was also suppressed by febuxostat. Interestingly, febuxostat, but not allopurinol (another xanthine oxidase inhibitor), rapidly induced the nuclear translocation of Nrf2 and facilitated the degradation of Keap1, similar to the electrophilic Nrf2 activator omaveloxolone. These results suggest that febuxostat alleviates adipogenesis under oxidative conditions, at least in part by suppressing ROS production and Nrf2 activation. Regulation of adipocytic differentiation by febuxostat is expected to inhibit obesity due to menopause or overeating.
(徳島大学機関リポジトリ): ● Metadata: 118313
(出版サイトへのリンク): ● Publication site (DOI): 10.3390/antiox12010133
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36670994; ● Search Scopus @ Elsevier (PMID): 36670994; ● Search Scopus @ Elsevier (DOI): 10.3390/antiox12010133

(徳島大学機関リポジトリ: 118313, DOI: 10.3390/antiox12010133, PubMed: 36670994) Taiki Hori, Saya Yasui, Minae Hosoki, Hiroki Yamagami, Toshiki Otoda, Tomoyuki Yuasa, Kenichi Aihara, Makoto Takishita, Akihiko Yokohama, Mitusharu Ueda, Masahiro Abe and Shingen Nakamura :
Systemic amyloidosis associated with non-IgM type paraprotein with lymphoplasmacytic lymphoma,
International Journal of Myeloma, Vol.13, No.2, 7-12, 2023.

(徳島大学機関リポジトリ): ● Metadata: 118610
(出版サイトへのリンク): ● Publication site (DOI): 10.57352/ijm.13.2_7
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.57352/ijm.13.2_7

(徳島大学機関リポジトリ: 118610, DOI: 10.57352/ijm.13.2_7) 高原由実子, 三木浩和, 中村信元, 林成樹, 住谷龍平, 大浦雅博, 曽我部公子, 髙橋真美子, 丸橋朋子, 富永誠記, 岡本秀樹, 岡田直人, 矢野由美子, 高橋真理, 大坂朱美, 原田武志, 藤井志朗, 菅俊行, 青田桂子, 尾崎修治, 安倍正博 :
徳島県におけるHIV感染症および後天性免疫不全症候群患者の臨床的特徴と今後の課題,
四国医学雑誌, Vol.78, No.5-6, 193-198, 2022年.

(要約): 【Introduction】The survival rate in patients with HIV infection and acquired immunodeficiency syndrome (AIDS) has been improved dramatically due to the advances in anti-HIV drug therapy, while aging-associated complications become a critical issue. The incidence of sudden occurrence of AIDS without prior detection of HIV infection, so called ``Ikinari AIDS'', still remains high. 【Objective】We retrospectively analyzed the incidence and clinical characteristics of HIV/AIDS patients in both Tokushima University Hospital and Tokushima Prefectural Central Hospital. 【Results】Eighty four patients (74 males and 10 females) with a median age of 39 years old (range 16 - 85) were enrolled. Thirty-four patients (40.5%) were diagnosed with ``Ikinari AIDS'' from 2001 to 2020. All 4 patients were diagnosed with ``Ikinari AIDS'' after 2020. AIDS-defining illnesses were diagnosed as follows ; pneumocystis pneumonia in 21 cases, CMV infection in 8 cases and candidiasis in 6 cases. All patients over 60 years old were suffered from AIDS. Other complications included syphilis in 17 cases, hepatitis B infection in 12 and herpes zoster in 7. 【Discussion/Conclusion】In Tokushima, the incidence rate of ``Ikinari AIDS'' appeared to be higher than that of national average. COVID - 19 pandemic hampered the public health care services of awareness-raising activity for HIV infection and telephone consultations about HIV, which may become more lease asymptomatic HIV patients without diagnosis. For early diagnosis of HIV/AIDS, it is becoming more important to share information to make early screening of HIV infection among medical staffs, such as medical doctors, dentists, nurses, pharmacists and MSWs.
(キーワード): HIV / AIDS / Ikinari AIDS
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1050295181679877760

(CiNii: 1050295181679877760) Bingzi Dong, Masahiro Hiasa, Yoshiki Higa, Yukiyo Ohnishi, Itsuro Endo, Takeshi Kondo, Yuichi Takashi, Maria Tsoumpra, Risa Kainuma, Shun Sawatsubashi, Hiroshi Kiyonari, Go Shioi, Hiroshi Sakaue, Tomoki Nakashima, Shigeaki Kato, Masahiro Abe, Seiji Fukumoto and Toshio Matsumoto :
Osteoblast/osteocyte-derived interleukin-11 regulates osteogenesis and systemic adipogenesis.,
Nature Communications, Vol.13, No.1, 2022.

(要約): did not exhibit any abnormalities. We demonstrate that osteoblast/osteocyte-derived IL-11 controls both osteogenesis and systemic adiposity in response to mechanical loading, an important insight for our understanding of osteoporosis and metabolic syndromes.
(キーワード): Animals / Mice / Adipogenesis / Interleukin-11 / Obesity / Osteoblasts / Osteocytes / Osteogenesis / Mice, Knockout
(徳島大学機関リポジトリ): ● Metadata: 118940
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/s41467-022-34869-3
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36424386; ● Search Scopus @ Elsevier (PMID): 36424386; ● Search Scopus @ Elsevier (DOI): 10.1038/s41467-022-34869-3

(徳島大学機関リポジトリ: 118940, DOI: 10.1038/s41467-022-34869-3, PubMed: 36424386) 板東真由, 峯田一秀, 長坂信司, 山下雄太郎, 安倍吉郎, 藤井志郎, 板東良美, 安倍正博, 橋本一郎 :
BIA ALCLを疑い検査を施行した乳房インプラント破損の2症例,
第10回日本乳房オンコプラスティックサージャリー学会総会, 2022年. Tomoyo Hara, Ryoko Uemoto, Akiko Sekine, Yukari Mitsui, Shiho Masuda, Hiroki Yamagami, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Yasumasa Ikeda, Itsuro Endo, Soichi Honda, Katsuhiko Yoshimoto, Akira Kondo, Toshiaki Tamaki, Toshio Matsumoto, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara :
Plasma Heparin Cofactor II Activity Is Inversely Associated with Hepatic Fibrosis of Non-Alcoholic Fatty Liver Disease in Patients with Type 2 Diabetes Mellitus.,
Journal of Atherosclerosis and Thrombosis, 2022.

(要約): Multiple regression analysis including confounding factors showed that plasma HCII activity independently contributed to decreases in FIB-4 index (p<0.001), NFS (p<0.001) and APRI (p=0.004). In addition, logistic regression analysis for the prevalence of advanced hepatic fibrosis defined by the cutoff points of the clinical scores showed that plasma HCII activity was the sole and common negative factor for prevalence of advanced hepatic fibrosis (FIB-4 index: p=0.002, NFS: p=0.026 and APRI: p=0.012).
(徳島大学機関リポジトリ): ● Metadata: 118258
(出版サイトへのリンク): ● Publication site (DOI): 10.5551/jat.63752
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36244745; ● Search Scopus @ Elsevier (PMID): 36244745; ● Search Scopus @ Elsevier (DOI): 10.5551/jat.63752

(徳島大学機関リポジトリ: 118258, DOI: 10.5551/jat.63752, PubMed: 36244745) Shingen Nakamura, Motoki Sugasaki, Masayoshi Souri, Hirohito Akazawa, Maiko Sogawa, Taiki Hori, Hiroki Yamagami, Makoto Takishita, Ken-ichi Aihara, Masahiro Abe, Atsushi Yasumoto, Eriko Morishita and Akitada Ichinose :
Autoimmune Acquired Factor XIII/13 Deficiency after SARS-CoV-2 mRNA Vaccination.,
Thrombosis and Haemostasis, 2022.

(徳島大学機関リポジトリ): ● Metadata: 118345
(出版サイトへのリンク): ● Publication site (DOI): 10.1055/a-1863-7265
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35636450; ● Search Scopus @ Elsevier (PMID): 35636450; ● Search Scopus @ Elsevier (DOI): 10.1055/a-1863-7265

(徳島大学機関リポジトリ: 118345, DOI: 10.1055/a-1863-7265, PubMed: 35636450) Naoto Okada, Akikazu Murakami, Masami Satou, Shingen Nakamura, Shiroh Fujii, Kimiko Sogabe, Mamiko Takahashi, Asami Okada, Akane Abe, Hideki Fujii, Masahiro Abe, Momoyo Azuma and Keisuke Ishizawa :
First reported case of Lachnoanaerobaculum gingivalis bacteremia in an acute myeloid leukemia patient with oral mucositis during high dose chemotherapy.,
Anaerobe, Vol.76, 2022.

(要約): During chemotherapy in patients with oral mucositis, we should consider the possibility of L. gingivalis bacteremia.
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.anaerobe.2022.102610
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35811059; ● Search Scopus @ Elsevier (PMID): 35811059; ● Search Scopus @ Elsevier (DOI): 10.1016/j.anaerobe.2022.102610

(DOI: 10.1016/j.anaerobe.2022.102610, PubMed: 35811059) Hiroki Yamada, Rio Ohmori, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato :
A machine learning model using SNPs obtained from a genome-wide association study predicts the onset of vincristine-induced peripheral neuropathy,
The Pharmacogenomics Journal, 2022.

(要約): Vincristine treatment may cause peripheral neuropathy. In this study, we identified the genes associated with the development of peripheral neuropathy due to vincristine therapy using a genome-wide association study (GWAS) and constructed a predictive model for the development of peripheral neuropathy using genetic information-based machine learning. The study included 72 patients admitted to the Department of Hematology, Tokushima University Hospital, who received vincristine. Of these, 56 were genotyped using the Illumina Asian Screening Array-24 Kit, and a GWAS for the onset of peripheral neuropathy caused by vincristine was conducted. Using Sanger sequencing for 16 validation samples, the top three single nucleotide polymorphisms (SNPs) associated with the onset of peripheral neuropathy were determined. Machine learning was performed using the statistical software R package "caret". The 56 GWAS and 16 validation samples were used as the training and test sets, respectively. Predictive models were constructed using random forest, support vector machine, naive Bayes, and neural network algorithms. According to the GWAS, rs2110179, rs7126100, and rs2076549 were associated with the development of peripheral neuropathy on vincristine administration. Machine learning was performed using these three SNPs to construct a prediction model. A high accuracy of 93.8% was obtained with the support vector machine and neural network using rs2110179 and rs2076549. Thus, peripheral neuropathy development due to vincristine therapy can be effectively predicted by a machine learning prediction model using SNPs associated with it.
(徳島大学機関リポジトリ): ● Metadata: 117583
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/s41397-022-00282-8
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35752658; ● Search Scopus @ Elsevier (PMID): 35752658; ● Search Scopus @ Elsevier (DOI): 10.1038/s41397-022-00282-8

(徳島大学機関リポジトリ: 117583, DOI: 10.1038/s41397-022-00282-8, PubMed: 35752658) Sou Shimizu, Jumpei Teramachi, Takeshi Harada, Masahiro Hiasa, Hirofumi Tenshin, A Oda, A Seki, Y Inoue, Kotaro Tanimoto, Yoshiki Higa, M Oura, K Sogabe, Takeshi Harada, Ryohei Sumitani, T Maruhashi, H Yamagami, Y Sawa, Itsuro Endo, K Tsuneyama, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe :
Aberrant upregulation of the endogenous PP2A inhibitor CIP2A is vital for myeloma cell growth and survival,
International Journal of Myeloma, Vol.12, No.2, 14-23, 2022.

(要約): The serine/threonine kinase TAK1 is constitutively overexpressed and auto-phosphorylated in multiple myeloma (MM) cells. Protein phosphatase 2A (PP2A) is a major serine/threonine phosphatase which dephosphorylates proteins phosphorylated by various serine/threonine kinases to regulate multiple cellular functions. We recently reported that the serine/threonine kinase TGF-β-activated kinase-1 (TAK1) is highly expressed and auto-phosphorylated to mediate critical growth and survival signaling in MM cells. We demonstrate here that regulation of PP2A activity inversely affects the phosphorylation levels of TAK1 in MM cells, and that MM cells aberrantly overexpress cancerous inhibitor of PP2A (CIP2A), an endogenous inhibitor for PP2A. CIP2A gene silencing as well as treatment with the CIP2A inhibitor TD52 potently induced MM cell death along with suppression of TAK1 expression in MM cells. These results suggest the critical role of PP2A inactivation via CIP2A upregulation in TAK1 phosphorylation and its protein expression and thereby MM cell growth and survival, posing the CIP2A-PP2A axis as an important therapeutic target.
(キーワード): multiple myeloma / TAK1 / CIP2A / PP2A (PP2A)
(徳島大学機関リポジトリ): ● Metadata: 117150
(出版サイトへのリンク): ● Publication site (DOI): 10.57352/ijm.12.2_14
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390573947533793024; ● Search Scopus @ Elsevier (DOI): 10.57352/ijm.12.2_14

(徳島大学機関リポジトリ: 117150, DOI: 10.57352/ijm.12.2_14, CiNii: 1390573947533793024) Shin Kondo, Tatsuro Inoue, Takashi Saito, Yuka Kawamura, Ayane Katayama, Masafumi Nakamura, Ryohei Sumitani, Mamiko Takahashi, Masahiro Oura, Kimiko Sogabe, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Nori Sato, Rei Ono, Masahiro Abe and Shinsuke Katoh :
Allogeneic haematopoietic stem cell transplantation and patient falls: impact of lower extremity muscle strength.,
BMJ Supportive & Palliative Care, 2022.

(要約): Pretransplant LEMS was a significant predictor of post-transplant falls. The results of this study may help to prevent falls in patients undergoing allo-HSCT.
(出版サイトへのリンク): ● Publication site (DOI): 10.1136/bmjspcare-2022-003582
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35534187; ● Search Scopus @ Elsevier (PMID): 35534187; ● Search Scopus @ Elsevier (DOI): 10.1136/bmjspcare-2022-003582

(DOI: 10.1136/bmjspcare-2022-003582, PubMed: 35534187) Asami Okada, Misuzu Yamada-Yamashita, Yukari Tominaga, Kyoka Jo, Hiroyasu Mori, Reiko Suzuki, Masashi Ishizu, Motoyuki Tamaki, Yuko Akehi, Yuichi Takashi, Daisuke Koga, Eisuke Shimokita, Fuminori Tanihara, Kiyoe Kurahashi, Sumiko Yoshida, Yukari Mitsui, Shiho Masuda, Itsuro Endo, Ken-ichi Aihara, Shoji Kagami, Masahiro Abe, Kevin Ferreri, Yoshio Fujitani, Munehide Matsuhisa and Akio Kuroda :
Novel method utilizing bisulfite conversion with dual amplification-refractory mutation system polymerase chain reaction to detect circulating pancreatic β-cell cfDNA.,
Journal of Diabetes Investigation, Vol.13, No.7, 1140-1148, 2022.

(要約): We developed a novel method for detecting unmethylated insulin DNA in circulation that can be performed using a conventional real-time PCR system. This method would be useful for analyzing dynamic profiles of β-cells in human disease such as type 1 diabetes.
(徳島大学機関リポジトリ): ● Metadata: 117206
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/jdi.13806
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35396829; ● Search Scopus @ Elsevier (PMID): 35396829; ● Search Scopus @ Elsevier (DOI): 10.1111/jdi.13806

(徳島大学機関リポジトリ: 117206, DOI: 10.1111/jdi.13806, PubMed: 35396829) Kotaro Tanimoto, Masahiro Hiasa, Hirofumi Tenshin, Jumpei Teramachi, Asuka Oda, Takeshi Harada, Yoshiki Higa, Kimiko Sogabe, Masahiro Oura, Ryohei Sumitani, Tomoyo Hara, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe :
Mechanical unloading aggravates bone destruction and tumor expansion in myeloma.,
Haematologica, Vol.107, No.3, 744-749, 2022.

(キーワード): Bone Resorption / Humans / Multiple Myeloma / Osteoclasts / Osteolysis
(徳島大学機関リポジトリ): ● Metadata: 116715
(出版サイトへのリンク): ● Publication site (DOI): 10.3324/haematol.2021.278295
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34788982; ● Search Scopus @ Elsevier (PMID): 34788982; ● Search Scopus @ Elsevier (DOI): 10.3324/haematol.2021.278295

(徳島大学機関リポジトリ: 116715, DOI: 10.3324/haematol.2021.278295, PubMed: 34788982) Yukari Mitsui, Akio Kuroda, Masashi Ishizu, Hiroyasu Mori, Kiyoe Kurahashi, Takeshi Kondo, Sumiko Yoshida, Yuko Akehi, Ken-ichi Aihara, Itsuro Endo, Masahiro Abe and Munehide Matsuhisa :
Basal insulin requirement in patients with type 1 diabetes depends on the age and body mass index.,
Journal of Diabetes Investigation, Vol.13, No.2, 292-298, 2022.

(要約): T
(徳島大学機関リポジトリ): ● Metadata: 116546
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/jdi.13547
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33740836; ● Search Scopus @ Elsevier (PMID): 33740836; ● Search Scopus @ Elsevier (DOI): 10.1111/jdi.13547

(徳島大学機関リポジトリ: 116546, DOI: 10.1111/jdi.13547, PubMed: 33740836) Hirofumi Tenshin, Jumpei Teramachi, Mohannad Ashtar, Masahiro Hiasa, Yusuke Inoue, Asuka Oda, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Tomoyo Hara, Ryohei Sumitani, Tomoko Maruhashi, Mayu Sebe, Rie Tsutsumi, Hiroshi Sakaue, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe :
TGF-β-activated kinase-1 inhibitor LL-Z1640-2 reduces joint inflammation and bone destruction in mouse models of rheumatoid arthritis by inhibiting NLRP3 inflammasome, TACE, TNF-α and RANKL expression.,
Clinical & translational immunology, Vol.11, No.1, 2022.

(要約): TAK1 inhibition with LLZ may become a novel treatment strategy to effectively alleviate inflammasome-mediated inflammation and RANKL-induced osteoclastic bone destruction in joints alongside its potent suppression of TNF-α and IL-6 production and proteinase-mediated pathological processes in RA.
(徳島大学機関リポジトリ): ● Metadata: 117260
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/cti2.1371
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35079379; ● Search Scopus @ Elsevier (PMID): 35079379; ● Search Scopus @ Elsevier (DOI): 10.1002/cti2.1371

(徳島大学機関リポジトリ: 117260, DOI: 10.1002/cti2.1371, PubMed: 35079379) Minori Takei, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato :
A genome-wide association study predicts the onset of dysgeusia due to anti-cancer drug treatment,
Biological & Pharmaceutical Bulletin, Vol.45, No.1, 114-117, 2022.

(要約): Dysgeusia is a major side effect of anti-cancer drug treatment. Since dysgeusia significantly lowers the patient's QOL, predicting and avoiding its onset in advance is desirable. Accordingly, aims of the present study were to use a genome-wide association study (GWAS) to identify genes associated with the development of dysgeusia in patients taking anti-cancer drugs and to predict the development of dysgeusia using associated single nucleotide polymorphisms (SNPs). GWAS was conducted on 76 patients admitted to the Department of Hematology, Tokushima University Hospital. Using Sanger sequencing for 23 separately collected validation samples, the top two SNPs associated with the development of dysgeusia were determined. GWAS identified rs73049478 and rs41396146 SNPs on the retinoic acid receptor beta (RARB) gene associated with dysgeusia development due to the administration of anti-cancer drugs. Evaluation of the two SNPs using 23 validation samples indicated that the accuracy rate of rs73049478 was relatively high (87.0%). Thus, the findings of the present study suggest that the rs73049478 SNP of RARB can be used to predict the onset of dysgeusia caused by the administration of anti-cancer drugs.
(キーワード): Antineoplastic Agents / Dysgeusia / Genetic Predisposition to Disease / Genome-Wide Association Study / Humans / Pharmaceutical Preparations / Polymorphism, Single Nucleotide / Quality of Life
(徳島大学機関リポジトリ): ● Metadata: 117584
(出版サイトへのリンク): ● Publication site (DOI): 10.1248/bpb.b21-00745
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34657909; ● CiNii @ 国立情報学研究所 (CRID): 1390290617368322560; ● Summary page in Scopus @ Elsevier: 2-s2.0-85123201593

(徳島大学機関リポジトリ: 117584, DOI: 10.1248/bpb.b21-00745, PubMed: 34657909, CiNii: 1390290617368322560, Elsevier: Scopus) Yukari Mitsui, Yuto Iizuka, Tomoaki Tanaka, Tomoyo Hara, Shiho Masuda, Yukiyo Ohnishi, Mai Kanai, Kiyoe Kurahashi, Sumiko Yoshida, Takeshi Kondo, Toshiko Kanezaki, Yasumi Shintani, Hiroki Yamagami, Hiroyuki Yamaguchi, Yuichi Fujinaka, Kana Morimoto, Atsuhisa Shirakami, Ken-ichi Aihara, Seiji Fukumoto, Masahiro Abe and Itsuro Endo :
An attempt to create a treatment algorithm of central adrenal insufficiency using CRH test, DHEA-S and clinical evaluation.,
The Journal of Medical Investigation : JMI, Vol.69, No.3.4, 287-293, 2022.

(要約): Objective : To examine diagnostic performance of corticotropin-releasing hormone (CRH) test combined with baseline dehydroepiandrosterone sulfate (DHEA-S) in patients with a suspect of central adrenal insufficiency. Methods : Patients (n=215) requiring daily or intermittent hydrocortisone replacement, or no replacement were retrospectively checked with their peak cortisol after CRH test and baseline DHEA-S. Results : None of 106 patients with the peak cortisol · 17.5 g /L after CRH test required replacement, and all 64 patients with the peak cortisol < 10.0 g /L required daily replacement. Among 8 patients with 10.0 g /L the peak cortisol < 17.5 g /L and baseline DHEA-S below the reference range, 6 patients required daily replacement and 1 patient was under intermittent replacement. Among 37 patients with 10.0 g /L the peak cortisol < 17.5 g /L and baseline DHEA-S within the reference range, 10 and 6 patients were under intermittent and daily replacement, respectively. Conclusions : No patients with the peak cortisol · 17.5 g /L required hydrocortisone replacement, and all patients with the peak cortisol below 10.0 g /L required daily replacement. Careful clinical evaluation was required to determine requirement for replacement in patients with 10.0 g /L the peak cortisol < 17.5 g /L even in combination with baseline DHEA-S. J. Med. Invest. 69 : 287-293, August, 2022.
(キーワード): Adrenal Insufficiency / Adrenocorticotropic Hormone / Algorithms / Corticotropin-Releasing Hormone / Dehydroepiandrosterone Sulfate / Humans / Hydrocortisone / Retrospective Studies
(徳島大学機関リポジトリ): ● Metadata: 117738
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.69.287
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36244782; ● CiNii @ 国立情報学研究所 (CRID): 1390575263318485248; ● Summary page in Scopus @ Elsevier: 2-s2.0-85139886801

(徳島大学機関リポジトリ: 117738, DOI: 10.2152/jmi.69.287, PubMed: 36244782, CiNii: 1390575263318485248, Elsevier: Scopus) 西條早希, 中村信元, 三木浩和, 谷口早紀, 岡本秀樹, 富永誠記, 岡田直人, 矢野由美子, 髙橋真理, 青田桂子, 菅俊行, 渡邊浩良, 大坂朱美, 安倍正博 :
徳島大学病院における先天性血友病患者(成人例)の実態調査∼移行期医療の重要性∼,
四国医学雑誌, Vol.77, No.5-6, 261-268, 2021年.

(要約): 【Introduction】Congenital hemophilia is a category of hemorrhagic disease caused by a genetic defect in the production of coagulation factors. It is treated by administering regular coagulation factor injections on an ongoing basis. Hemophilia is a hereditary illness, often causing social and psychological problems as a result of the disease. To analyze the objective effects of hemophilia, we conducted a retrospective analysis in Tokushima University Hospital. 【Result】All 23 cases were men between the ages of20and72. Hemophilia A was present in17cases, and hemophilia B was present in six. Nineteen out of 23 cases were severe, and the others were intermediate. Medical assessments were conducted at pediatrics in seven cases and hematology in 16 cases. Adoption of the self-injection technique was not realized in five cases. Seventeen cases were complicated by hemophilic arthropathy, seven with human immunodeficiency virus(HIV), and 12 with hepatitis C virus. Eight participants were unemployed, and17were unmarried. 【Discussion】 Many adult hemophilia patients still visit pediatrics in our hospital. Hemophilia in the period of growth between adolescence and young adulthood is often accompanied by life-altering events such as entering higher education, marriage, and work experience. Therefore, collaboration among professionals of multiple occupations, such as doctors, nurses, pharmacists, medical social workers, and clinical psychologists, is essential. Furthermore, there are many cases of HIV and hepatitis C virus infections complicating hemophilia study due to the stigma surrounding HIV-tainted blood. 【Conclusion】It is imperative that we establish a long-term, sustainable, and multi-disciplinary transitional care and medical support system for patients and their families.
(キーワード): Congenital Hemophilia / Transitional Care
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1050855267567099520

(CiNii: 1050855267567099520) 木村蘭子, 倉橋清衛, 細木美苗, 辻誠士郎, 三井由加里, 吉田守美子, 明比祐子, 遠藤逸朗, 福本誠二, 安倍正博 :
繰り返す脆弱性骨折を契機に発見されたクッシング症候群の一例,
四国医学雑誌, Vol.77, No.5-6, 269-274, 2021年.

(要約): A 38-year-old woman had suffered from an avulsion fracture of the left cuboid bone, a rib fracture, a fatigue fracture of the left second metatarsal bone and a pubic fracture within the last 4 years. She also realized that her face was getting rounded and became aware of edema on extremities. She had repeated fragile fractures before menopause and was referred to our department on suspicion of secondary osteoporosis. The patients showed physical signs of moon face, central obesity, and abdominal violaceous striae. Cushing's syndrome was suspected, therefore confirmatory studies were performed. Circadian variation of cortisol : serum cortisol19．3μg/dL(at7:00), 21．4μg/dL(at23:00), urinary free cortisol :247．4μg/24h, ACTH :2．5pg/mL. Low-dose(1mg) dexamethasone did not suppress cortisol level(18．9μg/dL). Based on these findings, we diagnosed as Cushing's syndrome and glucocorticoid excess seemed to be the cause of secondary osteoporosis. Abdominal CT identified a 2．7 cm tumor in the left adrenal gland, and in-phase T1‐weighted MRI showed decreased signal compared to out-phase, suggesting an adrenocortical adenoma. She underwent laparoscopic left adrenalectomy. Postoperative fasting serum cortisol decreased to2．2 μg/dL, and glucocorticoid replacement therapy was started. It is necessary to find out any secondary causes for premenopausal women with fragility fractures. It is well known that endocrine disorders including Cushing's syndrome are the most frequent associated diseases in patients with premenopausal osteoporosis. Cushing's syndrome should be considered as a causative disease in premenopausal women with osteoporosis.
(キーワード): Cushing syndrome / fragility fracture / Premenopausal woman
(徳島大学機関リポジトリ): ● Metadata: 116832
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1050573637786980224

(徳島大学機関リポジトリ: 116832, CiNii: 1050573637786980224) 吉川紘平, 金子遥祐, 辻誠士郎, 河田沙紀, 川原綾香, 森建介, 遠藤ふうり, 原倫世, 倉橋清衛, 吉田守美子, 黒田暁生, 明比祐子, 遠藤逸朗, 船木真理, 福本誠二, 安倍正博, 松久宗英 :
TIA様症状を契機に診断されたインスリノーマの1例,
四国医学雑誌, Vol.77, No.5-6, 275-280, 2021年.

(要約): We report the case of a67-year-old woman who had symptoms suggestive of a transient ischemic attack(TIA), such as lightheadedness and transient visual changes before meals for 4 months. She experienced altered consciousness before lunch and was taken to the emergency room2weeks ago. She had repeated hypoglycemia with a blood glucose level of 31 mg/dL. Insulin secretion was not suppressed, with an immunoreactive insulin level of 14．0 μU/mL and connecting peptide immunoreactivity of 1．83 ng/mL for occasional blood glucose levels of 49 mg/dL. Dynamic CT revealed a 17‐mm mass enhanced during the arterial phase in the pancreatic uncinate process, suggestive of a pancreatic neuroendocrine tumor. A selective arterial secretagogue(calcium)injection test revealed the localization of insulinoma in the head of the pancreas. Therefore, pancreatoduodenectomy was performed. Hyperglycemia occurred after the surgery, and it was judged that the insulinoma was resected. This case showed TIA-like symptoms without signs of sympathetic overdrive associated with hypoglycemia. Thus, the diagnosis was delayed. Insulinoma may present with symptoms of neuroglycopenia but not autonomic activity due to hypoglycemia. Insulinoma should be distinguished in patients with unknown neurological symptoms since neuroglycopenia caused by insulinoma is diverse.
(キーワード): Insulinoma / Hypoglycemia / Neuroglycopenia / Transient ischemic attack
(徳島大学機関リポジトリ): ● Metadata: 116831
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1050855112792865536

(徳島大学機関リポジトリ: 116831, CiNii: 1050855112792865536) Shin Kondo, Kumiko Kagawa, Takashi Saito, Masahiro Oura, Kimiko Sogabe, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Nori Sato, Rei Ono, Masahiro Abe and Shinsuke Katoh :
Allogeneic haematopoietic stem cell transplantation-clinical outcomes: impact of leg muscle strength.,
BMJ Supportive & Palliative Care, 2021.

(要約): Pre-transplant LEMS was a significant factor in predicting OS and NRM.
(出版サイトへのリンク): ● Publication site (DOI): 10.1136/bmjspcare-2021-003256
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34949601; ● Search Scopus @ Elsevier (PMID): 34949601; ● Search Scopus @ Elsevier (DOI): 10.1136/bmjspcare-2021-003256

(DOI: 10.1136/bmjspcare-2021-003256, PubMed: 34949601) 川原綾香, 倉橋清衛, 工藤千晶, 鎌田基夢, 加藤真介, 富岡有紀子, 辻本賀美, 安井沙耶, 遠藤ふうり, 桝田志保, 三井由加里, 吉田守美子, 粟飯原賢一, 遠藤逸朗, 福本誠二, 松久宗英, 安倍正博 :
歩行不能だったが，多職種の高度な連携と患者特性に配慮したケアにより自宅生活可能となった高度肥満症の一例,
四国医学雑誌, Vol.76, No.5-6, 317-322, 2021年.

(要約): A 48-year-old man who weighed 216 kg was significantly overweight with a body mass index (BMI)of 75．6kg/m2, and was unable to walk due to disuse syndrome. Because of the psychological and social problems in the background, a psychological examination was performed and the staff took time to build a trusting relationship with the patient, taking into account his characteristics. With diet and rehabilitation, he was able to lose weight to 124kg and BMI 43．9kg/m2 over 600 days, and was able to walk with assistive devices and defecate by himself. The patient was discharged from our hospital after a series of multidisciplinary meetings with medical, nursing, welfare, and governmental agencies to create an environment for home recuperation. The reasons for the improvement to enable him to be discharged from the hospital were due to the multi-disciplinary meetings among the staff inside and outside the hospital, information sharing and advanced coordination, and smooth communication with the patient by taking into account his characteristics from a psychological standpoint.
(キーワード): Sever obesity / 廃用症候群 (disuse syndrome) / Patient-specific care / Multidisciplinary team
(徳島大学機関リポジトリ): ● Metadata: 115801
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1050568937749256704

(徳島大学機関リポジトリ: 115801, CiNii: 1050568937749256704) Yousuke Kaneko, Motoki Sugasaki, Naoto Okada, Mako Niimi, Saya Yasui, Taiki Hori, Ken-ichi Aihara, Makoto Takishita, Masahiro Abe and Shingen Nakamura :
Artifactual prolongation of the activated partial thromboplastin time by amikacin or gentamicin with ellagic acid, but not silica activated reagent.,
International Journal of Laboratory Hematology, Vol.44, No.2, e72-e75, 2021.

(キーワード): Amikacin / Anti-Bacterial Agents / Ellagic Acid / Gentamicins / Humans / Indicators and Reagents / Partial Thromboplastin Time / Silicon Dioxide
(徳島大学機関リポジトリ): ● Metadata: 118369
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/ijlh.13718
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34585530; ● Search Scopus @ Elsevier (PMID): 34585530; ● Search Scopus @ Elsevier (DOI): 10.1111/ijlh.13718

(徳島大学機関リポジトリ: 118369, DOI: 10.1111/ijlh.13718, PubMed: 34585530) Masahiro Hiasa, Takeshi Harada, Eiji Tanaka and Masahiro Abe :
Pathogenesis and treatment of multiple myeloma bone disease.,
Japanese Dental Science Review, Vol.57, 164-173, 2021.

(要約): Multiple myeloma (Plasma cell myeloma), a malignancy of the plasma cells, exhibits tumor expansion preferentially in the bone marrow and the development of bone-destructive lesions. Multiple myeloma is still an incurable disease with changes in the bone marrow microenvironment in favor of the survival and proliferation of multiple myeloma cells and bone destruction. In this review, we described the recent findings on the regulators involved in the development of myeloma bone diseases, and succinctly summarize currently available therapeutic options and the development of novel bone modifying agents for myeloma treatment.
(徳島大学機関リポジトリ): ● Metadata: 117254
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.jdsr.2021.08.006
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34611468; ● Search Scopus @ Elsevier (PMID): 34611468; ● Search Scopus @ Elsevier (DOI): 10.1016/j.jdsr.2021.08.006

(徳島大学機関リポジトリ: 117254, DOI: 10.1016/j.jdsr.2021.08.006, PubMed: 34611468) Yuichi Takashi, Shun Sawatsubashi, Itsuro Endo, Yukiyo Ohnishi, Masahiro Abe, Munehide Matsuhisa, Daiji Kawanami, Toshio Matsumoto and Seiji Fukumoto :
Skeletal FGFR1 signaling is necessary for regulation of serum phosphate level by FGF23 and normal life span.,
Biochemistry and Biophysics Reports, Vol.27, 101107, 2021.

(要約): Fibroblast growth factor (FGF) 23 produced by the bone is the principal hormone to regulate serum phosphate level. Serum FGF23 needs to be tightly regulated to maintain serum phosphate in a narrow range. Thus, we hypothesized that the bone has some phosphate-sensing mechanism to regulate the production of FGF23. Previously we showed that extracellular phosphate induces the phosphorylation of FGF receptor 1 (FGFR1) and FGFR1 signaling regulates the expression of , whose product works to increase FGF23 production . In this study, we show the significance of FGFR1 in the regulated FGF23 production and serum phosphate level . We generated late-osteoblast/osteocyte-specific -knockout mice ( ) by crossing the and the floxed mouse lines. We evaluated serum phosphate and FGF23 levels, the expression of in the bone, the body weight and life span. A selective ablation of aborted the increase of serum active full-length FGF23 and the enhanced expression of in the bone by a high phosphate diet. These mice showed more pronounced hyperphosphatemia compared with control mice. In addition, these mice fed with a control diet showed body weight loss after 23 weeks of age and shorter life span. These results reveal a novel significance of FGFR1 signaling in the phosphate metabolism and normal life span.
(徳島大学機関リポジトリ): ● Metadata: 116283
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.bbrep.2021.101107
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34458594; ● Search Scopus @ Elsevier (PMID): 34458594; ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrep.2021.101107

(徳島大学機関リポジトリ: 116283, DOI: 10.1016/j.bbrep.2021.101107, PubMed: 34458594) Atsushi Nakayama, Tenta Nakamura, Tabassum Ara, tatsuya fukuta, Sangita Karanjit, Takeshi Harada, Asuka Oda, Hideo Sato, Masahiro Abe, Kentaro Kogure and Kosuke Namba :
Development of a novel antioxidant based on a dimeric dihydroisocoumarin derivative,
Tetrahedron Letters, Vol.74, 153176, 2021.

(徳島大学機関リポジトリ): ● Metadata: 116179
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.tetlet.2021.153176
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-85107022552

(徳島大学機関リポジトリ: 116179, DOI: 10.1016/j.tetlet.2021.153176, Elsevier: Scopus) Tomoyo Hara, Ryoko Uemoto, Akiko Sekine, Yukari Mitsui, Shiho Masuda, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Yasumasa Ikeda, Itsuro Endo, Soichi Honda, Katsuhiko Yoshimoto, Akira Kondo, Toshiaki Tamaki, Toshio Matsumoto, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara :
Plasma Heparin Cofactor II Activity Is Inversely Associated with Albuminuria and Its Annual Deterioration in Patients with Diabetes.,
Journal of Diabetes Investigation, 2021.

(要約): The plasma HCII activity was inversely and specifically associated with glomerular injury in patients with diabetes. The results suggest that HCII can serve as a novel predictive factor for early-stage DKD development, as represented by albuminuria.
(徳島大学機関リポジトリ): ● Metadata: 116545
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/jdi.13602
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34043882; ● Search Scopus @ Elsevier (PMID): 34043882; ● Search Scopus @ Elsevier (DOI): 10.1111/jdi.13602

(徳島大学機関リポジトリ: 116545, DOI: 10.1111/jdi.13602, PubMed: 34043882) Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Asuka Oda, Ariunzaya Bat-Erdene, Takeshi Harada, Shingen Nakamura, Mohannad Ashtar, Sou Shimizu, Masami Iwasa, Kimiko Sogabe, Masahiro Oura, Shiroh Fujii, Kumiko Kagawa, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe :
TAK1 is a pivotal therapeutic target for tumor progression and bone destruction in myeloma,
Haematologica, Vol.106, No.5, 1401-1413, 2021.

(要約): Along with the tumor progression, the bone marrow microenvironment is skewed in multiple myeloma (MM), which underlies the unique pathophysiology of MM and confers aggressiveness and drug resistance in MM cells. TGF-β-activated kinase-1 (TAK1) mediates a wide range of intracellular signaling pathways. We demonstrate here that TAK1 is constitutively overexpressed and phosphorylated in MM cells, and that TAK1 inhibition suppresses the activation of NF-κB, p38MAPK, ERK and STAT3 to decrease the expression of critical mediators for MM growth and survival, including PIM2, MYC, Mcl-1, IRF4, and Sp1, along with a substantial reduction in the angiogenic factor VEGF in MM cells. Intriguingly, TAK1 phosphorylation was also induced along with upregulation of vascular cell adhesion molecule-1 (VCAM-1) in bone marrow stromal cells (BMSCs) in cocultures with MM cells, which facilitated MM cell-BMSC adhesion while inducing IL-6 production and receptor activator of nuclear factor κ-Β ligand (RANKL) expression by BMSCs. TAK1 inhibition effectively impaired MM cell adhesion to BMSCs to disrupt the support of MM cell growth and survival by BMSCs. Furthermore, TAK1 inhibition suppressed osteoclastogenesis enhanced by RANKL in cocultures of bone marrow cells with MM cells, and restored osteoblastic differentiation suppressed by MM cells or inhibitory factors for osteoblastogenesis overproduced in MM. Finally, treatment with the TAK1 inhibitor LLZ1640-2 markedly suppressed MM tumor growth and prevented bone destruction and loss in mouse MM models. Therefore, TAK1 inhibition may be a promising therapeutic option targeting not only MM cells but also the skewed bone marrow microenvironment in MM.
(キーワード): Animals / Bone Marrow Cells / MAP Kinase Kinase Kinases / Mice / Multiple Myeloma / NF-kappa B / Osteoclasts / Osteolysis / RANK Ligand / Tumor Microenvironment
(徳島大学機関リポジトリ): ● Metadata: 116529
(出版サイトへのリンク): ● Publication site (DOI): 10.3324/haematol.2019.234476
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32273474; ● Search Scopus @ Elsevier (PMID): 32273474; ● Search Scopus @ Elsevier (DOI): 10.3324/haematol.2019.234476

(徳島大学機関リポジトリ: 116529, DOI: 10.3324/haematol.2019.234476, PubMed: 32273474) Ryohei Sumitani, Taiki Hori, Jumpei Murai, Shiyori Kawata, Masahiro Oura, Kimiko Sogabe, Mamiko Takahashi, Takeshi Harada, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, Masahiro Abe and Shingen Nakamura :
Acute Myeloid Leukemia Developing with Acute Pancreatitis Mimicking Autoimmune Pancreatitis.,
Internal Medicine, Vol.60, No.11, 1753-1757, 2021.

(要約): A 33-year-old man was admitted to our hospital for fever and abdominal pain. A blood analysis revealed pancytopenia and increased serum pancreatic enzymes with disseminated intravascular coagulation. A detailed examination revealed acute pancreatitis, with diffuse swelling of the pancreas and diffuse beaded dilatation of the main pancreatic duct, which mimicked autoimmune pancreatitis complicated by acute myeloid leukemia. Systemic cytotoxic chemotherapy led to the remission of leukemia and pancreatitis. We hypothesized that the etiology of acute pancreatitis was invasion of leukemia cells. Acute pancreatitis is rare as a symptom of leukemia; however, we should consider the possibility of leukemia during the differential diagnosis of acute pancreatitis.
(キーワード): Acute Disease / Adult / Autoimmune Diseases / Autoimmune Pancreatitis / Humans / Leukemia, Myeloid, Acute / Male / Pancreatitis
(徳島大学機関リポジトリ): ● Metadata: 116536
(出版サイトへのリンク): ● Publication site (DOI): 10.2169/internalmedicine.4916-20
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33456032; ● Search Scopus @ Elsevier (PMID): 33456032; ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.4916-20

(徳島大学機関リポジトリ: 116536, DOI: 10.2169/internalmedicine.4916-20, PubMed: 33456032) 桝田志保, 吉田守美子, 工藤千晶, 辻本賀美, 安井沙耶, 遠藤ふうり, 三井由加里, 倉橋清衛, 遠藤逸朗, 轟貴史, 安倍正博 :
診断に時間を要した高齢者の甲状腺クリーゼの1例,
日本老年医学会雑誌, Vol.58, No.1, 158-163, 2021年.

(要約): 甲状腺クリーゼは致死的かつ緊急疾患であるが，他疾患に起因する症状と区別がつきにくいことや，高齢者では典型的クリーゼ症状を呈さない場合があり，診断は容易ではない．今回，消化器症状で発症し，心房細動と心不全の加療中に，甲状腺クリーゼと未治療バセドウ病の診断に至った症例を経験したので報告する．症例は70歳の女性．甲状腺疾患の既往はなく，多発筋炎でプレドニゾロン服用中であった．X月中頃より下痢・嘔吐が出現し，徐々に増悪し，労作時呼吸困難も出現した．X+1月8日に嘔気と倦怠感のため消化器内科に入院し，脱水に対して補液を行った．さらに消化器症状，発熱，呼吸困難の症状が悪化し，入院4日目にうっ血性心不全，頻脈性心房細動の診断で循環器内科において利尿薬を中心とした治療が開始された．入院7日目にFT4 9.95 ng/dL，FT3 >30 pg/mL，TSH <0.01 μU/mLとTSH抑制を伴う甲状腺ホルモン過剰が判明し，内分泌代謝内科へ紹介された．TRAb 22.6 IU/Lと上昇がありバセドウ病と診断するとともに，不穏，39℃の発熱，140回/分以上の頻脈，肺水腫，頻回な下痢を認め，確実な甲状腺クリーゼの状態であった．チアマゾール，ヨウ化カリウム，ヒドロコルチゾン，ランジオロールなどによる甲状腺クリーゼの包括的治療を行い，後遺症を残すことなく救命できた．甲状腺ホルモンの低下とともに，心不全診断時に認めた左室壁の局所運動異常と心電図のST-T変化は改善し，たこつぼ型心筋症も合併していたと考えられた．後の検査で入院時から甲状腺中毒症が存在し，すでに甲状腺クリーゼの状態であったことが判明した．本症例は，入院時に高熱や多動などの意識障害を呈さず，倦怠感が目立ち，基礎疾患や服用薬の影響など診断を困難にする要因が重なり，甲状腺クリーゼの診断までに時間を要したと考えられた．
(キーワード): 甲状腺クリーゼ / バセドウ病 / 心房細動 / 心不全 / たこつぼ型心筋症
(出版サイトへのリンク): ● Publication site (DOI): 10.3143/geriatrics.58.158
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390568772520282112; ● Search Scopus @ Elsevier (DOI): 10.3143/geriatrics.58.158

(DOI: 10.3143/geriatrics.58.158, CiNii: 1390568772520282112) Tashima Hozumi, Endo Yuka, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato :
Association analysis between adverse drug reactions to cytarabine therapy and single nucleotide polymorphisms in cytarabine metabolic genes in patients with hematopoietic tumor,
Personalized Medicine Universe, Vol.10, 1-6, 2021.

(徳島大学機関リポジトリ): ● Metadata: 117585
(出版サイトへのリンク): ● Publication site (DOI): 10.46459/pmu.2021002
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.46459/pmu.2021002

(徳島大学機関リポジトリ: 117585, DOI: 10.46459/pmu.2021002) Mamiko Takahashi, Ryohei Sumitani, Taiki Hori, Jumpei Murai, Shiyori Kawata, Masahiro Oura, Kimiko Sogabe, Takeshi Harada, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, Masahiro Abe and Shingen Nakamura :
Intravenous busulfan-based conditioning with autologous stem cell transplantation for refractory B-cell lymphoma with central nervous system involvement.,
The Journal of Medical Investigation : JMI, Vol.68, No.1.2, 196-201, 2021.

(要約): The prognosis of relapsed or refractory lymphoma with central nervous system (CNS) involvement remains poor because of the lack of anticancer drugs with sufficient CNS penetration. [Case 1] A 65-year-old man was diagnosed with Stage IV mantle cell lymphoma. After two courses of chemotherapy and autologous hematopoietic stem cell (HSC) collection, urinary retention with fever developed. Cerebrospinal fluid analysis revealed leptomeningeal involvement, which was refractory to high-dose methotrexate therapy. Autologous peripheral blood stem cell transplantation (ASCT) was performed, followed by intravenous busulfan (ivBU), cyclophosphamide, and etoposide ; thereafter, no relapse has been detected for over six years. [Case 2] A 40-year-old woman with right lower hemiplegia was diagnosed with primary CNS lymphoma. Although four courses of high-dose methotrexate therapy were administered, the cerebral tumor increased in size. HSCs were collected after methotrexate therapy, and ASCT was performed in addition to conditioning using ivBU, cyclophosphamide, and etoposide, followed by whole-brain and local boost irradiation. She achieved complete remission, but relapsed two years after ASCT. High-dose ivBU-containing conditioning regimens with ASCT may be useful for refractory B-cell lymphoma with CNS involvement. J. Med. Invest. 68 : 196-201, February, 2021.
(徳島大学機関リポジトリ): ● Metadata: 116021
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.68.196
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33994471; ● Search Scopus @ Elsevier (PMID): 33994471; ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.68.196

(徳島大学機関リポジトリ: 116021, DOI: 10.2152/jmi.68.196, PubMed: 33994471) Yuka Sogawa, Makoto Fukui, Shingen Nakamura, Kimiko Sogabe, Ryohei Sumitani, Masami Yoshioka, Masahiro Abe and Daisuke Hinode :
Involvement of oral bacteria and oral immunity as risk factors for chemotherapy- induced fever with neutropenia in patients with hematological cancer,
International Journal of Hematology, Vol.112, No.6, 851-859, 2020.

(要約): The aim of this study is to investigate the association between chemotherapy-induced fever with neutropenia less than 1500/μL (FwN) and oral bacteria and/or oral immunity in patients with hematological cancer. Thirty-two patients with hematological cancer were enrolled in the study. Secretory immunoglobulin A (sIgA) in saliva and the anaerobic bacteria in tongue coating of each subject were assessed before the first chemotherapy. Eleven subjects had an onset of FwN and 21 subjects did not during the observation periods. It was revealed by the Cox-proportional hazard model analysis that the levels of sIgA were low (HR 0.98, p < 0.05) and the rate of Fusobacterium nucleatum [F. nucleatum count per total bacterial count (%)] was high (HR 1.65, p < 0.05) in patients with FwN onset. Using ROC curve analysis, the optimal cutoff point based on the AUC in the F. nucleatum/sIgA ratio was 0.023, and this model had a 78.4% probability (p < 0.01). The risk of FwN onset was also significantly higher among the group of ≥ 0.023 F. nucleatum/sIgA ratio (HR 66.06, p < 0.01). These results suggest that the rate of F. nucleatum and the levels of sIgA at baseline might be related to FwN onset as risk factors.
(キーワード): Adult / Aged / Aged, 80 and over / Antineoplastic Agents / Bacterial Load / Febrile Neutropenia / 女性 (female) / Fusobacterium nucleatum / Hematologic Neoplasms / Humans / Immunoglobulin A, Secretory / 男性 (male) / Middle Aged / Mouth / Risk Factors / Young Adult
(徳島大学機関リポジトリ): ● Metadata: 115932
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s12185-020-02975-x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32880823; ● Summary page in Scopus @ Elsevier: 2-s2.0-85090162636

(徳島大学機関リポジトリ: 115932, DOI: 10.1007/s12185-020-02975-x, PubMed: 32880823, Elsevier: Scopus) Michihiro Nakamura, Koichiro Hayashi, Junna Nakamura, Chihiro Mochizuki, Takuya Murakami, Hirokazu Miki, Shuji Ozaki and Masahiro Abe :
Near-Infrared Fluorescent Thiol-Organosilica Nanoparticles That Are Functionalized with IR-820 and Their Applications for Long-Term Imaging of in Situ Labeled Cells and Depth-Dependent Tumor in Vivo Imaging,
Chemistry of Materials, Vol.32, No.17, 7201-7214, 2020.

(出版サイトへのリンク): ● Publication site (DOI): 10.1021/acs.chemmater.0c01414
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-85090482286

(DOI: 10.1021/acs.chemmater.0c01414, Elsevier: Scopus) Mohannad Ashtar, Hirofumi Tenshin, Jumpei Teramachi, Ariunzaya Bat-Erdene, Masahiro Hiasa, Asuka Oda, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Shingen Nakamura, Shiroh Fujii, Ryohei Sumitani, Hirokazu Miki, Kengo Udaka, Mamiko Takahashi, Kumiko Kagawa, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
The Roles of ROS Generation in RANKL-Induced Osteoclastogenesis: Suppressive Effects of Febuxostat.,
Cancers, Vol.12, No.4, 2020.

(要約): Receptor activator of NF-κB ligand (RANKL), a critical mediator of osteoclastogenesis, is upregulated in multiple myeloma (MM). The xanthine oxidase inhibitor febuxostat, clinically used for prevention of tumor lysis syndrome, has been demonstrated to effectively inhibit not only the generation of uric acid but also the formation of reactive oxygen species (ROS). ROS has been demonstrated to mediate RANKL-mediated osteoclastogenesis. In the present study, we therefore explored the role of cancer-treatment-induced ROS in RANKL-mediated osteoclastogenesis and the suppressive effects of febuxostat on ROS generation and osteoclastogenesis. RANKL dose-dependently induced ROS production in RAW264.7 preosteoclastic cells; however, febuxostat inhibited the RANKL-induced ROS production and osteoclast (OC) formation. Interestingly, doxorubicin (Dox) further enhanced RANKL-induced osteoclastogenesis through upregulation of ROS production, which was mostly abolished by addition of febuxostat. Febuxostat also inhibited osteoclastogenesis enhanced in cocultures of bone marrow cells with MM cells. Importantly, febuxostat rather suppressed MM cell viability and did not compromise Dox's anti-MM activity. In addition, febuxostat was able to alleviate pathological osteoclastic activity and bone loss in ovariectomized mice. Collectively, these results suggest that excessive ROS production by aberrant RANKL overexpression and/or anticancer treatment disadvantageously impacts bone, and that febuxostat can prevent the ROS-mediated osteoclastic bone damage.
(徳島大学機関リポジトリ): ● Metadata: 115041
(出版サイトへのリンク): ● Publication site (DOI): 10.3390/cancers12040929
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32283857; ● Search Scopus @ Elsevier (PMID): 32283857; ● Search Scopus @ Elsevier (DOI): 10.3390/cancers12040929

(徳島大学機関リポジトリ: 115041, DOI: 10.3390/cancers12040929, PubMed: 32283857) Kengo Udaka, Shingen Nakamura, Shiroh Fujii, Ryosuke Miyamoto, Naoko Matsui, Shiyori Kawata, Taiki Hori, Junpei Murai, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Mamiko Takahashi, Takeshi Harada, Kumiko Kagawa, Yuishin Izumi, Masahiro Abe and Hirokazu Miki :
Successful treatment of progressive multifocal leukoencephalopathy with mirtazapine and mefloquine in refractory myeloma,
International Journal of Myeloma, Vol.10, No.1, 8-12, 2020. Shuji Ozaki, Takeshi Harada, Hikaru Yagi, Etsuko Sekimoto, Hironobu Shibata, Toshio Shigekiyo, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa and Masahiro Abe :
Polyclonal Immunoglobulin Recovery after Autologous Stem Cell Transplantation Is an Independent Prognostic Factor for Survival Outcome in Patients with Multiple Myeloma,
Cancers, Vol.12, No.1, 12, 2019.

(要約): We retrospectively analyzed multiple myeloma (MM) patients who underwent autologous stem cell transplantation (ASCT) without maintenance therapy to assess the impact of recovery of normal immunoglobulin (Ig) on clinical outcomes. The recovery of polyclonal Ig was defined as normalization of all values of serum IgG, IgA, and IgM 1 year after ASCT. Among 50 patients, 26 patients showed polyclonal Ig recovery; 14 patients were in ≥complete response (CR) and 12 remained in non-CR after ASCT. The patients with Ig recovery exhibited a significantly better progression-free survival (PFS, median, 46.8 vs 26.7 months, = 0.0071) and overall survival (OS, median, not reached vs 65.3 months, < 0.00001) compared with those without Ig recovery. The survival benefits of Ig recovery were similarly observed in ≥CR patients (median OS, not reached vs 80.5 months, = 0.061) and non-CR patients (median OS, not reached vs 53.2 months, = 0.00016). Multivariate analysis revealed that non-CR and not all Ig recovery were independent prognostic factors for PFS (HR, 4.284, 95%CI (1.868-9.826), = 0.00059; and HR, 2.804, 95%CI (1.334-5.896), = 0.0065, respectively) and also for OS (HR, 8.245, 95%CI (1.528-44.47), = 0.014; and HR, 36.55, 95%CI (3.942-338.8), = 0.0015, respectively). Therefore, in addition to the depth of response, the recovery of polyclonal Ig after ASCT is a useful indicator especially for long-term outcome and might be considered to prevent overtreatment with maintenance therapy in transplanted patients with MM.
(徳島大学機関リポジトリ): ● Metadata: 115047
(出版サイトへのリンク): ● Publication site (DOI): 10.3390/cancers12010012
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31861479; ● Summary page in Scopus @ Elsevier: 2-s2.0-85077198248

(徳島大学機関リポジトリ: 115047, DOI: 10.3390/cancers12010012, PubMed: 31861479, Elsevier: Scopus) Naoto Okada, Masayuki Chuma, Momoyo Azuma, Shingen Nakamura, Hirokazu Miki, Hirofumi Hamano, Mitsuhiro Goda, Kenshi Takechi, Yoshito Zamami, Masahiro Abe and Keisuke Ishizawa :
Effect of serum concentration and concomitant drugs on vancomycin-induced acute kidney injury in haematologic patients: a single-centre retrospective study.,
European Journal of Clinical Pharmacology, Vol.75, No.12, 1695-1704, 2019.

(要約): The optimal initial VCM trough concentration was 10-15 mg/L in haematologic patients, considering safety and effectiveness. There were differences in the effect of VCM-induced AKI between nephrotoxic drugs.
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s00228-019-02756-4
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31511938; ● Search Scopus @ Elsevier (PMID): 31511938; ● Search Scopus @ Elsevier (DOI): 10.1007/s00228-019-02756-4

(DOI: 10.1007/s00228-019-02756-4, PubMed: 31511938) 井上雄介, 池亀彰茂, 徳永尚樹, 井上千尋, 中尾隆之, 長井幸二郎, 高橋真美子, 藤井志朗, 中村信元, 安倍正博 :
芽球様の形態を示した肝脾型T細胞リンパ腫の一症例,
日本検査血液学会雑誌, Vol.20, No.2, 231-237, 2019年. Yuichi Takashi, Hidetaka Kosako, Shun Sawatsubashi, Yuka Kinoshita, Nobuaki Ito, Maria K. Tsoumpra, Masaomi Nangaku, Masahiro Abe, Munehide Matsuhisa, Shigeaki Kato, Toshio Matsumoto and Seiji Fukumoto :
Activation of unliganded FGF receptor by extracellular phosphate potentiates proteolytic protection of FGF23 by its O-glycosylation,
Proceedings of the National Academy of Sciences of the United States of America, Vol.116, No.23, 11418-11427, 2019.

(要約): Fibroblast growth factor (FGF) 23 produced by bone is a hormone that decreases serum phosphate (Pi). Reflecting its central role in Pi control, serum FGF23 is tightly regulated by serum Pi alterations. FGF23 levels are regulated by the transcriptional event and posttranslational cleavage into inactive fragments before its secretion. For the latter, O-glycosylation of FGF23 by gene product prevents the cleavage, leading to an increase in serum FGF23. However, the molecular basis of Pi sensing in the regulation of serum FGF23 remains elusive. In this study, we showed that high Pi diet enhanced the skeletal expression of , but not , with expected increases in serum FGF23 and Pi in mice. induction by high Pi was further observed in osteoblastic UMR 106 cells, and this was mediated by activation of the extracellular signal-regulated kinase (ERK) pathway. Through proteomic searches for the upstream sensor for high Pi, we identified one subtype of the FGF receptor (FGFR1c), which was phosphorylated by high Pi in the absence of FGFs. The mode of unliganded FGFR activation by high Pi appeared different from that of FGFR bound to a canonical FGFR ligand (FGF2) when phosphorylation of the FGFR substrate 2α and ERK was monitored. Finally, we showed that an FGFR inhibitor and conditional deletion of in osteoblasts/osteocytes abrogated high Pi diet-induced increases in serum FGF23 and femoral expression in mice. Thus, these findings uncover an unrecognized facet of unliganded FGFR function and illustrate a Pi-sensing pathway involved in regulation of FGF23 production.
(徳島大学機関リポジトリ): ● Metadata: 113621
(出版サイトへのリンク): ● Publication site (DOI): 10.1073/pnas.1815166116
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31097591; ● Search Scopus @ Elsevier (PMID): 31097591; ● Search Scopus @ Elsevier (DOI): 10.1073/pnas.1815166116

(徳島大学機関リポジトリ: 113621, DOI: 10.1073/pnas.1815166116, PubMed: 31097591) Dong Bingzi, Itsuro Endo, Ohnishi Yukoyo, Mitsui Yukari, Kiyoe Kurahashi, Mai Kanai, Masahiro Hiasa, Jumpei Teramachi, Hirofumi Tenshin, Seiji Fukumoto, Masahiro Abe and Toshio Matsumoto :
Persistent Activation of Calcium-Sensing Receptor Suppresses Bone Turnover, Increases Microcracks, and Decreases Bone Strength.,
JBMR Plus, Vol.3, No.7, e10182, 2019.

(要約): Activating mutations of calcium-sensing receptor (CaSR) cause autosomal dominant hypocalcemia type 1 (ADH1). Patients with ADH1 exhibit similar features to patients with hypoparathyroidism, including reduced serum parathyroid hormone (PTH) and Ca with low bone turnover. Although persistent suppression of bone turnover may increase bone fragility, bone strength in ADH1 patients has been unclear. We created knock-in mice harboring the A843E activating mutation of CaSR, mimicking severe features of ADH1 patients. The severe form of ADH1 model mice showed smaller body and bone size with lower bone mineral density (BMD) and cortical area of the femur compared with age-matched wild-type (WT) mice. Bone strength in the femur was lower in ADH1 mice even after correction by bone geometry and/or BMD. Microcracks were markedly increased in ADH1 mice, but were rarely detected in WT mice. There was a negative correlation between bone strength corrected by bone geometry and/or BMD and microcrack number or density in ADH1 and WT mice. Among ADH1 mice, negative correlation was still observed between bone strength and microcrack number or density. Microcracks increased with age in ADH1 mice, and were negatively correlated with bone strength. Treatment with PTH(1-34) or a calcilytic, JTT-305, increased bone turnover, reduced microcracks, and increased bone strength to similar levels to those in WT mice. The increase in microcracks was associated with a reduction in bone strength in ADH1 mice, and aging aggravates these changes. These results demonstrate that activating mutation of CaSR causes reduction in PTH secretion with suppressed bone turnover, that reduced bone turnover is associated with an age-dependent increase in microcracks with a reduction in bone strength, and that both PTH(1-34) and calcilytic ameliorate all these changes in bone turnover and strength. It is suggested that fracture susceptibility may be increased in severe types of ADH1 patients especially in the elderly. © 2019 The Authors. published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/jbm4.10182
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31372589; ● Search Scopus @ Elsevier (PMID): 31372589; ● Search Scopus @ Elsevier (DOI): 10.1002/jbm4.10182

(DOI: 10.1002/jbm4.10182, PubMed: 31372589) 宮上侑子, 中村信元, 大浦雅博, 岡本惠暢, 高橋真美子, 曽我部公子, 岩佐昌美, 原田武志, 藤井志朗, 三木浩和, 賀川久美子, 上原久典, 安倍正博 :
不明熱と著明な高CRP血症で発症したde novo CD20陰性びまん性大細胞型B細胞リンパ腫の1例,
四国医学雑誌, Vol.74, No.5-6, 193-200, 2018年.

(要約): A 68-year-old woman presented with sustained fever for more than 1 month and admitted due to hematemesis and systemic edema. Computed tomography scan revealed swelling of the cervical, paraaortic lymph nodes. Blood test results showed severe anemia, elevation of white blood cell count, elevation of liver enzyme and coagulopathy with high C-reactive protein. Biopsy of the right cervical lymph node showed proliferation of abnormal lymphoid cells with necrosis and hemorrhage, which are positive for CD79α, CD30, MUM-1, and bcl-6 and negative for CD20, CD5, CD10, ALK, CD38, CD138, and EBER. Gene rearrangement of immunoglobulin heavy chain was detected in tumor cells. Bone marrow aspiration showed tumor involvement. The patient was diagnosed with de novo CD20-negative diffuse large B-cell lymphoma(DLBCL)stage IV B. Reduced CHOP therapy was performed under artificial respiration due to pulmonary edema and takotsubo cardiomyopathy. Although her general condition and high CRP levels temporarily improved, she died 47 days after admission due to rapid relapse. De novo CD20-negative DLBCL was rare and presented with high CRP levels and rapid progression, and was thought to be clinically different from the existing DLBCL. It is imperative to elucidate molecular pathophysiology and establish new treatment strategy for de novo CD20-negative DLBCL.
(キーワード): CD20 / fever of unknown origin / diffuse large B-cell lymphoma / CRP
(徳島大学機関リポジトリ): ● Metadata: 112987
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1050845763422780928

(徳島大学機関リポジトリ: 112987, CiNii: 1050845763422780928) Ariunzaya Bat-Erdene, Shingen Nakamura, Asuka Oda, Masami Iwasa, Jumpei Teramachi, Mohannad Ashtar, Takeshi Harada, Hirokazu Miki, Hirofumi Tenshin, Masahiro Hiasa, Shiroh Fujii, Kimiko Sogabe, Masahiro Oura, Kengo Udaka, Kumiko Kagawa, Sumiko Yoshida, Ken-ichi Aihara, Kiyoe Kurahashi, Itsuro Endo and Masahiro Abe :
Class 1 HDAC and HDAC6 inhibition inversely regulates CD38 induction in myeloma cells via interferon-α and ATRA.,
British Journal of Haematology, 2018.

(徳島大学機関リポジトリ): ● Metadata: 113393
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/bjh.15673
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30474853; ● Summary page in Scopus @ Elsevier: 2-s2.0-85057280798

(徳島大学機関リポジトリ: 113393, DOI: 10.1111/bjh.15673, PubMed: 30474853, Elsevier: Scopus) Seiji Kishi, 小幡史明, Hirokazu Miki, Motokazu Matsuura, Masanori Tamaki, Fumi Kishi, 西村賢二, Taichi Murakami, Hideharu Abe, Kojiro Nagai, Masahiro Abe and Toshio Doi :
A case of Lambda Light Chain Noncrystalline Proximal Tubulopathy with IgD lambda myeloma,
Internal Medicine, 2018.

(徳島大学機関リポジトリ): ● Metadata: 114401
(出版サイトへのリンク): ● Publication site (DOI): 10.2169/internalmedicine.1323-18
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30101939; ● Search Scopus @ Elsevier (PMID): 30101939; ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.1323-18

(徳島大学機関リポジトリ: 114401, DOI: 10.2169/internalmedicine.1323-18, PubMed: 30101939) Kumiko Kagawa, Hikaru Fujino, Hirokazu Miki, Kimiko Sogabe, Mamiko Takahashi, Tomoko Maruhashi, Kengo Udaka, Masami Iwasa, Shiro Fujii, Shingen Nakamura and Masahiro Abe :
Cryptosporidiosis in a transplant recipient with severe intractable diarrhea: Detection of Cryptosporidium oocysts by intestinal biopsies.,
Transplant Infectious Disease, Vol.20, No.2, e12826, 2018.

(要約): Disseminated Cryptosporidium infection results in manifestations similar to those of graft-versus-host disease (GVHD), which hampers the detection of Cryptosporidium infection after allogeneic hematopoietic stem cell transplantation. Surveillance of oocysts on the surface of intestinal epithelial cells is needed for early and appropriate detection of Cryptosporidium infection in transplant recipients on immunosuppressants with severe intractable diarrhea. We present the first case of Cryptosporidium meleagridis infection in Japan after allogeneic cord blood transplantation.
(キーワード): Biopsy / Cord Blood Stem Cell Transplantation / Cryptosporidiosis / Cryptosporidium / Diarrhea / Female / Humans / Intestines / Middle Aged / Oocysts / Transplant Recipients
(徳島大学機関リポジトリ): ● Metadata: 115817
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/tid.12826
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29277954; ● Summary page in Scopus @ Elsevier: 2-s2.0-85041047530

(徳島大学機関リポジトリ: 115817, DOI: 10.1111/tid.12826, PubMed: 29277954, Elsevier: Scopus) Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Takeshi Harada, Shingen Nakamura, Ryota Amachi, Hirofumi Tenshin, Masami Iwasa, Shiroh Fujii, Kumiko Kagawa, Hirokazu Miki, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe :
Pim-2 is a critical target for treatment of osteoclastogenesis enhanced in myeloma.,
British Journal of Haematology, Vol.180, No.4, 581-585, 2018.

(徳島大学機関リポジトリ): ● Metadata: 112935
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/bjh.14388
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27748523; ● Search Scopus @ Elsevier (PMID): 27748523; ● Search Scopus @ Elsevier (DOI): 10.1111/bjh.14388

(徳島大学機関リポジトリ: 112935, DOI: 10.1111/bjh.14388, PubMed: 27748523) Shiroh Fujii, Shingen Nakamura, Asuka Oda, Hirokazu Miki, Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Ariunzaya Bat-Erdene, Yusaku Maeda, Masahiro Oura, Mamiko Takahashi, Masami Iwasa, Itsuro Endo, Sumiko Yoshida, Ken-ichi Aihara, Kiyoe Kurahashi, Takeshi Harada, Kumiko Kagawa, Michiyasu Nakao, Shigeki Sano and Masahiro Abe :
Unique anti-myeloma activity by thiazolidine-2,4-dione compounds with Pim inhibiting activity.,
British Journal of Haematology, Vol.180, No.2, 246-258, 2018.

(要約): Proviral Integrations of Moloney virus 2 (PIM2) is overexpressed in multiple myeloma (MM) cells, and regarded as an important therapeutic target. Here, we aimed to validate the therapeutic efficacy of different types of PIM inhibitors against MM cells for their possible clinical application. Intriguingly, the thiazolidine-2,4-dione-family compounds SMI-16a and SMI-4a reduced PIM2 protein levels and impaired MM cell survival preferentially in acidic conditions, in contrast to other types of PIM inhibitors, including AZD1208, CX-6258 and PIM447. SMI-16a also suppressed the drug efflux function of breast cancer resistance protein, minimized the sizes of side populations and reduced in vitro colony-forming capacity and in vivo tumourigenic activity in MM cells, suggesting impairment of their clonogenic capacity. PIM2 is known to be subject to ubiquitination-independent proteasomal degradation. Consistent with this, the proteasome inhibitors bortezomib and carfilzomib increased PIM2 protein levels in MM cells without affecting its mRNA levels. However, SMI-16a mitigated the PIM2 protein increase and cooperatively enhanced anti-MM effects in combination with carfilzomib. Collectively, the thiazolidine-2,4-dione-family compounds SMI-16a and SMI-4a uniquely reduce PIM2 protein in MM cells, which may contribute to their profound efficacy in addition to their immediate kinase inhibition. Their combination with proteasome inhibitors is envisioned.
(キーワード): Animals / Antineoplastic Agents / Cell Line, Tumor / Cell Survival / Cell Transformation, Neoplastic / Disease Models, Animal / Humans / Hydrogen-Ion Concentration / Mice / Multiple Myeloma / Proteasome Inhibitors / Protein-Serine-Threonine Kinases / Proteolysis / Proto-Oncogene Proteins / Thiazolidinediones
(徳島大学機関リポジトリ): ● Metadata: 112752
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/bjh.15033
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29327347; ● Summary page in Scopus @ Elsevier: 2-s2.0-85040344893

(徳島大学機関リポジトリ: 112752, DOI: 10.1111/bjh.15033, PubMed: 29327347, Elsevier: Scopus) 山口純代, 中村信元, 住田智志, 前田悠作, 大浦雅博, 高橋真美子, 岩佐昌美, 原田武志, 藤井志朗, 三木浩和, 賀川久美子, 岸潤, 安倍正博 :
リウマチ様関節炎に対する免疫抑制療法中に発症した成人T細胞性白血病/リンパ腫の1例,
四国医学雑誌, Vol.73, No.5,6, 301-308, 2017年.

(要約): A 64-year-old woman presented with lower leg edema, fever, and bilateral joint pain, involving the wrists, fingers, and knees, in April 201X. Serological test results were negative for rheumatoid factor, antinuclear antibody, and anti-cyclic citrullinated peptide antibody. A diagnosis of remitting seronegative symmetrical synovitis with pitting edema syndrome, a type of seronegative rheumatoid arthritis, was made and prednisolone was administered. The joint pain was refractory to prednisolone therapy. In February, 201X+2, the patient presented with right cervical lymphadenopathy. The CT scan revealed swelling of the cervical, axillary, and inguinal lymph nodes bilaterally and rapidly enlarged. In April, 18F-fluorodeoxyglucose PET/CT scan showed an abnormal collection in the enlarged lymph nodes. The patient subsequently developed hoarseness with dyspnea and attended our department. Blood test results showed high levels of lactate dehydrogenase (547U/L) and soluble interleukin‐2 receptor (34200 IU/L) and were positive for anti-human T-cell leukemia virus type1 (HTLV‐1) antibody. Biopsy of the right cervical lymph node showed proliferation of abnormal lymphoid cells positive for CD3, CD4, and CD25 and negative for CD7. Monoclonal integration of HTLV‐1 proviral DNA was detected in the lymph node. A diagnosis of adult T-cell leukemia/lymphoma (ATLL), lymphoma type was made. The pain involving multiple joints was attributed to HTLV‐1associated arthropathy. Immunosuppressive therapy for HTLV‐1 carrier status may have played a role in the development of ATLL.
(キーワード): Adult T-cell leukemia/lymphoma / HTLV-1 / rheumatoid arthritis / immunosuppressive therapy
(徳島大学機関リポジトリ): ● Metadata: 112059
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1050001338847982080

(徳島大学機関リポジトリ: 112059, CiNii: 1050001338847982080) Hirokazu Miki, Shingen Nakamura, Asuka Oda, Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Ariunzaya Bat-Erdene, Yusaku Maeda, Masahiro Oura, Mamiko Takahashi, Masami Iwasa, Takeshi Harada, Shiroh Fujii, Kiyoe Kurahashi, Sumiko Yoshida, Kumiko Kagawa, Itsuro Endo, Aihara Kenichi, Mariko Ikuo, Kouji Itou, Koichiro Hayashi, Michihiro Nakamura and Masahiro Abe :
Effective impairment of myeloma cells and their progenitors by hyperthermia.,
Oncotarget, Vol.9, No.12, 10307-10316, 2017.

(要約): Multiple myeloma (MM) remains incurable, and MM-initiating cells or MM progenitors are considered to contribute to disease relapse through their drug-resistant nature. In order to improve the therapeutic efficacy for MM, we recently developed novel superparamagnetic nanoparticles which selectively accumulate in MM tumors and extirpate them by heat generated with magnetic resonance. We here aimed to clarify the therapeutic effects on MM cells and their progenitors by hyperthermia. Heat treatment at 43°C time-dependently induced MM cell death. The treatment upregulated endoplasmic reticulum (ER) stress mediators, ATF4 and CHOP, while reducing the protein levels of Pim-2, IRF4, c-Myc and Mcl-1. Combination with the proteasome inhibitor bortezomib further enhanced ER stress to potentiate MM cell death. The Pim inhibitor SMI-16a also enhanced the reduction of the Pim-2-driven survival factors, IRF4 and c-Myc, in combination with the heat treatment. The heat treatment almost completely eradicated "side population" fractions in RPMI8226 and KMS-11 cells and suppressed their clonogenic capacity as determined by colony formation and tumorigenic capacity in SCID mice. These results collectively demonstrated that hyperthermia is able to impair clonogenic drug-resistant fractions of MM cells and enhance their susceptibility to chemotherapeutic drugs.
(徳島大学機関リポジトリ): ● Metadata: 113059
(出版サイトへのリンク): ● Publication site (DOI): 10.18632/oncotarget.23121
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29535808; ● Summary page in Scopus @ Elsevier: 2-s2.0-85041952629

(徳島大学機関リポジトリ: 113059, DOI: 10.18632/oncotarget.23121, PubMed: 29535808, Elsevier: Scopus) Hirofumi Tenshin, Jumpei Teramachi, Asuka Oda, Ryota Amachi, Masahiro Hiasa, Ariunzaya Bat-Erdene, Keiichiro Watanabe, Masami Iwasa, Takeshi Harada, Shiroh Fujii, Kumiko Kagawa, Kimiko Sogabe, Shingen Nakamura, Hirokazu Miki, Kiyoe Kurahashi, Sumiko Yoshida, Kenichi Aihara, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
TAK1 inhibition subverts the osteoclastogenic action of TRAIL while potentiating its antimyeloma effects.,
Blood Advances, Vol.1, No.24, 2124-2137, 2017.

(要約): Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) agonists induce tumor-specific apoptosis indicating that they may be an attractive therapeutic strategy against cancers, including multiple myeloma (MM). Osteoclastogenesis is highly induced in MM, which in turn enhances MM growth, thereby forming a vicious cycle between MM tumor expansion and bone destruction. However, the effects of TRAIL on MM-enhanced osteoclastogenesis remain largely unknown. Here, we show that TRAIL induced apoptosis in MM cells, but not in osteoclasts (OCs), and that it rather facilitated receptor activator of NF-B ligand-induced osteoclastogenesis along with upregulation of cellular FLICE inhibitory protein (c-FLIP). TRAIL did not induce death-inducing signaling complex formation in OCs, but formed secondary complex (complex II) with the phosphorylation of transforming growth factor -activated kinase-1 (TAK1), and thus activated NF-B signaling. c-FLIP knockdown abolished complex II formation, thus permitting TRAIL induction of OC cell death. The TAK1 inhibitor LLZ1640-2 abrogated the TRAIL-induced c-FLIP upregulation and NF-B activation, and triggered TRAIL-induced caspase-8 activation and cell death in OCs. Interestingly, the TRAIL-induced caspase-8 activation caused enzymatic degradation of the transcription factor Sp1 to noticeably reduce c-FLIP expression, which further sensitized OCs to TRAIL-induced apoptosis. Furthermore, the TAK1 inhibition induced antiosteoclastogenic activity by TRAIL even in cocultures with MM cells while potentiating TRAIL's anti-MM effects. These results demonstrated that osteoclastic lineage cells use TRAIL for their differentiation and activation through tilting caspase-8-dependent apoptosis toward NF-B activation, and that TAK1 inhibition subverts TRAIL-mediated NF-B activation to resume TRAIL-induced apoptosis in OCs while further enhancing MM cell death in combination with TRAIL.
(徳島大学機関リポジトリ): ● Metadata: 111724
(出版サイトへのリンク): ● Publication site (DOI): 10.1182/bloodadvances.2017008813
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29296860; ● Search Scopus @ Elsevier (PMID): 29296860; ● Search Scopus @ Elsevier (DOI): 10.1182/bloodadvances.2017008813

(徳島大学機関リポジトリ: 111724, DOI: 10.1182/bloodadvances.2017008813, PubMed: 29296860) Kiyoe Kurahashi, Itsuro Endo, Takeshi Kondo, Kana Morimoto, Sumiko Yoshida, Akio Kuroda, Ken-ichi Aihara, Munehide Matsuhisa, Kohhei Nakajima, Yoshifumi Mizobuchi, Shinji Nagahiro, Masahiro Abe and Seiji Fukumoto :
Remarkable Shrinkage of a Growth Hormone (GH)-secreting Macroadenoma Induced by Somatostatin Analogue Administration: A Case Report and Literature Review.,
Internal Medicine, Vol.56, No.18, 2455-2461, 2017.

(要約): Acromegaly is caused by excessive growth hormone secretion, usually from pituitary adenomas. Somoatostatin analogues are widely used as primary or adjunctive therapy in the management of acromegaly. In this report, we present a case with remarkable shrinkage of a tumor after relatively short-term octreotide long-acting release (LAR) administration. During the 30-month follow-up after starting octreotide LAR, there was no recurrence of acromegaly with remarkable shrinkage of the tumor on pituitary magnetic resonance imaging. A literature review of the predictors for tumor shrinkage after the administration of somatostatin analogues in patients with acromegaly is also discussed in relation to this case.
(徳島大学機関リポジトリ): ● Metadata: 114396
(出版サイトへのリンク): ● Publication site (DOI): 10.2169/internalmedicine.8223-16
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28824054; ● Summary page in Scopus @ Elsevier: 2-s2.0-85029653591

(徳島大学機関リポジトリ: 114396, DOI: 10.2169/internalmedicine.8223-16, PubMed: 28824054, Elsevier: Scopus) Muto Kohei, Naoko Matsui, Unai Yuki, Sakai Waka, Haji Shotaro, Udaka Kengo, Hirokazu Miki, Takahiro Furukawa, Masahiro Abe and Ryuji Kaji :
Memory B cell resurgence requires repeated rituximab in myasthenia gravis,
Neuromuscular Disorders, Vol.27, No.16, 918-922, 2017.

(要約): The immunologic effects of rituximab (RTX) in myasthenia gravis (MG) remain to be explored. We aimed to clarify immunologic reactions and their association with response to RTX in MG. Regulatory T cell and B cell profiles of MG patients were monitored. Two patients presenting with generalized MG with anti-acetylcholine receptor antibodies were treated with RTX. The treatment led to sustained clinical improvement, discontinuation of intravenous immunoglobulin or plasma exchange, and reduction of prednisolone and other drugs. One patient was in remission for more than one year, whereas the other patient exhibited deterioration of symptoms within one year. Disease activity was associated with the repopulation of IgDCD27 and IgDCD27 memory B cells. Clinicians should be aware of the possibility that MG ranges in the duration of B cell depletion and additional RTX should be prescribed upon resurgence of memory B cells.
(キーワード): Adult / Autoantibodies / B-Lymphocytes / Female / Humans / Immunoglobulins, Intravenous / Immunologic Factors / Middle Aged / Myasthenia Gravis / Receptors, Cholinergic / Rituximab / Treatment Outcome
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.nmd.2017.06.012
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28694074; ● Search Scopus @ Elsevier (PMID): 28694074; ● Search Scopus @ Elsevier (DOI): 10.1016/j.nmd.2017.06.012

(DOI: 10.1016/j.nmd.2017.06.012, PubMed: 28694074) Jun Okazaki, Naoki Muguruma, Shinji Kitamura, Tetsuo Kimura, Koichi Okamoto, Hiroshi Miyamoto, Kazuhiro Kishi, Yoshimi Bando, Takeshi Kondo, Itsuro Endo, Masahiro Abe and Tetsuji Takayama :
Paraneoplastic hypocalcemia developed in gastric cancer accompanied by osteoblastic metastasis,
Internal Medicine, Vol.56, No.11, 1345-1349, 2017.

(要約): Paraneoplastic syndromes are generally defined as clinical disorders associated with malignant diseases, and hypocalcemia associated with cancer is a rare condition. A woman in her 60s was referred to our hospital for the further examination of massive ascites due to carcinoma of unknown primary origin. She complained of numbness around her lips, and marked hypocalcemia of 5.0 mg/dL was noted. After two courses of chemotherapy, computed tomography showed a decrease in the ascites, and her serum calcium level increased. Although hypocalcemia is a very rare condition in patients with gastric cancer, serum calcium values should be evaluated when neurological symptoms are observed.
(キーワード): Adult / Aged / Female / Humans / Hypocalcemia / Middle Aged / Neoplasm Metastasis / Osteoblasts / Paraneoplastic Syndromes / Stomach Neoplasms / Tomography, X-Ray Computed / Treatment Outcome / Young Adult
(徳島大学機関リポジトリ): ● Metadata: 114393
(出版サイトへのリンク): ● Publication site (DOI): 10.2169/internalmedicine.56.8545
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28566596; ● Summary page in Scopus @ Elsevier: 2-s2.0-85020067897

(徳島大学機関リポジトリ: 114393, DOI: 10.2169/internalmedicine.56.8545, PubMed: 28566596, Elsevier: Scopus) Kiyoe Kurahashi, Seika Inoue, Sumiko Yoshida, Yasumasa Ikeda, Kana Morimoto, Ryoko Uemoto, Kazue Ishikawa, Takeshi Kondo, Tomoyuki Yuasa, Itsuro Endo, Masato Miyake, Seiichi Oyadomari, Toshio Matsumoto, Masahiro Abe, Hiroshi Sakaue and Ken-ichi Aihara :
The Role of Heparin Cofactor in the Regulation of Insulin Sensitivity and Maintenance of Glucose Homeostasis in Humans and Mice.,
Journal of Atherosclerosis and Thrombosis, 2017.

(要約): The present studies provide evidence to support the idea that HC plays an important role in the maintenance of glucose homeostasis by regulating insulin sensitivity in both humans and mice. Stimulators of HC production may serve as novel therapeutic tools for the treatment of type 2 diabetes.
(徳島大学機関リポジトリ): ● Metadata: 110925
(出版サイトへのリンク): ● Publication site (DOI): 10.5551/jat.37739
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28502917; ● Search Scopus @ Elsevier (PMID): 28502917; ● Search Scopus @ Elsevier (DOI): 10.5551/jat.37739

(徳島大学機関リポジトリ: 110925, DOI: 10.5551/jat.37739, PubMed: 28502917) Akio Kuroda, Tsuruo Miho, Aki Nanako, Takeshi Kondo, Oguro Yukari, Motoyuki Tamaki, Ken-ichi Aihara, Itsuro Endo, Toshio Matsumoto, Masahiro Abe and Munehide Matsuhisa :
A Pirot study comparing the CGM-assessed glycemic profiles of patients with type 1 diabetes on insulin degludec and insulin glargine,
Diabetology International, Vol.8, No.1, 112-115, 2017.

(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s13340-016-0289-4
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-85013200573

(DOI: 10.1007/s13340-016-0289-4, Elsevier: Scopus) Takeshi Kondo, Itsuro Endo, Yukari Ooguro, Kana Morimoto, Kiyoe Kurahashi, Sumiko Yoshida, Akio Kuroda, Ken-ichi Aihara, Munehide Matsuhisa, Masahiro Abe and Seiji Fukumoto :
Suppression of the Hypothalamic-pituitary-adrenal Axis by Maximum Androgen Blockade in a Patient with Prostate Cancer.,
Internal Medicine, Vol.55, No.24, 3623-3626, 2016.

(要約): A 78-year-old Japanese man showed suppression of the hypothalamic-pituitary-adrenal axis during maximum androgen blockade (MAB) therapy including chlormadinone acetate (CMA) for prostate cancer. After stopping the MAB therapy, both the basal ACTH level and the response to CRH recovered. While no reports have indicated that CMA suppresses the hypothalamic-pituitary-adrenal axis in patients with prostate cancer, CMA has been shown to inhibit this axis in animals. These observations suggest that we must monitor the hypothalamic-pituitary-adrenal axis in patients treated with CMA, especially under stressful conditions.
(キーワード): Adrenal Glands / Adrenocorticotropic Hormone / Aged / Androgen Antagonists / Animals / Antineoplastic Agents / Chlormadinone Acetate / Corticotropin-Releasing Hormone / Diabetes Mellitus, Type 2 / Humans / Hypothalamo-Hypophyseal System / Male / Pituitary-Adrenal System / Prostatic Neoplasms / Treatment Outcome
(徳島大学機関リポジトリ): ● Metadata: 114392
(出版サイトへのリンク): ● Publication site (DOI): 10.2169/internalmedicine.55.7359
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27980263; ● Summary page in Scopus @ Elsevier: 2-s2.0-85007140325

(徳島大学機関リポジトリ: 114392, DOI: 10.2169/internalmedicine.55.7359, PubMed: 27980263, Elsevier: Scopus) Ariunzaya Bat-Erdene, Hirokazu Miki, Asuko Oda, Shingen Nakamura, Jumpei Teramachi, Ryota Amachi, Hirofumi Tenshin, Masahiro Hiasa, Masami Iwasa, Takeshi Harada, Shiroh Fujii, Kimiko Sogabe, Kumiko Kagawa, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara and Masahiro Abe :
Synergistic targeting of Sp1, a critical transcription factor for myeloma cell growth and survival, by panobinostat and proteasome inhibitors.,
Oncotarget, Vol.7, No.48, 79064-79075, 2016.

(要約): Panobinostat, a pan-deacetylase inhibitor, synergistically elicits cytotoxic activity against myeloma (MM) cells in combination with the proteasome inhibitor bortezomib. Because precise mechanisms for panobinostat's anti-MM action still remain elusive, we aimed to clarify the mechanisms of anti-MM effects of panobinostat and its synergism with proteasome inhibitors. Although the transcription factor Sp1 was overexpressed in MM cells, the Sp1 inhibitor terameprocol induced MM cell death in parallel with reduction of IRF4 and cMyc. Panobinostat induced activation of caspase-8, which was inversely correlated with reduction of Sp1 protein levels in MM cells. The panobinostat-mediated effects were further potentiated to effectively induce MM cell death in combination with bortezomib or carfilzomib even at suboptimal concentrations as a single agent. Addition of the caspase-8 inhibitor z-IETD-FMK abolished the Sp1 reduction not only by panobinostat alone but also by its combination with bortezomib, suggesting caspase-8-mediated Sp1 degradation. The synergistic Sp1 reduction markedly suppressed Sp1-driven prosurvival factors, IRF4 and cMyc. Besides, the combinatory treatment reduced HDAC1, another Sp1 target, in MM cells, which may potentiate HDAC inhibition. Collectively, caspase-8-mediated post-translational Sp1 degradation appears to be among major mechanisms for synergistic anti-MM effects of panobinostat and proteasome inhibitors in combination.
(徳島大学機関リポジトリ): ● Metadata: 109988
(出版サイトへのリンク): ● Publication site (DOI): 10.18632/oncotarget.12594
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27738323; ● Search Scopus @ Elsevier (PMID): 27738323; ● Search Scopus @ Elsevier (DOI): 10.18632/oncotarget.12594

(徳島大学機関リポジトリ: 109988, DOI: 10.18632/oncotarget.12594, PubMed: 27738323) Ryota Amachi, Masahiro Hiasa, Jumpei Teramachi, Takeshi Harada, Asuka Oda, Shingen Nakamura, Derek Hanson, Keiichiro Watanabe, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, Masami Iwasa, Itsuro Endo, Takeshi Kondo, Sumiko Yoshida, Ken-ichi Aihara, Kiyoe Kurahashi, Yoshiaki Kuroda, Hideaki Horikawa, Eiji Tanaka, Masahiro Abe and Toshio Matsumoto :
A vicious cycle between acid sensing and survival signaling in myeloma cells: acid-induced epigenetic alteration.,
Oncotarget, Vol.7, No.43, 70447-70461, 2016.

(要約): Myeloma (MM) cells and osteoclasts are mutually interacted to enhance MM growth while creating acidic bone lesions. Here, we explored acid sensing of MM cells and its role in MM cell response to acidic conditions. Acidic conditions activated the PI3K-Akt signaling in MM cells while upregulating the pH sensor transient receptor potential cation channel subfamily V member 1 (TRPV1) in a manner inhibitable by PI3K inhibition. The acid-activated PI3K-Akt signaling facilitated the nuclear localization of the transcription factor Sp1 to trigger the expression of its target genes, including TRPV1 and HDAC1. Consistently, histone deacetylation was enhanced in MM cells in acidic conditions, while repressing a wide variety of genes, including DR4. Indeed, acidic conditions deacetylated histone H3K9 in a DR4 gene promoter and curtailed DR4 expression in MM cells. However, inhibition of HDAC as well as either Sp1 or PI3K was able to restore DR4 expression in MM cells suppressed in acidic conditions. These results collectively demonstrate that acid activates the TRPV1-PI3K-Akt-Sp1 signaling in MM cells while inducing HDAC-mediated gene repression, and suggest that a positive feedback loop between acid sensing and the PI3K-Akt signaling is formed in MM cells, leading to MM cell response to acidic bone lesions.
(徳島大学機関リポジトリ): ● Metadata: 113048
(出版サイトへのリンク): ● Publication site (DOI): 10.18632/oncotarget.11927
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27626482; ● Search Scopus @ Elsevier (PMID): 27626482; ● Search Scopus @ Elsevier (DOI): 10.18632/oncotarget.11927

(徳島大学機関リポジトリ: 113048, DOI: 10.18632/oncotarget.11927, PubMed: 27626482) Takeshi Harada, Hirokazu Miki, Q Cui, A Oda, Ryota Amachi, Jumpei Teramachi, A Bat-Erdene, K Sogabe, M Iwasa, Shiroh Fujii, Shingen Nakamura, Kumiko Kagawa, Sumiko Yoshida, I Endo, Ken-ichi Aihara, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe :
Expansion of Th1-like V9V2T cells by new-generation IMiDs, lenalidomide and pomalidomide, in combination with zoledronic acid.,
Leukemia, Vol.31, No.1, 258-262, 2016.

(出版サイトへのリンク): ● Publication site (DOI): 10.1038/leu.2016.273
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27698446; ● Search Scopus @ Elsevier (PMID): 27698446; ● Search Scopus @ Elsevier (DOI): 10.1038/leu.2016.273

(DOI: 10.1038/leu.2016.273, PubMed: 27698446) Naoto Okada, Takeshi Hanafusa, Shinji Abe, Chiemi Sato, Toshimi Nakamura, Kazuhiko Teraoka, Masahiro Abe, Kazuyoshi Kawazoe and Keisuke Ishizawa :
Evaluation of the risk factors associated with high-dose chemotherapyinduced dysgeusia in patients undergoing autologous hematopoietic stem cell transplantation: Possible usefulness of cryotherapy in dysgeusia prevention,
Supportive Care in Cancer, Vol.24, No.9, 3979-3985, 2016.

(要約): Dysgeusia is one of the sporadic adverse effects induced by chemotherapy, but it remains poorly understood. The aim of this study was to retrospectively identify the risk factors related with dysgeusia in patients undergoing autologous hematopoietic stem cell transplantation (AHSCT). Forty-eight patients with myeloma or lymphoma undergoing AHSCT were enrolled in this study. Data regarding dysgeusia and symptoms were collected by interviews conducted by medical workers. Patient characteristics and unfavorable effects induced by dysgeusia were obtained from medical records and analyzed. Logistic regression analysis was performed to identify the risk factors related with dysgeusia. Of the 48 patients, 20 (42 %) had dysgeusia after AHSCT. The total period of parenteral nutrition (TPN) administration and period of decreased oral intake in the dysgeusia group were statistically longer than those in the non-dysgeusia group. Multivariate analyses revealed that oral mucositis (odds ratio: 30.3; p < 0.01) and the type of chemotherapy prior to AHSCT (odds ratio: 6.56; p < 0.05) were independent risk factors, while oral cryotherapy was the independent suppressive factor of dysgeusia (odds ratio: 0.14; p < 0.05). Our study showed that dysgeusia after AHSCT led to the decrease in oral intake and extended the TPN administration period. Moreover, MEAM or LEED chemotherapy and oral mucositis were independent risk factors for dysgeusia in patients undergoing AHSCT, while oral cryotherapy was an independent suppressive factor for dysgeusia. Therefore, oral cryotherapy should be implemented into the regimen of supportive care management in patients undergoing AHSCT.
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s00520-016-3244-9
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27129837; ● Search Scopus @ Elsevier (PMID): 27129837; ● Search Scopus @ Elsevier (DOI): 10.1007/s00520-016-3244-9

(DOI: 10.1007/s00520-016-3244-9, PubMed: 27129837) Takeshi Kondo, Itsuro Endo, Ken-ichi Aihara, Ohnishi Yukiyo, Dong Bingzi, Oguro Yukari, Kiyoe Kurahashi, Sumiko Yoshida, Yuichi Fujinaka, Akio Kuroda, Munehide Matsuhisa, Seiji Fukumoto, Toshio Matsumoto and Masahiro Abe :
Serum carboxy-terminal telopeptide of type I collagen levels are associated with carotid atherosclerosis in patients with cardiovascular risk factors.,
Endocrine Journal, Vol.63, No.4, 397-404, 2016.

(要約): Carboxy-terminal telopeptide of type I collagen (ICTP) is generated through matrix metalloproteinase (MMP)-dependent type I collagen digestion, and has been widely utilized as a biomarker for bone turnover. The fact that atherosclerotic lesions are rich in both type I collagen and MMP-producing macrophages led to the hypothesis that serum ICTP concentrations may serve as a non-invasive clinical biomarker for atherosclerosis. Therefore, the association of serum ICTP concentrations with the maximum intima-media thickness (IMT) of carotid arteries, a surrogate index of systemic atherosclerosis, or brachial-ankle pulse wave velocity (baPWV) in patients with atherosclerotic risk factors was evaluated. A total of 52 male and 65 female (mean age: 62.8 yrs) patients without renal failure, malignancies or bone diseases known to affect serum ICTP concentrations were recruited. Patients with max IMTs ≥1.1 mm showed significantly higher serum ICTP concentrations compared with patients with max IMTs <1.1 mm (3.33 ± 0.97 vs 2.82 ± 0.65 ng/mL, p<0.05). Serum ICTP concentration was also positively correlated with max IMT (p<0.001) or baPWV values (p<0.05). Multivariate analyses also revealed that serum ICTP concentrations were correlated with max IMT (p<0.001; 95% CI 0.200 to 0.454). These results suggest that serum ICTP concentrations can be used as a non-invasive biomarker for systemic atherosclerosis.
(徳島大学機関リポジトリ): ● Metadata: 109666
(出版サイトへのリンク): ● Publication site (DOI): 10.1507/endocrj.EJ15-0589
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26877258; ● Summary page in Scopus @ Elsevier: 2-s2.0-84964267287

(徳島大学機関リポジトリ: 109666, DOI: 10.1507/endocrj.EJ15-0589, PubMed: 26877258, Elsevier: Scopus) Naoto Okada, Shuji Fushitani, Momoyo Azuma, Shingen Nakamura, Toshimi Nakamura, Kazuhiko Teraoka, Hiroyoshi Watanabe, Masahiro Abe, Kazuyoshi Kawazoe and Keisuke Ishizawa :
Clinical evaluation of pharmacist interventions in patients treated with anti-methicillin-resistant Staphylococcus aureus agents in a hematological ward,
Biological & Pharmaceutical Bulletin, Vol.39, No.2, 295-300, 2015.

(要約): The therapeutic effects of anti-methicillin-resistant Staphylococcus aureus (MRSA) agents, vancomycin (VCM), teicoplanin (TEIC), and arbekacin (ABK), depend on their concentrations in blood. Therefore, therapeutic drug monitoring (TDM) is important when these antibiotics are used. In the hematological ward at Tokushima University Hospital, pharmacists have ordered the measurement of blood VCM, TEIC, and ABK concentrations to promote the use of TDM in accordance with an agreed protocol since 2013. Moreover, the infection control team includes several medical disciplines and has advised on the optimal treatment using VCM, TEIC, and ABK since 2013. This study aimed to investigate the clinical effectiveness of these pharmacist interventions. We retrospectively studied 145 cases in which patients were treated with VCM, TEIC, or ABK between January 2012 and December 2013 in the hematological ward at Tokushima University Hospital. The patients were divided into a control group (71 cases) and an intervention group (74 cases), and their clinical outcomes were compared. The rate of achievement of effective drug concentrations significantly increased in the intervention group (74%), compared to the rate in the control group (55%). Moreover, univariate and multivariate Cox proportional hazard regression revealed that pharmacist intervention and appropriate concentrations of anti-MRSA agents were independent factors associated with reduced hospitalization periods in patients with lymphoma. Our study revealed that proactive pharmacist intervention may improve the therapeutic effect of anti-MRSA agents in hematology ward patients.
(出版サイトへのリンク): ● Publication site (DOI): 10.1248/bpb.b15-00774
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26830489; ● Search Scopus @ Elsevier (PMID): 26830489; ● Search Scopus @ Elsevier (DOI): 10.1248/bpb.b15-00774

(DOI: 10.1248/bpb.b15-00774, PubMed: 26830489) James Derek Hanson, Shingen Nakamura, Ryota Amachi, Masahiro Hiasa, Asuka Oda, Daisuke Tsuji, Kohji Itoh, Takeshi Harada, Kazuki Horikawa, Jumpei Teramachi, Hirokazu Miki, Toshio Matsumoto and Masahiro Abe :
Effective impairment of myeloma cells and their progenitors by blockade of monocarboxylate transportation.,
Oncotarget, Vol.6, No.32, 33568-33586, 2015.

(要約): Cancer cells robustly expel lactate produced through enhanced glycolysis via monocarboxylate transporters (MCTs) and maintain alkaline intracellular pH. To develop a novel therapeutic strategy against multiple myeloma (MM), which still remains incurable, we explored the impact of perturbing a metabolism via inhibiting MCTs. All MM cells tested constitutively expressed MCT1 and MCT4, and most expressed MCT2. Lactate export was substantially suppressed to induce death along with lowering intracellular pH in MM cells by blockade of all three MCT molecules with -cyano-4-hydroxy cinnamate (CHC) or the MCT1 and MCT2 inhibitor AR-C155858 in combination with MCT4 knockdown, although only partially by knockdown of each MCT. CHC lowered intracellular pH and severely curtailed lactate secretion even when combined with metformin, which further lowered intracellular pH and enhanced cytotoxicity. Interestingly, an ambient acidic pH markedly enhanced CHC-mediated cytotoxicity, suggesting preferential targeting of MM cells in acidic MM bone lesions. Furthermore, treatment with CHC suppressed hexokinase II expression and ATP production to reduce side populations and colony formation. Finally, CHC caused downregulation of homing receptor CXCR4 and abrogated SDF-1-induced migration. Targeting tumor metabolism by MCT blockade therefore may become an effective therapeutic option for drug-resistant MM cells with elevated glycolysis.
(徳島大学機関リポジトリ): ● Metadata: 109501
(出版サイトへのリンク): ● Publication site (DOI): 10.18632/oncotarget.5598
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26384349; ● Summary page in Scopus @ Elsevier: 2-s2.0-84946086135

(徳島大学機関リポジトリ: 109501, DOI: 10.18632/oncotarget.5598, PubMed: 26384349, Elsevier: Scopus) Michiko Yamashita, Yoshiyuki Fujii, Keiji Ozaki, Yoshio Urano, Masami Iwasa, Shingen Nakamura, Shiroh Fujii, Masahiro Abe, Yasuharu Sato and Tadashi Yoshino :
Human immunodeficiency virus-positive secondary syphilis mimicking cutaneous T-cell lymphoma.,
Diagnostic Pathology, Vol.10, 185, 2015.

(要約): Malignant syphilis or lues maligna is a severe form of secondary syphilis that was commonly reported in the pre-antibiotic era, and has now reemerged with the advent of the human immunodeficiency virus (HIV) epidemic. However, the characteristic histopathological findings of malignant syphilis remain controversial. The aim of this case report was to clarify the clinical and histopathological findings of HIV-positive malignant secondary syphilis. A Japanese man in his forties complained of fever, skin lesions, headache, and myalgia without lymphadenopathy during the previous 4 weeks. The skin lesions manifested as erythematous, nonhealing, ulcerated papules scattered on his trunk, extremities, palm, and face. Although the skin lesions were suspected to be cutaneous T-cell lymphomas on histological analyses, they lacked T-cell receptor Jγ rearrangement; moreover, immunohistochemical analyses confirmed the presence of spirochetes. The patient was administered antibiotics and anti-retroviral therapy, which dramatically improved the symptoms. On the basis of these observations of the skin lesions, we finally diagnosed the patient with HIV-associated secondary syphilis that mimicked cutaneous T-cell lymphoma. The patient's systemic CD4+ lymphocyte count was very low, and the infiltrate was almost exclusively composed of CD8+ atypical lymphocytes; therefore, the condition was easily misdiagnosed as cutaneous lymphoma. Although the abundance of plasma cells is a good indicator of malignant syphilis on skin histological analyses, in some cases, the plasma cell count may be very low. Therefore, a diagnosis of malignant secondary syphilis should be considered before making a diagnosis of primary cutaneous peripheral T-cell lymphoma or lymphoma associated with HIV infection.
(キーワード): AIDS-Related Opportunistic Infections / Anti-Bacterial Agents / Anti-HIV Agents / Biopsy / Coinfection / Diagnosis, Differential / HIV Infections / Humans / 免疫組織化学 (immunohistochemistry) / Lymphoma, T-Cell, Cutaneous / 男性 (male) / Predictive Value of Tests / 皮膚 (skin) / Skin Neoplasms / Syphilis / Syphilis, Cutaneous / Treatment Outcome
(出版サイトへのリンク): ● Publication site (DOI): 10.1186/s13000-015-0419-5
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26449225; ● Summary page in Scopus @ Elsevier: 2-s2.0-84943540407

(DOI: 10.1186/s13000-015-0419-5, PubMed: 26449225, Elsevier: Scopus) Shingen Nakamura, Hirokazu Miki, Asuka Oda, Ryota Amachi, Jumpei Teramachi, Kimiko Sogabe, Hikaru Fujino, Tomoko Maruhashi, Shiroh Fujii, Kumiko Kagawa and Masahiro Abe :
Susceptibility to bendamustine considerably varies among myeloma cells, but is enhanced in acidic conditions,
International Journal of Myeloma, Vol.6, No.1, 7-11, 2015. Bingzi Dong, Itsuro Endo, Yukiyo Ohnishi, Takeshi Kondo, Tomoka Hasegawa, Norio Amizuka, Hiroshi Kiyonari, Go Shioi, Masahiro Abe, Seiji Fukumoto and Toshio Matsumoto :
Calcilytic Ameliorates Abnormalities of Mutant Calcium-Sensing Receptor (CaSR) Knock-In Mice Mimicking Autosomal Dominant Hypocalcemia (ADH).,
Journal of Bone and Mineral Research, Vol.30, No.11, 1980-1993, 2015.

(要約): Activating mutations of calcium-sensing receptor (CaSR) cause autosomal dominant hypocalcemia (ADH). ADH patients develop hypocalcemia, hyperphosphatemia, and hypercalciuria, similar to the clinical features of hypoparathyroidism. The current treatment of ADH is similar to the other forms of hypoparathyroidism, using active vitamin D3 or parathyroid hormone (PTH). However, these treatments aggravate hypercalciuria and renal calcification. Thus, new therapeutic strategies for ADH are needed. Calcilytics are allosteric antagonists of CaSR, and may be effective for the treatment of ADH caused by activating mutations of CaSR. In order to examine the effect of calcilytic JTT-305/MK-5442 on CaSR harboring activating mutations in the extracellular and transmembrane domains in vitro, we first transfected a mutated CaSR gene into HEK cells. JTT-305/MK-5442 suppressed the hypersensitivity to extracellular Ca(2+) of HEK cells transfected with the CaSR gene with activating mutations in the extracellular and transmembrane domains. We then selected two activating mutations locating in the extracellular (C129S) and transmembrane (A843E) domains, and generated two strains of CaSR knock-in mice to build an ADH mouse model. Both mutant mice mimicked almost all the clinical features of human ADH. JTT-305/MK-5442 treatment in vivo increased urinary cAMP excretion, improved serum and urinary calcium and phosphate levels by stimulating endogenous PTH secretion, and prevented renal calcification. In contrast, PTH(1-34) treatment normalized serum calcium and phosphate but could not reduce hypercalciuria or renal calcification. CaSR knock-in mice exhibited low bone turnover due to the deficiency of PTH, and JTT-305/MK-5442 as well as PTH(1-34) increased bone turnover and bone mineral density (BMD) in these mice. These results demonstrate that calcilytics can reverse almost all the phenotypes of ADH including hypercalciuria and renal calcification, and suggest that calcilytics can become a novel therapeutic agent for ADH.
(徳島大学機関リポジトリ): ● Metadata: 109486
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/jbmr.2551
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25967373; ● Summary page in Scopus @ Elsevier: 2-s2.0-84945482381

(徳島大学機関リポジトリ: 109486, DOI: 10.1002/jbmr.2551, PubMed: 25967373, Elsevier: Scopus) Jin Temma, Munehide Matsuhisa, Toru Horie, Akio Kuroda, Hiroyasu Mori, Motoyuki Tamaki, Itsuro Endo, Ken-ichi Aihara, Masahiro Abe and Toshio Matsumoto :
Non-invasive Measurement of Skin Autofluorescence as a Beneficial Surrogate Marker for Atherosclerosis in Patients with Type 2 Diabetes,
The Journal of Medical Investigation : JMI, Vol.62, No.3-4, 126-129, 2015.

(要約): Advanced glycation end-products (AGEs) are thought to play a major role in the pathogenesis of diabetic vascular complications. Skin autofluorescence (AF) was recently reported to represent tissue AGEs accumulation with a non-invasive method. The aim of the present study was to evaluate association between AF value and diabetic vascular complications, such as retinopathy, nephropathy and cervical atherosclerosis using the carotid intima-media thickness (IMT), an established marker of cardiovascular disease in patients with type 2 diabetes. A total of 68 patients with type 2 diabetes were enrolled in a cross-sectional manner. AGEs accumulation was measured with AF reader. Clinical parameters were collected at the time of AF and IMT measurement. Max-IMT was correlated with age and AF (r=0.407, p=0.001), but not with HbA1c, GA, and pentosidine. Also, AF was not correlated with HbA1c, GA and pentosidine, but was correlated with age (r=0.560, p<0.001), duration of diabetes (r=0.256, p<0.05). Multivariate regression analysis revealed that AF, but not age, was an independent determinant of max-IMT. In conclusion, AF might be a beneficial surrogate marker for evaluating carotid atherosclerosis in patients with type 2 diabetes non-invasively. J. Med. Invest. 62: 126-129, August, 2015.
(徳島大学機関リポジトリ): ● Metadata: 111266
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.62.126
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26399335; ● Summary page in Scopus @ Elsevier: 2-s2.0-84942054596

(徳島大学機関リポジトリ: 111266, DOI: 10.2152/jmi.62.126, PubMed: 26399335, Elsevier: Scopus) T Watanabe, M Mitsuhashi, M Sagawa, M Ri, K Suzuki, Masahiro Abe, K Ohmachi, Y Nakagawa, Shingen Nakamura, S Iida and M Kizaki :
Lipopolysaccharide-Induced CXCL10 mRNA Level and Six Stimulant-mRNA Combinations in Whole Blood: Novel Biomarkers for Bortezomib Responses Obtained from a Prospective Multicenter Trial for Patients with Multiple Myeloma,
PLoS ONE, Vol.10, No.6, e0128662, 2015.

(要約): To identify predictive biomarkers for clinical responses to bortezomib treatment, 0.06 mL of each whole blood without any cell separation procedures was stimulated ex vivo using five agents, and eight mRNAs were quantified. In six centers, heparinized peripheral blood was prospectively obtained from 80 previously treated or untreated, symptomatic multiple myeloma (MM) patients with measurable levels of M-proteins. The blood sample was procured prior to treatment as well as 2-3 days and 1-3 weeks after the first dose of bortezomib, which was intravenously administered biweekly or weekly, during the first cycle. Six stimulant-mRNA combinations; that is, lipopolysaccharide (LPS)-granulocyte-macrophage colony-stimulating factor (GM-CSF), LPS-CXCL chemokine 10 (CXCL10), LPS-CCL chemokine 4 (CCL4), phytohemagglutinin-CCL4, zymosan A (ZA)-GMCSF and ZA-CCL4 showed significantly higher induction in the complete and very good partial response group than in the stable and progressive disease group, as determined by both parametric (t-test) and non-parametric (unpaired Mann-Whitney test) tests. Moreover, LPS-induced CXCL10 mRNA expression was significantly suppressed 2-3 days after the first dose of bortezomib in all patients, as determined by both parametric (t-test) and non-parametric (paired Wilcoxon test) tests, whereas the complete and very good partial response group showed sustained suppression 1-3 weeks after the first dose. Thus, pretreatment LPS-CXCL10 mRNA and/or the six combinations may serve as potential biomarkers for the response to bortezomib treatment in MM patients.
(徳島大学機関リポジトリ): ● Metadata: 114924
(出版サイトへのリンク): ● Publication site (DOI): 10.1371/journal.pone.0128662
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26115406; ● Summary page in Scopus @ Elsevier: 2-s2.0-84938631804

(徳島大学機関リポジトリ: 114924, DOI: 10.1371/journal.pone.0128662, PubMed: 26115406, Elsevier: Scopus) Hirokazu Miki, Shingen Nakamura, A Oda, R Amachi, Keiichiro Watanabe, D Hanson, Jumpei Teramachi, Masahiro Hiasa, H Yagi, K Sogabe, M Takahashi, T Maruhashi, K Udaka, T Harada, Shiroh Fujii, A Nakano, Kumiko Kagawa, M Ri, S Iida, Shuji Ozaki, T Matsumoto and Masahiro Abe :
Induction of endoplasmic reticulum stress by bortezomib sensitizes myeloma cells to DR5-mediated cell death,
International Journal of Myeloma, Vol.5, No.1, 1-7, 2015.

(要約): TNF-related apoptosis-including ligand/Apo2 (TRAIL)-mediated immunotherapy is an attractive anti-tumor modality with high tumor specificity. In order to improve its therapeutic efficacy, we further need to implement a novel maneuver for sensitization of malignant cells to TRAIL. Bortezomib (BTZ), a novel anti-myeloma (MM) agent, potently induces endoplasmic reticulum (ER) stress to cause apoptosis. Here, we explored the roles of BTZ in the cytotoxicity of anti-TRAIL receptor agonistic antibodies against MM cells with special reference to ER stress. BTZ enhanced the expression of death receptor 5 (DR5) but not DR4 in MM cells at surface protein as well as mRNA levels. However, the DR5 expression was not affected by BTZ without ER stress induction in MM cells with a point mutation in a BTZ-binding proteasome β5 subunit. Tunicamycin, an ER stress inducer, was able to enhance the DR5 expression even in the BTZ-resistant MM cells, suggesting the role of ER stress in up-regulation of DR5 expression. Interestingly, BTZ facilitated extrinsic caspase-mediated apoptosis by anti-DR5 agonistic antibody in MM cells along with reducing c-FLICE-like interleukin protein, a caspase 8 inhibitor. These results suggest that BTZ enhances DR5 expression and its downstream apoptotic signaling through ER stress to sensitize MM cells to TRAIL-mediated immunotherapy.
(キーワード): multiple myeloma / bortezomib / TRAIL / DR5 / ER stress
(出版サイトへのリンク): ● Publication site (DOI): 10.57352/ijm.5.1_1
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390292815284471040; ● Search Scopus @ Elsevier (DOI): 10.57352/ijm.5.1_1

(DOI: 10.57352/ijm.5.1_1, CiNii: 1390292815284471040) Koichiro Hayashi, Michihiro Nakamura, Hirokazu Miki, Shuji Ozaki, Masahiro Abe, Toshio Matsumoto, Sakamoto Wataru, Yogo Toshinobu and Kazunori Ishimura :
Magnetically Responsive Smart Nanoparticles for Cancer Treatment with a Combination of Magnetic Hyperthermia and Remote-Control Drug Release,
Theranostics, Vol.4, No.8, 834-844, 2014.

(要約): We report the synthesis of smart nanoparticles (NPs) that generate heat in response to an alternating current magnetic field (ACMF) and that sequentially release an anticancer drug (doxorubicin, DOX). We further study the in vivo therapeutic efficacy of the combination of magnetic hyperthermia (MHT) and chemotherapy using the smart NPs for the treatment of multiple myeloma. The smart NPs are composed of a polymer with a glass-transition temperature (T g) of 44°C, which contains clustered Fe3O4 NPs and DOX. The clustered Fe3O4 NPs produce heat when the ACMF is applied and rise above 44°C, which softens the polymer phase and leads to the release of DOX. The combination of MHT and chemotherapy using the smart NPs destroys cancer cells in the entire tumor and achieves a complete cure in one treatment without the recurrence of malignancy. Furthermore, the smart NPs have no significant toxicity.
(キーワード): Animals / Body Weight / Drug Liberation / Female / Hyperthermia, Induced / Magnetic Phenomena / Mice / Nanoparticles / Neoplasms / Organ Size / Telemedicine
(出版サイトへのリンク): ● Publication site (DOI): 10.7150/thno.9199
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24955144; ● Summary page in Scopus @ Elsevier: 2-s2.0-84902517614

(DOI: 10.7150/thno.9199, PubMed: 24955144, Elsevier: Scopus) 賀川久美子, 中村信元, 八木ひかる, 曽我部公子, 髙橋真美子, 丸橋朋子, 宇髙憲吾, 藤井志朗, 三木浩和, 安倍正博 :
同系骨髄移植が著効した最重症再生不良性貧血の1例,
四国医学雑誌, Vol.70, No.3,4, 77-80, 2014年.

(要約): Aplastic anemia is a bone marrow failure caused by severely curtailed hematopoietic stem cells (HSCs) and dysregulation of ambient immune cells. Immumo-suppressive conditioning followed by allogeneic HSC transplantation is currently a mainstay in treatment for patients at a younger age or those refractory to conventional immunosuppressive remedies. Syngeneic HSC transplantation appears to be promising, but has been very rarely performed ; therefore, its impact on a long-term outcome as well as the best preparative measures for HSC engraftment and immune amelioration are still largely unknown. Here, we reported a successful and beneficial syngeneic HSC transplantation for a refractory case with very severe aplastic anemia. A 30-year-old female presented high fever after tooth extraction, and was diagnosed with very severe aplastic anemia. Cyclosporine and anti-thymocyte globulin were initiated, but showed no hematological effects. After obtaining an informed consent, she underwent bone marrow transplantation from a genetically identical twin following an non-myeloablative conditioning regimen consisted of cyclophosphamide (750mg/m2, 4 days), fludarabine phosphate (25mg/m2, 4 days). Cyclosporine was given for acute GvHD prophylaxis. Her neutrophils recovered over 500/μl on 12 days after the transplantation, and her blood counts have been maintained in a normal range over 7 years thereafter. Although a fate of HSCs from a genetically identical twin and an immune response of ambient cells in the bone marrow in recipients remains largely unknown, from the present case and previously reported cases, we dare to recommend immunoablative conditioning and acute GvHD prophylaxis in syngeneic HSC transplantation for a refractory case with aplastic anemia for better engraftment and sustained onward recovery of hematopoiesis.
(キーワード): aplastic anemia / genetically identical twin / syngeneic hematopoietic stem cell transplantation
(徳島大学機関リポジトリ): ● Metadata: 109757
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1050001337464993408

(徳島大学機関リポジトリ: 109757, CiNii: 1050001337464993408) Naoto Okada, Takeshi Hanafusa, Takumi Sakurada, Kazuhiko Teraoka, Toshihide Kujime, Masahiro Abe, Yasuo Shinohara, Kazuyoshi Kawazoe and Kazuo Minakuchi :
Risk Factors for Early-Onset Peripheral Neuropathy Caused by Vincristine in Patients With a First Administration of R-CHOP or R-CHOP-Like Chemotherapy,
Journal of Clinical Medicine Research, Vol.6, No.4, 252-260, 2014.

(要約): Peripheral neuropathy is a well-known side effect of vincristine (VCR), a microtubule inhibitor used for R-CHOP or R-CHOP-like (namely R-CVP and R-THP-COP) regimens. Previous studies have shown that both the total dose of VCR and the number of treatment cycles are related to the incidence of VCR-induced peripheral neuropathy (VIPN). However, VIPN will also occur during the first treatment cycle regardless of the total dose of VCR or number of treatment cycles (early-onset VIPN). There is little information about early-onset VIPN, and it is difficult to predict. The present study's goal was to identify risk factors for early-onset VIPN. We analyzed the case records of patients who had their first administration of an R-CHOP or R-CHOP-like regimen between April 2008 and August 2013 at Tokushima University Hospital in Tokushima, Japan. To identify the risk factors for early-onset VIPN, we performed univariate and multivariate logistic regression analyses. Forty-one patients underwent an R-CHOP or R-CHOP-like regimen for the first time at Tokushima University Hospital between April 2008 and August 2013, and 14 patients had grade 1 or higher early-onset VIPN. A univariate analysis revealed that age, the dose of VCR and the concomitant use of aprepitant appeared to be the risk factors of early-onset VIPN. In our calculation using receiver-operator characteristics curves, the cut-off value for patient age was 65 years and that of the dose of VCR was 1.9 mg. A multivariate analysis revealed that VCR dose ≥ 1.9 mg and the concomitant use of the antiemetic aprepitant were independent risk factors for early-onset VIPN. Our present study showed that the patients who had VCR dose ≥ 1.9 mg and the concomitant use of aprepitant had the risk for early-onset VIPN. This suggests that it is important to use aprepitant in light of the risk of early-onset VIPN and the benefit of aprepitant's antiemetic effect in R-CHOP and R-CHOP-like regimens.
(出版サイトへのリンク): ● Publication site (DOI): 10.14740/jocmr1856w
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24883150; ● Search Scopus @ Elsevier (PMID): 24883150; ● Search Scopus @ Elsevier (DOI): 10.14740/jocmr1856w

(DOI: 10.14740/jocmr1856w, PubMed: 24883150) Masahiro Hiasa, Jumpei Teramachi, A Oda, Ryota Amachi, T Harada, Shingen Nakamura, Hirokazu Miki, Shiroh Fujii, Kumiko Kagawa, Keiichiro Watanabe, Itsuro Endo, Y Kuroda, T Yoneda, Daisuke Tsuji, Michiyasu Nakao, Eiji Tanaka, Kenichi Hamada, Shigeki Sano, Kouji Itou, Toshio Matsumoto and Masahiro Abe :
Pim-2 kinase is an important target of treatment for tumor progression and bone loss in myeloma.,
Leukemia, 2014.

(要約): Pim-2 kinase is overexpressed in multiple myeloma (MM) cells to enhance their growth and survival, and regarded as a novel therapeutic target in MM. However, the impact of Pim-2 inhibition on bone disease in MM remains unknown. We demonstrated here that Pim-2 expression was also upregulated in bone marrow stromal cells and MC3T3-E1 preosteoblastic cells in the presence of cytokines known as the inhibitors of osteoblastogenesis in MM, including interleukin-3 (IL-3), IL-7, tumor necrosis factor-, transforming growth factor- (TGF-) and activin A, as well as MM cell conditioned media. The enforced expression of Pim-2 abrogated in vitro osteoblastogenesis by BMP-2, which suggested Pim-2 as a negative regulator for osteoblastogenesis. Treatment with Pim-2 short-interference RNA as well as the Pim inhibitor SMI-16a successfully restored osteoblastogenesis suppressed by all the above inhibitory factors and MM cells. The SMI-16a treatment potentiated BMP-2-mediated anabolic signaling while suppressing TGF- signaling. Furthermore, treatment with the newly synthesized thiazolidine-2,4-dione congener, 12a-OH, as well as its prototypic SMI-16a effectively prevented bone destruction while suppressing MM tumor growth in MM animal models. Thus, Pim-2 may have a pivotal role in tumor progression and bone loss in MM, and Pim-2 inhibition may become an important therapeutic strategy to target the MM cell-bone marrow interaction.Leukemia advance online publication, 30 May 2014; doi:10.1038/leu.2014.147.
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/leu.2014.147
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24787487; ● Search Scopus @ Elsevier (PMID): 24787487; ● Search Scopus @ Elsevier (DOI): 10.1038/leu.2014.147

(DOI: 10.1038/leu.2014.147, PubMed: 24787487) Masahiro Abe, Takeshi Harada and Toshio Matsumoto :
Concise review: Defining and targeting myeloma stem cell-like cells.,
Stem Cells, Vol.32, No.5, 1067-1073, 2014.

(要約): Multiple myeloma (MM) remains incurable despite recent advances in the treatment of MM. Although the idea of MM cancer stem cells (CSCs) has been proposed for the drug resistance in MM, MM CSCs have not been properly defined yet. Besides clonotypic B cells, phenotypically distinct MM plasma cell fractions have been demonstrated to possess a clonogenic capacity, leading to long-lasting controversies regarding the cells of origin in MM or MM-initiating cells. However, MM CSCs may not be a static population and survive as phenotypically and functionally different cell types via the transition between stem-like and non-stem-like states in local microenvironments, as observed in other types of cancers. Targeting MM CSCs is clinically relevant, and different approaches have been suggested to target molecular, metabolic and epigenetic signatures, and the self-renewal signaling characteristic of MM CSC-like cells.
(キーワード): Animals / Cell Differentiation / Clone Cells / Humans / Models, Biological / Multiple Myeloma / Neoplastic Stem Cells / Stem Cell Niche / Tumor Microenvironment
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/stem.1643
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24449391; ● Search Scopus @ Elsevier (PMID): 24449391; ● Search Scopus @ Elsevier (DOI): 10.1002/stem.1643

(DOI: 10.1002/stem.1643, PubMed: 24449391) Koichiro Hayashi, Michihiro Nakamura, Hirokazu Miki, Shuji Ozaki, Masahiro Abe, Toshio Matsumoto, Toshinari Kori and Kazunori Ishimura :
Photostable Iodinated Silica/Porphyrin Hybrid Nanoparticles with Heavy-Atom Effect for Wide-Field Photodynamic/Photothermal Therapy Using Single Light Source,
Advanced Functional Materials, Vol.24, No.4, 503-513, 2014.

(出版サイトへのリンク): ● Publication site (DOI): 10.1002/adfm.201301771
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-84892950115

(DOI: 10.1002/adfm.201301771, Elsevier: Scopus) Takeshi Harada, Shuji Ozaki, Asuka Oda, Daisuke Tsuji, Akishige Ikegame, Masami Iwasa, Kengo Udaka, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Yoshiaki Kuroda, Shigeto Kawai, Kouji Itou, Hisafumi Yamada-Okabe, Toshio Matsumoto and Masahiro Abe :
Combination with a Defucosylated Anti-HM1.24 Monoclonal Antibody plus Lenalidomide Induces Marked ADCC against Myeloma Cells and Their Progenitors,
PLoS ONE, Vol.8, No.12, e83905, 2013.

(要約): The immunomodulatory drug lenalidomide (Len) has drawn attention to potentiate antibody-dependent cellular cytotoxicity (ADCC)-mediated immunotherapies. We developed the defucosylated version (YB-AHM) of humanized monoclonal antibody against HM1.24 (CD317) overexpressed in multiple myeloma (MM) cells. In this study, we evaluated ADCC by YB-AHM and Len in combination against MM cells and their progenitors. YB-AHM was able to selectively kill via ADCC MM cells in bone marrow samples from patients with MM with low effector/target ratios, which was further enhanced by treatment with Len. Interestingly, Len also up-regulated HM1.24 expression on MM cells in an effector-dependent manner. HM1.24 was found to be highly expressed in a drug-resistant clonogenic "side population" in MM cells; and this combinatory treatment successfully reduced SP fractions in RPMI 8226 and KMS-11 cells in the presence of effector cells, and suppressed a clonogenic potential of MM cells in colony-forming assays. Collectively, the present study suggests that YB-AHM and Len in combination may become an effective therapeutic strategy in MM, warranting further study to target drug-resistant MM clonogenic cells.
(キーワード): Aged / Aged, 80 and over / Antibodies, Monoclonal, Humanized / Antibody-Dependent Cell Cytotoxicity / Antigens, CD / Antineoplastic Combined Chemotherapy Protocols / Cell Line, Tumor / Drug Synergism / Female / GPI-Linked Proteins / Glycosylation / Humans / 免疫療法 (immunotherapy) / Lenalidomide / Male / Middle Aged / Multiple Myeloma / Neoplastic Stem Cells / Side-Population Cells / Thalidomide / Up-Regulation
(徳島大学機関リポジトリ): ● Metadata: 106068
(出版サイトへのリンク): ● Publication site (DOI): 10.1371/journal.pone.0083905
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24386306; ● Summary page in Scopus @ Elsevier: 2-s2.0-84891280322

(徳島大学機関リポジトリ: 106068, DOI: 10.1371/journal.pone.0083905, PubMed: 24386306, Elsevier: Scopus) Masahiro Abe :
Bench work for targeted therapy to the microenvironment of myeloma bone disease.,
Clinical Lymphoma, Myeloma & Leukemia, Vol.14, No.1, 8-9, 2013.

(キーワード): Animals / Bone Diseases / Cell Differentiation / Disease Progression / Humans / Molecular Targeted Therapy / Multiple Myeloma / Osteoclasts / Tumor Microenvironment
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.clml.2013.12.006
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24461802; ● Search Scopus @ Elsevier (PMID): 24461802; ● Search Scopus @ Elsevier (DOI): 10.1016/j.clml.2013.12.006

(DOI: 10.1016/j.clml.2013.12.006, PubMed: 24461802) Naoto Okada, Kazuyoshi Kawazoe, Kazuhiko Teraoka, Toshihide Kujime, Masahiro Abe, Yasuo Shinohara and Kazuo Minakuchi :
Identification of the Risk Factors Associated with Hypocalcemia Induced by Denosumab,
Biological & Pharmaceutical Bulletin, Vol.36, No.10, 1622-1626, 2013.

(要約): Denosumab, a fully human monoclonal antibody that inhibits the receptor activator of nuclear factor-κB ligand, inhibits the activation of osteoclasts. Some clinical trials have shown that denosumab suppresses bone resorption in patients with advanced cancer, but hypocalcemia has been reported as a serious adverse effect after the administration of denosumab. It is difficult to predict hypocalcemia in such cases because the risk factors for denosumab-induced hypocalcemia have not been reported. Accordingly, the aim of the present study was to identify the risk factors for hypocalcemia induced by denosumab. We retrospectively reviewed the records of patients who had received denosumab at Tokushima University Hospital between April 2012 and May 2013. Fifty-three patients were analyzed and eleven patients had hypocalcemia after administration of denosumab. Univariate logistic regression analysis revealed that the patients who had not been administered zoledronic acid before receiving denosumab or had lower creatinine clearance (CCr) appeared to have a higher risk of hypocalcemia (p<0.05). The cut off value of CCr was 50.4 ml/min calculated by receiver-operator characteristics curves. Moreover, multivariate logistic regression analysis revealed that non-administration of zoledronic acid (odds ratio 10.43, p<0.05) and CCr less than 50.0 ml/min (odds ratio 5.90, p<0.05) were independent risk factors for denosumab-induced hypocalcemia. These findings provide useful information regarding the monitoring of hypocalcemia in patients receiving denosumab.
(キーワード): denosumab / hypocalcemia / risk factor / zoledronic acid / creatinine clearance
(出版サイトへのリンク): ● Publication site (DOI): 10.1248/bpb.b13-00496
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23934346; ● CiNii @ 国立情報学研究所 (CRID): 1390282679608990592; ● Summary page in Scopus @ Elsevier: 2-s2.0-84887114892

(DOI: 10.1248/bpb.b13-00496, PubMed: 23934346, CiNii: 1390282679608990592, Elsevier: Scopus) Shingen Nakamura, Hirokazu Miki, Shinsuke Kido, Ayako Nakano, Masahiro Hiasa, Asuka Oda, Hiroe Amou, Keiichiro Watanabe, Takeshi Harada, Shiroh Fujii, Kyoko Takeuchi, Kumiko Kagawa, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe :
Activating transcription factor 4, an ER stress mediator, is required for, but exce ssive ER stress suppresses osteoblastogenesis by bortezomib.,
International Journal of Hematology, Vol.98, No.1, 66-73, 2013.

(要約): Endoplasmic reticulum (ER) stress is induced in matrix-producing osteoblasts and plays an essential role in osteoblastogenesis. Although the bone anabolic activity of proteasome inhibitors has been demonstrated, the roles of ER stress induced by proteasome inhibition in osteoblastogenesis remain largely unknown. Here we show that bortezomib translationally increases protein levels of activating transcription factor 4 (ATF4), a downstream mediator of ER stress, in bone marrow stromal cells and MC3T3-E1 preosteoblastic cells. The suppression of ATF4 expression by siRNA abrogated osteocalcin expression and mineralized nodule formation by MC3T3-E1 cells induced by bortezomib, indicating a critical role for ATF4 in bortezomib-mediated osteoblastogenesis. However, bortezomib at 20 nM or higher abolished the mineralized nodule formation along with reductions in the expression of osteoblastogenesis mediators β-catenin and Osterix. Furthermore, at 50 nM, bortezomib induced the expression of C/EBP homologous protein (CHOP), suggesting activation of the ATF4-CHOP pro-apoptotic pathway. These results suggest that a low dose of bortezomib induces osteogenic activity, but that, in contrast, excessive ER stress caused by bortezomib at higher doses hampers osteoblastogenesis. Therefore, dosing schedules for proteasome inhibitors warrant further study to maximize anabolic actions without compromising anti-MM activity in patients with multiple myeloma (MM).
(キーワード): 3T3 Cells / Activating Transcription Factor 4 / Animals / Antineoplastic Agents / Biological Markers / Bone Marrow Cells / Boronic Acids / Calcification, Physiologic / Cells, Cultured / Endoplasmic Reticulum Stress / Gene Expression Regulation / Gene Silencing / Humans / Mice / Multiple Myeloma / Neoplasm Proteins / Osteoblasts / Osteocalcin / Osteogenesis / Proteasome Inhibitors / Pyrazines / RNA, Small Interfering / Stromal Cells
(徳島大学機関リポジトリ): ● Metadata: 105938
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s12185-013-1367-z
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23708974; ● Summary page in Scopus @ Elsevier: 2-s2.0-84880304849

(徳島大学機関リポジトリ: 105938, DOI: 10.1007/s12185-013-1367-z, PubMed: 23708974, Elsevier: Scopus) Koichiro Hayashi, Michihiro Nakamura, Hirokazu Miki, Shuji Ozaki, Masahiro Abe, Toshio Matsumoto and Kazunori Ishimura :
Gold Nanoparticle Cluster/Plasmon-Enhanced Fluorescent Silica Core-Shell Nanoparticles for X-Ray Computed Tomography/Fluorescence Dual-Mode Imaging of Tumors,
Chemical Communications, Vol.49, 5334-5336, 2013.

(要約): Owing to the surface plasmon resonance-enhanced electromagnetic field, clustered gold nanoparticles-fluorescent silica core-shell nanoparticles became excited within the therapeutic window and fluoresced strongly in this window. The nanoparticles enabled tumor detection using fluorescence imaging and X-ray computed tomography.
(キーワード): Animals / Fluorescence / Fluorescent Dyes / Gold / Mice / Nanoparticles / Neoplasms / Optical Imaging / Silicon Dioxide / Surface Plasmon Resonance / Tomography, X-Ray Computed
(出版サイトへのリンク): ● Publication site (DOI): 10.1039/c3cc41876f
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23648868; ● Search Scopus @ Elsevier (PMID): 23648868; ● Search Scopus @ Elsevier (DOI): 10.1039/c3cc41876f

(DOI: 10.1039/c3cc41876f, PubMed: 23648868) Koichiro Hayashi, Michihiro Nakamura, Wataru Sakamoto, Toshinobu Yogo, Hirokazu Miki, Shuji Ozaki, Masahiro Abe, Toshio Matsumoto and Kazunori Ishimura :
"Superparamagnetic Nanoparticle Clusters for Cancer Theranostics Combining Magnetic Resonance Imaging and Hyperthermia Treatment,
Theranostics, Vol.3, No.6, 366-376, 2013.

(要約): Superparamagnetic nanoparticles (SPIONs) could enable cancer theranostics if magnetic resonance imaging (MRI) and magnetic hyperthermia treatment (MHT) were combined. However, the particle size of SPIONs is smaller than the pores of fenestrated capillaries in normal tissues because superparamagnetism is expressed only at a particle size <10 nm. Therefore, SPIONs leak from the capillaries of normal tissues, resulting in low accumulation in tumors. Furthermore, MHT studies have been conducted in an impractical way: direct injection of magnetic materials into tumor and application of hazardous alternating current (AC) magnetic fields. To accomplish effective enhancement of MRI contrast agents in tumors and inhibition of tumor growth by MHT with intravenous injection and a safe AC magnetic field, we clustered SPIONs not only to prevent their leakage from fenestrated capillaries in normal tissues, but also for increasing their relaxivity and the specific absorption rate. We modified the clusters with folic acid (FA) and polyethylene glycol (PEG) to promote their accumulation in tumors. SPION clustering and cluster modification with FA and PEG were achieved simultaneously via the thiol-ene click reaction. Twenty-four hours after intravenous injection of FA- and PEG-modified SPION nanoclusters (FA-PEG-SPION NCs), they accumulated locally in cancer (not necrotic) tissues within the tumor and enhanced the MRI contrast. Furthermore, 24 h after intravenous injection of the NCs, the mice were placed in an AC magnetic field with H = 8 kA/m and f = 230 kHz (Hf = 1.8×10(9) A/m∙s) for 20 min. The tumors of the mice underwent local heating by application of an AC magnetic field. The temperature of the tumor was higher than the surrounding tissues by ≈6°C at 20 min after treatment. Thirty-five days after treatment, the tumor volume of treated mice was one-tenth that of the control mice. Furthermore, the treated mice were alive after 12 weeks; control mice died up to 8 weeks after treatment.
(出版サイトへのリンク): ● Publication site (DOI): 10.7150/thno.5860
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23781284; ● Summary page in Scopus @ Elsevier: 2-s2.0-84882252518

(DOI: 10.7150/thno.5860, PubMed: 23781284, Elsevier: Scopus) Shuji Kato, Itsuro Endo, Mitsunori Fujimura, Rika Kuriwaka-Kido, Yuichi Fujinaka, Ken-ichi Aihara, Takashi Iwase, Daisuke Inoue, Masashi Akaike, Masahiro Abe and Toshio Matsumoto :
Serum carboxy-terminal telopeptide of type I collagen (ICTP) as a surrogate marker for vulnerable plaques in atherosclerotic patients: A pilot study.,
Atherosclerosis, Vol.229, No.1, 182-185, 2013.

(要約): Evaluation of atherosclerotic plaques depends on invasive intravascular ultrasonography (IVUS). Carboxy-terminal telopeptide of type I collagen (ICTP) is produced by matrix metalloproteinase (MMP)-dependent digestion of type I collagen. Because vulnerable plaques are rich in type I collagen and MMPs from macrophages, we examined the association between serum ICTP and coronary plaques in patients with coronary disease. We recruited 46 men and 17 women without renal failure or bone diseases affecting serum ICTP, who underwent coronary IVUS. Serum ICTP levels were higher in patients with coronary plaques containing more than 10% necrotic core area than in patients with less than 10% necrotic core area. A positive correlation was found between serum ICTP and necrotic core area. Only serum ICTP was positively correlated with necrotic core area by multivariate analysis (p < 0.05). These results suggest that serum ICTP can be used as a non-invasive marker of vulnerable plaques in atherosclerotic patients.
(徳島大学機関リポジトリ): ● Metadata: 105936
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.atherosclerosis.2013.03.030
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23639859; ● Search Scopus @ Elsevier (PMID): 23639859; ● Search Scopus @ Elsevier (DOI): 10.1016/j.atherosclerosis.2013.03.030

(徳島大学機関リポジトリ: 105936, DOI: 10.1016/j.atherosclerosis.2013.03.030, PubMed: 23639859) Koichiro Hayashi, Michihiro Nakamura, Hirokazu Miki, Shuji Ozaki, Masahiro Abe, Toshio Matsumoto and Kazunori Ishimura :
Near-Infrared Fluorescent Silica/Porphyrin Hybrid Nanorings for In Vivo Cancer Imaging,
Advanced Functional Materials, Vol.22, No.17, 3539-3546, 2012.

(出版サイトへのリンク): ● Publication site (DOI): 10.1002/adfm.201200219
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.1002/adfm.201200219

(DOI: 10.1002/adfm.201200219) N Hosen, Y Matsuoka, S Kishida, J Nakata, Y Mizutani, K Hasegawa, A Mugitani, H Ichihara, Y Aoyama, S Nishida, A Tsuboi, F Fujiki, N Tatsumi, H Nakajima, M Hino, T Kimura, K Yata, Masahiro Abe, Y Oka, Y Oji, A Kumanogoh and H Sugiyama :
CD138-negative clonogenic cells are plasma cells but not B cells in some multiple myeloma patients.,
Leukemia, Vol.26, No.9, 2135-2141, 2012.

(要約): Clonogenic multiple myeloma (MM) cells reportedly lacked expression of plasma cell marker CD138. It was also shown that CD19(+) clonotypic B cells can serve as MM progenitor cells in some patients. However, it is unclear whether CD138-negative clonogenic MM plasma cells are identical to clonotypic CD19(+) B cells. We found that in vitro MM colony-forming cells were enriched in CD138(-)CD19(-)CD38(++) plasma cells, while CD19(+) B cells never formed MM colonies in 16 samples examined in this study. We next used the SCID-rab model, which enables engraftment of human MM in vivo. CD138(-)CD19(-)CD38(++) plasma cells engrafted in this model rapidly propagated MM in 3 out of 9 cases, while no engraftment of CD19(+) B cells was detected. In 4 out of 9 cases, CD138(+) plasma cells propagated MM, although more slowly than CD138(-) cells. Finally, we transplanted CD19(+) B cells from 13 MM patients into NOD/SCID IL2Rγc(-/-) mice, but MM did not develop. These results suggest that at least in some MM patients CD138-negative clonogenic cells are plasma cells rather than B cells, and that MM plasma cells including CD138(-) and CD138(+) cells have the potential to propagate MM clones in vivo in the absence of CD19(+) B cells.
(キーワード): Animals / B-Lymphocytes / Bone Marrow Transplantation / Colony-Forming Units Assay / Humans / Immunophenotyping / Mice / Mice, Inbred NOD / Mice, SCID / Multiple Myeloma / Plasma Cells / Rabbits / Syndecan-1
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/leu.2012.80
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22430638; ● Search Scopus @ Elsevier (PMID): 22430638; ● Search Scopus @ Elsevier (DOI): 10.1038/leu.2012.80

(DOI: 10.1038/leu.2012.80, PubMed: 22430638) Tamotsu Kanbara, Hirotsugu Kurobe, Takashi Kitaichi, Mikio Sugano, Nakayama Taisuke, Hajime Kinoshita, Takashi Iwase, Akaike Masafumi, Masahiro Abe, Masataka Sata, Toshio Matsumoto and Tetsuya Kitagawa :
Autologous Peripheral Blood-Derived Mononuclear Cells Induced by Erythropoietin Improve Critical Ischemic Limbs.,
Annals of Vascular Diseases, Vol.5, No.1, 52-60, 2012.

(要約): Purpose: Efficient and secure collection of CD34+ cells are crucial for the angiogenic therapies. We have developed autologous peripheral blood-mononuclear cell (MNC) transplantation induced by erythropoietin (rhEPO) for critical ischemic limbs. Methods: Seven patients, including five with arteriosclerosis obliterans, one with Buerger's disease and one with progressive systemic sclerosis, underwent ten cell therapies. The first administration of rhEPO was performed two weeks before apheresis, and the second administration and blood donation were performed one week before apheresis to activate bone marrow. MNCs including CD34+ cells, isolated from peripheral blood by apheresis, were immediately injected intramuscularly into ischemic limbs. Results: The number of peripheral blood-CD34 + cells had significantly increased from 1.32 ± 0.83/microL, before the rhEPO induction, to 1.86 ± 0.94/microL, before the apheresis. The number of transplanted MNCs ranged between 0.5 × 10(9) and 16.5 × 10(9), and that of CD34+ cells, between 0.1 × 10(6) and 12.7 × 10(6), accounting for 0.02%-0.1% of MNCs. There were no serious complications. Finger ulcers with Buerger's disease were significantly improved one month after the transplantations, but the same or other ulcer(s) appeared 2-6 months later. Three patients had an improvement in rest pain, and one patient extended maximum pain-free walking distance. Conclusions: Erythropoietin-induced autologous peripheral blood-MNC transplantation is a useful and safe alternative for ischemic limbs.
(出版サイトへのリンク): ● Publication site (DOI): 10.3400/avd.oa.11.00070
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23555486; ● Search Scopus @ Elsevier (PMID): 23555486; ● Search Scopus @ Elsevier (DOI): 10.3400/avd.oa.11.00070

(DOI: 10.3400/avd.oa.11.00070, PubMed: 23555486) Kumiko Kagawa, Ayako Nakano, Hirokazu Miki, Asuka Oda, Hiroe Amou, Kyoko Takeuchi, Shingen Nakamura, Takeshi Harada, Shiro Fujii, Kenichiro Yata, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe :
Inhibition of TACE activity enhances the susceptibility of myeloma cells to TRAIL.,
PLoS ONE, Vol.7, No.2, 2012.

(要約): These results demonstrate that MM cells post-translationally down-modulate the cell surface expression of DR4 through ectodomain shedding by endogenous TACE, and that TACE inhibition is able to restore cell surface DR4 levels and the susceptibility of MM cells to TRAIL or an agonistic antibody against DR4. Thus, TACE may protect MM cells from TRAIL-mediated death through down-modulation of cell-surface DR4. It can be envisaged that TACE inhibition augments clinical efficacy of TRAIL-based immunotherapy against MM, which eventually becomes resistant to the present therapeutic modalities.
(キーワード): ADAM Proteins / Blotting, Western / Cell Line, Tumor / Cell Survival / Flow Cytometry / HL-60 Cells / Humans / Multiple Myeloma / Receptors, TNF-Related Apoptosis-Inducing Ligand / Reverse Transcriptase Polymerase Chain Reaction / TNF-Related Apoptosis-Inducing Ligand / U937 Cells
(出版サイトへのリンク): ● Publication site (DOI): 10.1371/journal.pone.0031594
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22389670; ● Search Scopus @ Elsevier (PMID): 22389670; ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0031594

(DOI: 10.1371/journal.pone.0031594, PubMed: 22389670) Ayako Nakano, Hirokazu Miki, Shingen Nakamura, Takeshi Harada, Asuka Oda, Hiroe Amou, Shiro Fujii, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe :
Up-regulation of hexokinaseII in myeloma cells: targeting myeloma cells with 3-bromopyruvate.,
Journal of Bioenergetics and Biomembranes, Vol.44, No.1, 31-38, 2012.

(要約): Hexokinase II (HKII), a key enzyme of glycolysis, is widely over-expressed in cancer cells. However, HKII levels and its roles in ATP production and ATP-dependent cellular process have not been well studied in hematopoietic malignant cells including multiple myeloma (MM) cells.We demonstrate herein that HKII is constitutively over-expressed in MM cells. 3-bromopyruvate (3BrPA), an inhibitor of HKII, promptly and substantially suppresses ATP production and induces cell death in MM cells. Interestingly, cocultures with osteoclasts (OCs) but not bone marrow stromal cells (BMSCs) enhanced the phosphorylation of Akt along with an increase in HKII levels and lactate production in MM cells. The enhancement of HKII levels and lactate production in MM cells by OCs were mostly abrogated by the PI3K inhibitor LY294002, suggesting activation of glycolysis in MM cells by OCs via the PI3K-Akt-HKII pathway. Although BMSCs and OCs stimulate MM cell growth and survival, 3BrPA induces cell death in MM cells even in cocultures with OCs as well as BMSCs. Furthermore, 3BrPA was able to diminish ATP-dependent ABC transporter activity to restore drug retention in MM cells in the presence of OCs. These results may underpin possible clinical application of 3BrPA in patients with MM.
(キーワード): Adenosine Triphosphate / Analysis of Variance / Antineoplastic Agents, Alkylating / Apoptosis / Cell Line, Tumor / Gene Expression Regulation, Enzymologic / Gene Expression Regulation, Neoplastic / Hexokinase / Humans / Immunohistochemistry / Multiple Myeloma / Pyruvates / Real-Time Polymerase Chain Reaction
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10863-012-9412-9
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22298254; ● Search Scopus @ Elsevier (PMID): 22298254; ● Search Scopus @ Elsevier (DOI): 10.1007/s10863-012-9412-9

(DOI: 10.1007/s10863-012-9412-9, PubMed: 22298254) Yawara Kawano, Shikiko Ueno, Masahiro Abe, Yoshitaka Kikukawa, Hiromichi Yuki, Kenichi Iyama, Yutaka Okuno, Hiroaki Mitsuya and Hiroyuki Hata :
TRAIL produced from multiple myeloma cells is associated with osteolytic markers.,
Oncology Reports, Vol.27, No.1, 39-44, 2012.

(要約): Skeletal complications represent major clinical problems in multiple myeloma (MM). MM cells are known to induce differentiation of osteoclasts and inhibit osteoblasts. Receptor activator of nuclear factor-B ligand (RANKL) and osteoprotegerin (OPG) are key molecules for osteoclastogenesis. Although OPG interacts with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), the contribution of TRAIL to skeletal-related events (SRE) remains a matter of debate. In the present study, we examined the role of TRAIL in MM bone lesions. Myeloma cells were purified from 56 MM patients by CD138-immunomagnetic beads. TRAIL, DKK-1 and MIP1 RNA expression in purified MM cells was analyzed by real-time PCR. Immunohistochemistry of TRAIL was performed on paraffin-embedded plasmacytoma tissue sections. The concentration of TRAIL in the serum and bone marrow plasma from MM patients was analyzed by ELISA. TRAIL expression was significantly higher in MM cells than in plasma cells from patients with monoclonal gammopathy of undetermined significance (MGUS). TRAIL staining was detected in the cytoplasm of myeloma cells. TRAIL expression in MM cells correlated with bone marrow plasma TRAIL concentration. TRAIL expression had a positive correlation with osteolytic markers, such as serum calcium and urinary deoxypyridinoline. These results suggest that TRAIL, produced from myeloma cells, may play an important role in bone resorption of MM patients. Inhibition of this pathway may lead to development of a new therapeutic approach preventing bone resorption in MM.
(キーワード): Adult / Aged / Aged, 80 and over / Amino Acids / Calcium / Enzyme-Linked Immunosorbent Assay / Female / Humans / Immunohistochemistry / Male / Middle Aged / Multiple Myeloma / Osteolysis / Real-Time Polymerase Chain Reaction / Reverse Transcriptase Polymerase Chain Reaction / TNF-Related Apoptosis-Inducing Ligand
(出版サイトへのリンク): ● Publication site (DOI): 10.3892/or.2011.1491
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21993926; ● Search Scopus @ Elsevier (PMID): 21993926; ● Search Scopus @ Elsevier (DOI): 10.3892/or.2011.1491

(DOI: 10.3892/or.2011.1491, PubMed: 21993926) 藤岡啓介, 西條敦郎, 豊田優子, 柿内聡司, 埴淵昌毅, 吾妻雅彦, 竹内恭子, 藤井志朗, 中村信元, 宇高憲吾, 賀川久美子, 安倍正博, 水谷友哉, 西岡安彦 :
皮膚ランダム生検が診断に有用であった血管内リンパ腫の一例,
四国医学雑誌, Vol.67, No.5,6, 257-262, 2011年.

(要約): A62‐year‐old woman was referred to our hospital for further examination of fever of unknownorigin, splenomegaly and pancytopenia. On admission, she had persistent fever and psychologicalsymptoms. Blood examination showed pancytopenia and elevated level of LDH, soluble IL‐2receptorand ferritin. Computed tomography showed multiple low density areas in the spleen, but no systemiclymphadenopathy. In magnetic resonance imaging of the pons, a low and high intensity area onT1‐and T2‐weighted image, respectively, was detected. Taken together these findings, she wassuspected to have hepatosplentic T-cell lymphoma or intravascular large B-cell lymphoma. To makea definite diagnosis, random skin biopsy was performed. Immunohistochemical stainings revealedthe massive infiltration of CD20‐and CD79α‐positive large lymphoid cells inside the vessels, whichyielded the diagnosis of intravascular large B-cell lymphoma.
(キーワード): fever of unknown origin / intravascular large B-cell lymphoma / random skin biopsy
(徳島大学機関リポジトリ): ● Metadata: 97858
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1050001337463886208

(徳島大学機関リポジトリ: 97858, CiNii: 1050001337463886208) Ayako Nakano, Daisuke Tsuji, Hirokazu Miki, Qu Cui, Mohamed Sayed Salah El, Akishige Ikegame, Asuka Oda, Hiroe Amou, Shingen Nakamura, Takeshi Harada, Shiro Fujii, Kumiko Kagawa, Kyoko Takeuchi, Akira Sakai, Shuji Ozaki, Kazuma Okano, Takahiro Nakamura, Kouji Itou, Toshio Matsumoto and Masahiro Abe :
Glycolysis inhibition inactivates ABC transporters to restore drug sensitivity in malignant cells.,
PLoS ONE, Vol.6, No.11, 2011.

(要約): Cancer cells eventually acquire drug resistance largely via the aberrant expression of ATP-binding cassette (ABC) transporters, ATP-dependent efflux pumps. Because cancer cells produce ATP mostly through glycolysis, in the present study we explored the effects of inhibiting glycolysis on the ABC transporter function and drug sensitivity of malignant cells. Inhibition of glycolysis by 3-bromopyruvate (3BrPA) suppressed ATP production in malignant cells, and restored the retention of daunorubicin or mitoxantrone in ABC transporter-expressing, RPMI8226 (ABCG2), KG-1 (ABCB1) and HepG2 cells (ABCB1 and ABCG2). Interestingly, although side population (SP) cells isolated from RPMI8226 cells exhibited higher levels of glycolysis with an increased expression of genes involved in the glycolytic pathway, 3BrPA abolished Hoechst 33342 exclusion in SP cells. 3BrPA also disrupted clonogenic capacity in malignant cell lines including RPMI8226, KG-1, and HepG2. Furthermore, 3BrPA restored cytotoxic effects of daunorubicin and doxorubicin on KG-1 and RPMI8226 cells, and markedly suppressed subcutaneous tumor growth in combination with doxorubicin in RPMI8226-implanted mice. These results collectively suggest that the inhibition of glycolysis is able to overcome drug resistance in ABC transporter-expressing malignant cells through the inactivation of ABC transporters and impairment of SP cells with enhanced glycolysis as well as clonogenic cells.
(キーワード): ATP-Binding Cassette Transporters / Adenosine Triphosphate / Antineoplastic Agents / Base Sequence / Cell Line, Tumor / DNA Primers / Daunorubicin / Doxorubicin / Flow Cytometry / Glycolysis / Humans / Mitoxantrone / Real-Time Polymerase Chain Reaction
(出版サイトへのリンク): ● Publication site (DOI): 10.1371/journal.pone.0027222
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22073292; ● Search Scopus @ Elsevier (PMID): 22073292; ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0027222

(DOI: 10.1371/journal.pone.0027222, PubMed: 22073292) Hirokazu Miki, Shingen Nakamura, Shuji Ozaki, A Oda, H Amou, Akishige Ikegame, Keiichiro Watanabe, Masahiro Hiasa, Q Cui, T Harada, Shiroh Fujii, A Nakano, Kumiko Kagawa, Kyoko Takeuchi, Ken-ichiro Yata, A Sakai, Masahiro Abe and Toshio Matsumoto :
KRN5500, a spicamycin derivative, exerts anti-myeloma effects through impairing both myeloma cells and osteoclasts.,
British Journal of Haematology, Vol.155, No.3, 328-339, 2011.

(要約): The spicamycin analogue KRN5500 alters glycoprotein processing and induces damage in the endoplasmic reticulum (ER)-Golgi apparatus in cancer cells. In the present study, we explored the cytotoxic effects of KRN5500 on multiple myeloma (MM) cells and the bone marrow microenvironment with special reference to ER stress. Cell proliferation assay showed that KRN5500 induced G1 arrest and apoptosis in MM cells in a time- and dose-dependent manner. KRN5500 enhanced ER stress independently of caspase activation in MM cells. This cell death was observed even in the presence of bone marrow stroma cells or osteoclasts. Notably, KRN5500 induced cell death also in osteoclasts. In vivo effects of KRN5500 were evaluated using two xenograft models established in severe combined immunodeficient (SCID) mice by either subcutaneous injection of RPMI 8226 cells or intra-bone injection of INA-6 cells to subcutaneously implanted rabbit bones (SCID-rab model). KRN5500 significantly inhibited tumour growth in both animal models, and decreased the number of osteoclasts, which resulted in prevention of bone destruction in the SCID-rab model. These results suggest that KRN5500 exerts anti-MM effects through impairing both MM cells and osteoclasts. Therefore, this unique mechanism of KRN5500 might be a useful therapeutic option in patients with MM.
(キーワード): Animals / Apoptosis / Bone Marrow Cells / Caspases / Cell Line, Tumor / Cell Proliferation / Dose-Response Relationship, Drug / Female / G1 Phase / Humans / Mice / Mice, SCID / Multiple Myeloma / Osteoclasts / Purine Nucleosides / Rabbits / Random Allocation / Stromal Cells / Tumor Microenvironment / Xenograft Model Antitumor Assays
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/j.1365-2141.2011.08844.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21902681; ● Search Scopus @ Elsevier (PMID): 21902681; ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2141.2011.08844.x

(DOI: 10.1111/j.1365-2141.2011.08844.x, PubMed: 21902681) Masahiro Abe :
Targeting the interplay between myeloma cells and the bone marrow microenvironment in myeloma.,
International Journal of Hematology, Vol.94, No.4, 334-343, 2011.

(要約): Cellular interplay in the bone marrow (BM) microenvironment in multiple myeloma (MM) mediates MM growth and the formation of bone-destructive lesions. MM cells show enhanced osteoclastogenesis, and stimulate angiogenesis in concert with BM stromal cells and osteoclasts, whereas they suppress osteoblastic differentiation, leading to devastating bone destruction and the rapid loss of bone. Importantly, osteoclasts, vascular endothelial cells, and BM stromal cells with defective osteoblastic differentiation create a cellular microenvironment suitable for MM growth and survival and confer a drug resistance to MM cells, which can be construed as the "MM niche". Therefore, the MM niche must be targeted and disrupted to improve the efficacy of anti-tumor treatment and prevent the progression of bone disease in MM. Clarifying molecular mechanisms leading to the formation of the MM niche along with bone disease will help in the development of novel approaches targeting the interplay between MM cells and the BM microenvironment.
(キーワード): Bone Diseases / Bone Marrow / Cellular Microenvironment / Humans / Molecular Targeted Therapy / Multiple Myeloma / Neovascularization, Pathologic / Osteoclasts
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s12185-011-0949-x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22005835; ● Search Scopus @ Elsevier (PMID): 22005835; ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-011-0949-x

(DOI: 10.1007/s12185-011-0949-x, PubMed: 22005835) Masahiro Abe :
Guest editorial: understanding the pathogenesis and the evolving treatment paradigm for multiple myeloma in the era of novel agents.,
International Journal of Hematology, Vol.94, No.4, 307-309, 2011.

(キーワード): Antineoplastic Agents / Bone Marrow / Hematopoietic Stem Cell Transplantation / Humans / Molecular Targeted Therapy / Multiple Myeloma / Prognosis / Risk Assessment
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s12185-011-0950-4
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21993876; ● Search Scopus @ Elsevier (PMID): 21993876; ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-011-0950-4

(DOI: 10.1007/s12185-011-0950-4, PubMed: 21993876) Qu Cui, Hironobu Shibata, Asuka Oda, Hiroe Amou, Ayako Nakano, Kenichiro Yata, Masahiro Hiasa, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Takeshi Harada, Shiroh Fujii, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe :
Targeting myeloma-osteoclast interaction with V9V2 T cells.,
International Journal of Hematology, Vol.94, No.1, 63-70, 2011.

(要約): Multiple myeloma (MM) cells stimulate osteoclastogenesis, and osteoclasts (OCs) in turn enhance MM growth and drug resistance, resulting in a vicious cycle. V9V2 T cells exert potent anti-tumor effects, making T cell-based immunotherapies using these cells attractive candidates for currently incurable malignancies, such as MM. However, the impact of such treatments on the MM-OC interaction is largely unknown. We demonstrate here that V9V2 T cells expanded by zoledronic acid and IL-2 exerted potent cytotoxic effects on both MM cells and OCs, even in coculture settings, but showed no such effect on bone marrow stromal cells. V9V2 T cells marginally affected colony formation from normal hematopoietic progenitors, and furthermore migrated toward osteopontin and MIP-1, factors produced by the MM-OC interaction. These results suggest that V9V2 T cells expanded by zoledronic acid and IL-2 are able to migrate to MM bone lesions and preferentially target OCs as well as MM cells, thereby inhibiting both tumor expansion and bone destruction.
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s12185-011-0885-9
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21698356; ● Search Scopus @ Elsevier (PMID): 21698356; ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-011-0885-9

(DOI: 10.1007/s12185-011-0885-9, PubMed: 21698356) Ayako Nakano, Masahiro Abe, Asuka Oda, Hiroe Amou, Masahiro Hiasa, Shingen Nakamura, Hirokazu Miki, Takeshi Harada, Shirou Fujii, Kumiko Kagawa, Kyoko Takeuchi, Takashi Watanabe, Shuji Ozaki and Toshio Matsumoto :
Delayed treatment with vitamin C and N-acetyl-L: -cysteine protects Schwann cells without compromising the anti-myeloma activity of bortezomib.,
International Journal of Hematology, Vol.93, No.6, 727-735, 2011.

(要約): Bortezomib-induced peripheral neuropathy (BIPN) emerges as a disabling adverse effect. As rat models for BIPN have demonstrated damage in nerve Schwann cells, we screened for cytoprotective agents to devise a method of rescuing Schwann cells from the cytotoxic effects of bortezomib without compromising its anti-myeloma effects. Schwann cells underwent macroautophagy along with cytoplasmic inclusion body and vacuole formation, and appeared much less susceptible to bortezomib-induced cytotoxicity than did myeloma cells. Vitamin C or N-acetyl-L: -cysteine (NAC) achieved near-complete rescue of Schwann cells treated with bortezomib at 30 nM or less, and these agents in combination are able to cooperatively inhibit the morphological changes and the cytotoxicity in Schwann cells with higher doses of bortezomib. The delayed addition of vitamin C and/or NAC after the exposure to bortezomib alleviated the cytotoxicity in Schwann cells but not myeloma cells. These results suggest that delayed treatment with these agents may be instrumental in prophylaxis of BIPN.
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s12185-011-0850-7
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21526377; ● Search Scopus @ Elsevier (PMID): 21526377; ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-011-0850-7

(DOI: 10.1007/s12185-011-0850-7, PubMed: 21526377) J Asano, A Nakano, A Oda, H Amou, Masahiro Hiasa, Kyoko Takeuchi, H Miki, S Nakamura, T Harada, Shiroh Fujii, Kumiko Kagawa, Itsuro Endo, Ken-ichiro Yata, A Sakai, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe :
The serine/threonine kinase Pim-2 is a novel anti-apoptotic mediator in myeloma cells.,
Leukemia, 2011.

(要約): Bone marrow stromal cells (BMSCs) and osteoclasts (OCs) confer multiple myeloma (MM) cell survival through elaborating factors. We demonstrate herein that IL-6 and TNF family cytokines, TNF, BAFF and APRIL, but not IGF-1 cooperatively enhance the expression of the serine/threonine kinase Pim-2 in MM cells. BMSCs and OCs upregulate Pim-2 expression in MM cells largely via the IL-6/STAT3 and NF-B pathway, respectively. Pim-2 short interfering RNA reduces MM cell viability in cocultures with BMSCs or OCs. Thus, upregulation of Pim-2 appears to be a novel anti-apoptotic mechanism for MM cell survival. Interestingly, the mammalian target of rapamycin inhibitor rapamycin further suppresses the MM cell viability in combination with the Pim-2 silencing. The Pim inhibitor (Z)-5-(4-propoxybenzylidene) thiazolidine-2, 4-dione and the PI3K inhibitor LY294002 cooperatively enhance MM cell death. The Pim inhibitor suppresses 4E-BP1 phosphorylation along with the reduction of Mcl-1 and c-Myc. Pim-2 may therefore become a new target for MM treatment.Leukemia advance online publication, 8 April 2011; doi:10.1038/leu.2011.60.
(徳島大学機関リポジトリ): ● Metadata: 106134
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/leu.2011.60
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21475253; ● Search Scopus @ Elsevier (PMID): 21475253; ● Search Scopus @ Elsevier (DOI): 10.1038/leu.2011.60

(徳島大学機関リポジトリ: 106134, DOI: 10.1038/leu.2011.60, PubMed: 21475253) Shuji Ozaki, Takeshi Harada, Shiro Fujii, Shingen Nakamura, Hirokazu Miki, Ayako Nakano, Kumiko Kagawa, Kyoko Takeuchi, Masahiro Abe and Toshio Matsumoto :
Transient inflammatory reaction during lenalidomide plus reduced-dose dexamethasone therapy in two patients with relapsed multiple myeloma.,
International Journal of Hematology, Vol.93, No.2, 257-259, 2011.

(キーワード): Antineoplastic Agents / Antineoplastic Combined Chemotherapy Protocols / Dexamethasone / Humans / Inflammation Mediators / Male / Middle Aged / Multiple Myeloma / Recurrence / Thalidomide
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s12185-011-0775-1
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21279817; ● Search Scopus @ Elsevier (PMID): 21279817; ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-011-0775-1

(DOI: 10.1007/s12185-011-0775-1, PubMed: 21279817) Michihiro Nakamura, Shuji Ozaki, Masahiro Abe, Toshio Matsumoto and Kazunori Ishimura :
One-pot synthesis and characterization of dual fluorescent thiol-organosilica nanoparticles as non-photoblinking quantum dots and their applications for biological imaging,
Journal of Materials Chemistry, Vol.21, 4689-4695, 2011.

(出版サイトへのリンク): ● Publication site (DOI): 10.1039/C0JM04259E
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.1039/C0JM04259E

(DOI: 10.1039/C0JM04259E) Shunji Hashizume, Masashi Akaike, Hiroyuki Azuma, Kazue Ishikawa, Sumiko Yoshida, Yuka Ueda, Shusuke Yagi, Yasumasa Ikeda, Takashi Iwase, Ken-ichi Aihara, Masahiro Abe, Masataka Sata and Toshio Matsumoto :
Activation of peroxisome proliferator-activated receptor α in megakaryocytes reduces platelet-derived growth factor-BB in platelets.,
Journal of Atherosclerosis and Thrombosis, Vol.18, No.2, 138-147, 2011.

(要約): Platelet-derived growth factor (PDGF)-BB plays a crucial role in atherosclerosis and vascular remodeling by promoting the migration and proliferation of vascular smooth muscle cells. The objective of this study was to clarify the pleiotropic effect of peroxisome proliferator-activated receptor α (PPARα) activators on PDGF-BB expression in megakaryocytes and platelets. The expression of PPARα in a human erythroleukemia (HEL) cells was clearly detected by reverse transcriptase-PCR and immunofluorescence microscopy. The expression level of PPARα in HEL cells was unchanged regardless of differentiation into megakaryocytic cells by treatment with phorbol 12-myristate 13 acetate (TPA). The TPA-induced expression of PDGF-B mRNA and PDGF-BB protein levels in culture media was significantly decreased by treatment with PPARα activators, Wy14643 and fenofibric acid, in a dose-dependent manner. PDGF-BB expression induced by inflammatory cytokines, including interleukin-1β or interleukin-6, was also significantly suppressed by treatment with PPARα activators. Immunohistochemistry of human bone marrow showed the expression of PPARα in both the nucleus and cytoplasm of megakaryocytes. In addition, PDGF-BB levels in platelets were significantly decreased from 1,800±870 to 1,470±840 pg/10(5) platelets (mean±SD, p<0.05) by treatment with 300 mg fenofibrate once daily for 4 weeks in 13 patients with dyslipidemia. Activation of PPARα in megakaryocytes reduces PDGF-BB expression in platelets. PPARα activators may exert vasculo-protective action through suppression of PDGF-BB production in a megakaryocyte/platelet pathway.
(キーワード): Adult / Blood Platelets / 細胞分化 (cell differentiation) / Cell Line, Tumor / Dyslipidemias / Female / Fenofibrate / 遺伝子発現 (gene expression) / Humans / 免疫組織化学 (immunohistochemistry) / Lipids / Male / Megakaryocytes / Middle Aged / PPAR alpha / Platelet-Derived Growth Factor / Pyrimidines / RNA, Messenger / Tetradecanoylphorbol Acetate
(出版サイトへのリンク): ● Publication site (DOI): 10.5551/jat.5868
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21060209; ● Search Scopus @ Elsevier (PMID): 21060209; ● Search Scopus @ Elsevier (DOI): 10.5551/jat.5868

(DOI: 10.5551/jat.5868, PubMed: 21060209) Takako Taniguchi, Shinsuke Kido, Emiko Yamauchi, Masahiro Abe, Toshio Matsumoto and Hisaaki Taniguchi :
Induction of endosomal/lysosomal pathways in differentiating osteoblasts as revealed by combined proteomic and transcriptomic analyses.,
FEBS Letters, Vol.584, No.18, 3969-3974, 2010.

(要約): We have analyzed proteome changes associated with bone-forming osteoblast differentiation by quantitative differential proteomic and transcriptomic analyses using in vitro differentiation model. Sixty nine proteins were found up-regulated (>2-fold) and 18 were down-regulated (<0.5-fold) at protein level. The mRNA levels of these proteins were then analyzed by quantitative real-time PCR combined with clustering analysis. The most prominent cluster with increased protein and mRNA levels contains endosomal and lysosomal proteins, demonstrating the drastic induction of degradative endosomal/lysosomal pathways in osteoblasts. Osteoblasts, therefore, are involved not only in the synthesis but also in the turnover of the extracellular matrix proteins such as collagens.
(キーワード): Animals / 細胞分化 (cell differentiation) / Gene Expression Profiling / Lysosomes / Mice / Mice, Inbred ICR / Osteoblasts / Plasmids / プロテオーム (proteome) / プロテオミクス (proteomics)
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.febslet.2010.07.055
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20682313; ● Search Scopus @ Elsevier (PMID): 20682313; ● Search Scopus @ Elsevier (DOI): 10.1016/j.febslet.2010.07.055

(DOI: 10.1016/j.febslet.2010.07.055, PubMed: 20682313) 中村信元, 矢田健一郎, 神野雅, 原田武志, 藤井志朗, 三木浩和, 中野綾子, 賀川久美子, 竹内恭子, 尾崎修治, 安倍正博, 松本俊夫 :
ボルテゾミブ療法後に播種性接合菌症を合併した多発性骨髄腫,
臨床血液, Vol.51, No.8, 690-695, 2010年.

(要約): 67歳男性，背部痛を契機に2001年10月に多発性骨髄腫IgA-λ stage IIIAと診断された．VAD療法5コース後の2003年3月に自家末梢血幹細胞移植併用大量化学療法を行うも再発した．以後，サリドマイド療法などを行うも再燃し，2007年6月入院した．入院後のボルテゾミブ(Bor)療法で，2度の腫瘍崩壊症候群をきたした．その後のCTで右肺上葉，膵尾部，脾臓の腫瘤が急速に出現し，ミカファンギンやボリコナゾールを投与するも，入院85日後に死亡した．剖検で，肺，脾臓に多発性の真菌塊と出血性梗塞が認められ，僧帽弁には真菌塊の疣贅を認め，組織学的に播種性接合菌症と診断した．Bor療法後の腫瘍崩壊によるアシドーシスや，コントロール不良の糖尿病，輸血による鉄過剰，抗真菌薬投与中のブレークスルー感染症などが発症の誘因と考えられた．
(キーワード): Zygomycosis / Multiple myeloma / Bortezomib / Tumor lysis syndrome
(出版サイトへのリンク): ● Publication site (DOI): 10.11406/rinketsu.51.690
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20805677; ● CiNii @ 国立情報学研究所 (CRID): 1390001205037088512; ● Summary page in Scopus @ Elsevier: 2-s2.0-78349258607

(DOI: 10.11406/rinketsu.51.690, PubMed: 20805677, CiNii: 1390001205037088512, Elsevier: Scopus) Michihiro Nakamura, Shuji Ozaki, Masahiro Abe, Hiroyuki Doi, Toshio Matsumoto and Kazunori Ishimura :
Size-controlled synthesis, surface functionalization, and biological applications of thiol-organosilica particles.,
Colloids and Surfaces B:Biointerfaces, Vol.79, No.1, 19-26, 2010.

(要約): Thiol-organosilica particles of a narrow size distribution, made from 3-mercaptopropyltrimethoxysilane (MPMS), were prepared by means of a one-pot synthesis. We examined three synthetic conditions at high temperature (100 degrees C), including the Stöber synthesis and two entirely aqueous syntheses. Under all conditions, the sizes of MPMS particles were well controlled, and the average of the coefficient of variation for the size distribution was less than 20%. The incubation times required for formation of MPMS particles were shorter at high temperature than at low temperature. MPMS particles internally functionalized with fluorescent dye were also prepared by means of the same one-pot synthesis. On flow cytometry analysis these MPMS particles showed distinct peaks of scattering due to well-controlled sizes of particles as well as due to fluorescence signals. Real-time observation of interaction between fluorescent MPMPS particles and cultured cells could be observed under fluorescent microscopy with bright light. The surface of the as-prepared MPMS particles contained exposed mercaptopropyl residues, and the ability to adsorb proteins was at least 6 times higher than that of gold nanopaticles. In addition, fluorescein-labeled proteins adsorbed to the surface of the particles were quantitatively detected at the pg/ml level by flow cytometry. MPMS particles surface functionalized with anti-CD20 antibody using adsorption could bind with lymphoma cells expressing CD20 specifically. In this paper, we demonstrated the possibility of size-controlled thiol-organosilica particles for wild range of biological applications.
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.colsurfb.2010.03.008
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20417071; ● Search Scopus @ Elsevier (PMID): 20417071; ● Search Scopus @ Elsevier (DOI): 10.1016/j.colsurfb.2010.03.008

(DOI: 10.1016/j.colsurfb.2010.03.008, PubMed: 20417071) Kyoko Takeuchi, Masahiro Abe, Masahiro Hiasa, Asuka Oda, Hiroe Amou, Shinsuke Kido, Takeshi Harada, Osamu Tanaka, Hirokazu Miki, Shingen Nakamura, Ayako Nakano, Kumiko Kagawa, Kenichiro Yata, Shuji Ozaki and Toshio Matsumoto :
Tgf-Beta inhibition restores terminal osteoblast differentiation to suppress myeloma growth.,
PLoS ONE, Vol.5, No.3, e9870, 2010.

(要約): BACKGROUND: Multiple myeloma (MM) expands almost exclusively in the bone marrow and generates devastating bone lesions, in which bone formation is impaired and osteoclastic bone resorption is enhanced. TGF-beta, a potent inhibitor of terminal osteoblast (OB) differentiation, is abundantly deposited in the bone matrix, and released and activated by the enhanced bone resorption in MM. The present study was therefore undertaken to clarify the role of TGF-beta and its inhibition in bone formation and tumor growth in MM. METHODOLOGY/PRINCIPAL FINDINGS: TGF-beta suppressed OB differentiation from bone marrow stromal cells and MC3T3-E1 preosteoblastic cells, and also inhibited adipogenesis from C3H10T1/2 immature mesenchymal cells, suggesting differentiation arrest by TGF-beta. Inhibitors for a TGF-beta type I receptor kinase, SB431542 and Ki26894, potently enhanced OB differentiation from bone marrow stromal cells as well as MC3T3-E1 cells. The TGF-beta inhibition was able to restore OB differentiation suppressed by MM cell conditioned medium as well as bone marrow plasma from MM patients. Interestingly, TGF-beta inhibition expedited OB differentiation in parallel with suppression of MM cell growth. The anti-MM activity was elaborated exclusively by terminally differentiated OBs, which potentiated the cytotoxic effects of melphalan and dexamethasone on MM cells. Furthermore, TGF-beta inhibition was able to suppress MM cell growth within the bone marrow while preventing bone destruction in MM-bearing animal models. CONCLUSIONS/SIGNIFICANCE: The present study demonstrates that TGF-beta inhibition releases stromal cells from their differentiation arrest by MM and facilitates the formation of terminally differentiated OBs, and that terminally differentiated OBs inhibit MM cell growth and survival and enhance the susceptibility of MM cells to anti-MM agents to overcome the drug resistance mediated by stromal cells. Therefore, TGF-beta appears to be an important therapeutic target in MM bone lesions.
(出版サイトへのリンク): ● Publication site (DOI): 10.1371/journal.pone.0009870
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20360846; ● Search Scopus @ Elsevier (PMID): 20360846; ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0009870

(DOI: 10.1371/journal.pone.0009870, PubMed: 20360846) Masahiro Hiasa, Masahiro Abe, Ayako Nakano, Asuka Oda, Hiroe Amou, Shinsuke Kido, Kyoko Takeuchi, Kumiko Kagawa, Kenichiro Yata, Toshihiro Hashimoto, Shuji Ozaki, Kenzo Asaoka, Eiji Tanaka, Keiji Moriyama and Toshio Matsumoto :
GM-CSF and IL-4 induce dendritic cell differentiation and disrupt osteoclastogenesis through M-CSF receptor shedding by up-regulation of TNF-{alpha} converting enzyme (TACE),
Blood, Vol.114, No.20, 4517-4526, 2009.

(要約): Monocytes give rise to macrophages, osteoclasts (OCs), and dendritic cells (DCs). M-CSF and RANK ligand induce OC differentiation from monocytes, while GM-CSF and IL-4 trigger monocytic differentiation into DCs. These two differentiation pathways occur in a mutually exclusive manner. However, regulatory mechanisms for the polarization of monocytic differentiation are still unclear. The present study was undertaken to clarify the mechanism of triggering the deflection of OC and DC differentiation from monocytes. GM-CSF and IL-4 abolished monocytic differentiation into OCs while inducing DC differentiation even in the presence of M-CSF and RANK ligand. GM-CSF and IL-4 in combination potently up-regulate TNF-alpha converting enzyme (TACE) expression and activity in monocytes, causing ectodomain shedding of the membrane-bound M-CSF receptor, resulting in the disruption of its phosphorylation by M-CSF as well as the induction of osteoclastogenesis from monocytes by M-CSF and RANK ligand. Interestingly, TACE inhibition robustly causes the resumption of the surface expression of M-CSF receptors on monocytes, which facilitates M-CSF-mediated phosphorylation of M-CSF receptors and macrophage/OC differentiation while impairing GM-CSF and IL-4-mediated DC differentiation from monocytes. These results reveal a novel proteolytic regulation of M-CSF receptor expression in monocytes to control M-CSF signaling and monocytic differentiation into macrophage/OC-lineage cells or DCs.
(キーワード): ADAM Proteins / Blotting, Western / Cell Differentiation / Dendritic Cells / Fluorescent Antibody Technique / Granulocyte-Macrophage Colony-Stimulating Factor / Humans / Interleukin-4 / Macrophages / Monocytes / Osteoclasts / RANK Ligand / Receptor, Macrophage Colony-Stimulating Factor / Reverse Transcriptase Polymerase Chain Reaction / Up-Regulation
(出版サイトへのリンク): ● Publication site (DOI): 10.1182/blood-2009-04-215020
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19762488; ● Search Scopus @ Elsevier (PMID): 19762488; ● Search Scopus @ Elsevier (DOI): 10.1182/blood-2009-04-215020

(DOI: 10.1182/blood-2009-04-215020, PubMed: 19762488) Ken-ichi Kitazoe, Masahiro Abe, Masahiro Hiasa, Asuka Oda, Hiroe Amou, Takeshi Harada, Ayako Nakano, Kyoko Takeuchi, Toshihiro Hashimoto, Ken-ichiro Yata, Shuji Ozaki and Toshio Matsumoto :
Valproic acid exerts anti-tumor as well as anti-angiogenic effects on myeloma.,
International Journal of Hematology, Vol.89, No.1, 45-57, 2008.

(要約): Multiple myeloma is still an incurable disease, most commonly occurring in the elderly. The myeloma-induced bone marrow microenvironment protects myeloma cells from drug-induced apoptosis. Therefore, the development of novel and tolerable therapeutic alternatives to overcome the drug resistance is an important clinical issue. Valproic acid (VPA), a safe and widely used anti-epileptic agent, is revisited as a class I- and IIa-specific histone deacetylase inhibitor. In the present study, we evaluated the effect as well as a mechanism of actions of VPA on myeloma cell growth and survival, with special reference to the myeloma-induced bone marrow microenvironment. VPA at therapeutic concentrations for epilepsy induced cell death in primary CD138-positive myeloma cells as well as myeloma cell lines, but not in CD138-negative bone marrow cells. VPA suppressed osteoclastogenesis as well as osteoclast-mediated myeloma cell growth. VPA also inhibited vascular tubule formation enhanced by co-cultures of myeloma cells and osteoclasts in concert with thalidomide. In addition, VPA induced both caspase-dependent and -independent cell death in myeloma cells, and potentiated the anti-myeloma effects of melphalan and dexamethasone. Collectively, VPA is suggested to exert multi-factorial anti-myeloma actions, and may serve as a safe adjuvant to be included in conventional chemotherapies against myeloma.
(キーワード): Antineoplastic Combined Chemotherapy Protocols / Bone Marrow / 細胞増殖·分化 (cell proliferation and differentiation) / Cell Survival / Coculture Techniques / Drug Synergism / Histone Deacetylase Inhibitors / Humans / Multiple Myeloma / Osteoclasts / Thalidomide / Tumor Cells, Cultured / Valproic Acid
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s12185-008-0226-9
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19093163; ● Search Scopus @ Elsevier (PMID): 19093163; ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-008-0226-9

(DOI: 10.1007/s12185-008-0226-9, PubMed: 19093163) Youichi Tanaka, Masahiro Abe, Masahiro Hiasa, Asuka Oda, Hiroe Amou, Ayako Nakano, Kyoko Takeuchi, Kenichi Kitazoe, Shinsuke Kido, Daisuke Inoue, Keiji Moriyama, Toshihiro Hashimoto, Shuji Ozaki and Toshio Matsumoto :
Myeloma Cell-Osteoclast Interaction Enhances Angiogenesis Together with Bone Resorption: A Role for Vascular Endothelial Cell Growth Factor and Osteopontin,
Clinical Cancer Research, Vol.13, No.3, 816-823, 2007.

(要約): Similar to osteoclastogenesis, angiogenesis is enhanced in the bone marrow in myeloma in parallel with tumor progression. We showed previously that myeloma cells and osteoclasts are mutually stimulated to form a vicious cycle to lead to enhance both osteoclastogenesis and tumor growth. The present study was undertaken to clarify whether myeloma cell-osteoclast interaction enhances angiogenesis and whether there is any mutual stimulation between osteoclastogenesis and angiogenesis. Myeloma cells and monocyte-derived osteoclasts were cocultured, and angiogenic activity produced by the cocultures was assessed with in vitro vascular tubule formation assays and human umbilical vascular endothelial cell (HUVEC) migration and survival. Osteoclastogenic activity was determined with rabbit bone cell cultures on dentine slices. Myeloma cells and osteoclasts constitutively secrete proangiogenic factors, vascular endothelial growth factor (VEGF) and osteopontin, respectively. A cell-to-cell interaction between myeloma cells and osteoclasts potently enhanced vascular tubule formation. Blockade of both VEGF and osteopontin actions almost completely abrogated such vascular tubule formation as well as migration and survival of HUVECs enhanced by conditioned medium from cocultures of myeloma cells and osteoclasts. Furthermore, these factors in combination triggered the production of osteoclastogenic activity by HUVEC. Osteoclast-derived osteopontin and VEGF from myeloma cells cooperatively enhance angiogenesis and also induce osteoclastogenic activity by vascular endothelial cells. These observations suggest the presence of a close link between myeloma cells, osteoclasts, and vascular endothelial cells to form a vicious cycle between bone destruction, angiogenesis, and myeloma expansion.
(キーワード): Bone Resorption / Cell Movement / Cell Survival / Coculture Techniques / Culture Media, Conditioned / Disease Progression / Endothelium, Vascular / Humans / Monocytes / Multiple Myeloma / Neovascularization, Pathologic / Osteoclasts / Osteopontin / Umbilical Veins / Vascular Endothelial Growth Factor A
(出版サイトへのリンク): ● Publication site (DOI): 10.1158/1078-0432.CCR-06-2258
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17289872; ● Search Scopus @ Elsevier (PMID): 17289872; ● Search Scopus @ Elsevier (DOI): 10.1158/1078-0432.CCR-06-2258

(DOI: 10.1158/1078-0432.CCR-06-2258, PubMed: 17289872) Masahiro Abe, Shinsuke Kido, Masahiro Hiasa, Nakano Ayako, Oda Asuka, Amou Hiroe and Toshio Matsumoto :
BAFF and APRIL as osteoclast-derived survival factors for myeloma cells: a rationale for TACI-Fc tratment in patients with multiple myeloma.,
Leukemia, Vol.20, No.7, 1313-1315, 2006.

(キーワード): B-Cell Activating Factor / Cell Survival / Humans / Immunoglobulin Fc Fragments / Multiple Myeloma / Osteoclasts / Transmembrane Activator and CAML Interactor Protein / Tumor Necrosis Factor Ligand Superfamily Member 13
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/sj.leu.2404228
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16617317; ● Search Scopus @ Elsevier (PMID): 16617317; ● Search Scopus @ Elsevier (DOI): 10.1038/sj.leu.2404228

(DOI: 10.1038/sj.leu.2404228, PubMed: 16617317) Ali Jalili, Shuji Ozaki, Tomoko Hara, Hironobu Shibata, Toshihiro Hashimoto, Masahiro Abe, Yasuhiko Nishioka and Toshio Matsumoto :
Induction of HM1.24 peptide specific cytotoxic T lymphocytes by using peripheral-blood stem-cell harvests in patients with multiple myeloma,
Blood, Vol.106, No.10, 3538-3545, 2005.

(要約): HM1.24 antigen is preferentially overexpressed in multiple myeloma (MM) cells but not in normal cells. To explore the potential of HM1.24 as a target for cellular immunotherapy, we selected 4 HM1.24-derived peptides that possess binding motifs for HLA-A2 or HLA-A24 by using 2 computer-based algorithms. The ability of these peptides to generate cytotoxic T lymphocytes (CTLs) was examined in 20 healthy donors and 6 patients with MM by a reverse immunologic approach. Dendritic cells (DCs) were induced from peripheral-blood mononuclear cells of healthy donors or peripheral-blood stem-cell (PBSC) harvests from patients with MM, and autologous CD8(+) T cells were stimulated with HM1.24 peptide-pulsed DCs. Both interferon-gamma-producing and cytotoxic responses were observed after stimulation with either HM1.24-126 or HM1.24-165 peptides in HLA-A2 or HLA-A24 individuals. The peptide-specific recognition of these CTLs was further confirmed by tetramer assay and cold target inhibition assay. Importantly, HM1.24-specific CTLs were also induced from PBSC harvests from patients with MM and these CTLs were able to kill MM cells in an HLA-restricted manner. These results indicate the existence of functional DCs and HM1.24-specific CTL precursors within PBSC harvests and provide the basis for cellular immunotherapy in combination with autologous PBSC transplantation in MM.
(キーワード): Antigens, CD / Cell Line, Tumor / Dendritic Cells / Female / GPI-Linked Proteins / HLA-A Antigens / HLA-A2 Antigen / HLA-A24 Antigen / Hematopoietic Stem Cells / Humans / Interferon-gamma / Male / Membrane Glycoproteins / Multiple Myeloma / Peptides / Peripheral Blood Stem Cell Transplantation / T-Lymphocytes, Cytotoxic / Transplantation, Homologous
(出版サイトへのリンク): ● Publication site (DOI): 10.1182/blood-2005-04-1438
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16037388; ● Search Scopus @ Elsevier (PMID): 16037388; ● Search Scopus @ Elsevier (DOI): 10.1182/blood-2005-04-1438

(DOI: 10.1182/blood-2005-04-1438, PubMed: 16037388) Takashi Oshima, Masahiro Abe, Jin Asano, Tomoko Hara, Kenichi Kitazoe, Etsuko Sekimoto, Yoichi Tanaka, Hironobu Shibata, Toshihiro Hashimoto, Shuji Ozaki, Shinsuke Kido, Daisuke Inoue and Toshio Matsumoto :
Myeloma cells suppress bone formation by secreting a soluble Wnt inhibitor, sFRP-2,
Blood, Vol.106, No.9, 3160-3165, 2005.

(要約): Multiple myeloma (MM) develops devastating bone destruction with enhanced bone resorption and suppressed bone formation. In contrast to enhanced osteoclastogenesis, little is known about the mechanism of impaired bone formation in MM. Because a canonical Wingless-type (Wnt) signaling pathway has recently been shown to play an important role in osteoblast differentiation, we examined whether MM cells affect a canonical Wnt pathway to suppress bone formation. Conditioned media from RPMI8226 and U266 MM cell lines and primary MM cells suppressed in vitro mineralization as well as alkaline phosphatase activity in osteoblasts induced by bone morphogenetic protein 2 (BMP-2). These cell lines constitutively produced a soluble Wnt inhibitor, secreted Frizzled-related protein 2 (sFRP-2), but not other Wnt inhibitors including sFRP-1, sFRP-3, and dickkopf 1 (DKK-1) at the protein level. Most MM cells from patients with advanced bone destructive lesions also expressed sFRP-2. Furthermore, exogenous sFRP-2 suppressed osteoblast differentiation induced by BMP-2, and immunodepletion of sFRP-2 significantly restored mineralized nodule formation in vitro, suggesting a predominant role for MM cell-derived sFRP-2 in the impairment of bone formation by MM. Thus, in addition to enhanced osteolysis, MM cells also suppress bone formation at least in part through an inhibition of the canonical Wnt pathway by secreting sFRP-2.
(キーワード): Animals / Antibodies / Bone Morphogenetic Protein 2 / Bone Morphogenetic Proteins / Calcification, Physiologic / Cell Differentiation / Genes, Reporter / Humans / Melanoma / Membrane Proteins / Mice / Osteoblasts / Osteogenesis / Solubility / Transforming Growth Factor beta / Tumor Cells, Cultured / Wnt Proteins
(出版サイトへのリンク): ● Publication site (DOI): 10.1182/blood-2004-12-4940
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16030194; ● Search Scopus @ Elsevier (PMID): 16030194; ● Search Scopus @ Elsevier (DOI): 10.1182/blood-2004-12-4940

(DOI: 10.1182/blood-2004-12-4940, PubMed: 16030194) Hironobu Shibata, Masahiro Abe, Kenji Hiura, Javier Wilde, Keiji Moriyama, Toshiaki Sano, Ken-ichi Kitazoe, Toshihiro Hashimoto, Shuji Ozaki, Shingo Wakatsuki, Shinsuke Kido, Daisuke Inoue and Toshio Matsumoto :
Malignant B-lymphoid cells with bone lesions express receptor activator of nuclear factor-kappaB ligand and vascular endothelial growth factor to enhance osteoclastogenesis.,
Clinical Cancer Research, Vol.11, No.17, 6109-6115, 2005.

(要約): Receptor activator of nuclear factor-kappaB ligand (RANKL) is a key mediator of osteoclastogenesis. Because certain types of tumor cells aberrantly express RANKL, and because bone destruction also develops in B-cell lymphomas of bone origin, we investigated RANKL expression and the mechanisms of osteoclastogenesis in B-lymphoid neoplasms. Immunohistochemistry of bone specimens resected from patients with primary B-cell lymphoma of bone with bone destruction revealed that lymphoma cells express RANKL as well as vascular endothelial cell growth factor (VEGF). The tumor cells isolated from the bone specimens enhanced osteoclastogenesis in vitro. In contrast, B-cell lymphoma infiltrating to the bone marrow without bone destruction did not express RANKL. Both RANKL and VEGF were expressed by a portion of B-lymphoid cell lines, including Daudi and IM-9. These RANKL-expressing tumor cells enhanced osteoclastogenesis from RAW264.7 cells and human monocyte-derived preosteoclasts in the absence of stromal cells/osteoblasts in a RANKL-dependent manner. Furthermore, conditioned media from Daudi cells enhanced transmigration of preosteoclasts that was inhibited by anti-VEGF antibody, suggesting that tumor cell-derived VEGF mediates recruitment of osteoclast precursors. Moreover, cocultures of B-lymphoid cell lines with osteoclasts enhanced the growth of B-lymphoid cells. Some malignant B cells aberrantly express functional RANKL as well as VEGF to enhance osteoclastogenesis. The coexpression of RANKL and VEGF may also contribute to the close cellular interactions with osteoclastic cells, thereby forming a vicious cycle between osteoclastic bone destruction and tumor expansion in bone.
(キーワード): Bone Neoplasms / Carrier Proteins / Cell Movement / Culture Media, Conditioned / Flow Cytometry / Humans / Immunoenzyme Techniques / Lymphoma, B-Cell / Membrane Glycoproteins / Osteoclasts / RANK Ligand / Receptor Activator of Nuclear Factor-kappa B / Stromal Cells / Tumor Cells, Cultured / Vascular Endothelial Growth Factor A
(出版サイトへのリンク): ● Publication site (DOI): 10.1158/1078-0432.CCR-05-0181
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16144909; ● Search Scopus @ Elsevier (PMID): 16144909; ● Search Scopus @ Elsevier (DOI): 10.1158/1078-0432.CCR-05-0181

(DOI: 10.1158/1078-0432.CCR-05-0181, PubMed: 16144909) Shoji Sakiyama, Kazuya Kondo, Mitsuteru Yoshida, Hiromitsu Takizawa, Koichiro Kenzaki, Takanori Miyoshi, Masahiro Abe, Shingo Wakatsuki and Yasumasa Monden :
Extramedullary plasmacytoma immunoglobulin D (λ) in the chest wall and the subglottic region,
Journal of Thoracic and Cardiovascular Surgery, Vol.129, No.5, 1168-1169, 2005.

(キーワード): Antineoplastic Combined Chemotherapy Protocols / Biopsy / Dexamethasone / Doxorubicin / Female / Glottis / Humans / Immunoglobulin D / Ki-67 Antigen / Laryngeal Neoplasms / Magnetic Resonance Imaging / Middle Aged / Neoplasms, Second Primary / Plasmacytoma / Prognosis / Radiotherapy, Adjuvant / Rare Diseases / Remission, Spontaneous / Thoracic Neoplasms / Thoracic Wall / Tomography, X-Ray Computed / Vincristine
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.jtcvs.2004.08.037
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15867795; ● Search Scopus @ Elsevier (PMID): 15867795; ● Search Scopus @ Elsevier (DOI): 10.1016/j.jtcvs.2004.08.037

(DOI: 10.1016/j.jtcvs.2004.08.037, PubMed: 15867795) Toshio Matsumoto and Masahiro Abe :
The Importance of Notch Signaling in Myeloma Cell-Osteoclast Interactions,
BoneKEy Osteovision, Vol.2, No.2, 7-10, 2005.

(出版サイトへのリンク): ● Publication site (DOI): 10.1138/20050148
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.1138/20050148

(DOI: 10.1138/20050148) Naoki Kimura, Shigeto Kawai, Yasuko Kinoshita, Takahiro Ishiguro, Yumiko Azuma, Shuji Ozaki, Masahiro Abe, Masamichi Sugimoto, Yuichi Hirata, Tetsuro Orita, Hisafumi Okabe, Toshio Matsumoto and Masayuki Tsuchiya :
2D7 diabody bound to the α2 domain of HLA class I efficiently induces caspase-independent cell death against malignant and activated lymphoid cells,
Biochemical and Biophysical Research Communications, Vol.325, No.4, 1201-1209, 2004.

(要約): A mouse monoclonal antibody (2D7 mAb), which specifically bound to the alpha2 domain of HLA class I, rapidly induces cell aggregation accompanied by weak cytotoxicity against ARH-77 cells, suggesting that 2D7 mAb had a potential for agonist antibody. In order to enhance this cytotoxicity, 2D7 mAb was engineered to be a small bivalent antibody fragment, 2D7 diabody. The resultant 2D7 diabody showed a strong cytotoxicity against ARH-77 cells. As a notable characteristic feature, the lethal effect of 2D7 diabody was quite rapid, mediated by a caspase-independent death pathway. Furthermore, 2D7 diabody also showed cytotoxicity against several leukemia and lymphoma cell lines, and mitogen-activated peripheral blood mononuclear cells (PBMC), but not for normal resting PBMC and adherent cell lines such as HUVEC. These results suggest that 2D7 diabody could be expected as a novel therapeutic antibody for hematological malignancies as well as inflammatory diseases.
(キーワード): Agonist antibody / Diabody / HLA class I / 細胞死 (cell death) / Therapeutic antibody / Hematological malignancy
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.bbrc.2004.10.163
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15555554; ● Search Scopus @ Elsevier (PMID): 15555554; ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2004.10.163

(DOI: 10.1016/j.bbrc.2004.10.163, PubMed: 15555554) Masahiro Abe, Kenji Hiura, Javier Wilde, Atsushi Shioyasono, Keiji Moriyama, Toshihiro Hashimoto, Shinsuke Kido, Takashi Oshima, Hironobu Shibata, Shuji Ozaki, Daisuke Inoue and Toshio Matsumoto :
Osteoclasts enhance myeloma cell growth and survival via cell-cell contact: a vicious cycle between bone destruction and myeloma expansion.,
Blood, Vol.104, No.8, 2484-2491, 2004.

(要約): Multiple myeloma (MM) expands in the bone marrow and causes devastating bone destruction by enhancing osteoclastic bone resorption in its vicinity, suggesting a close interaction between MM cells and osteoclasts (OCs). Here, we show that peripheral blood mononuclear cell-derived OCs enhanced growth and survival of primary MM cells as well as MM cell lines more potently than stromal cells, and that OCs protected MM cells from apoptosis induced by serum depletion or doxorubicin. OCs produced osteopontin (OPN) and interleukin 6 (IL-6), and adhesion of MM cells to OCs increased IL-6 production from OCs. In addition, IL-6 and OPN in combination enhanced MM cell growth and survival. However, the effects of OCs on MM cell growth and survival were only partially suppressed by a simultaneous addition of anti-IL-6 and anti-OPN antibodies and were completely abrogated by inhibition of cellular contact between MM cells and OCs. These results demonstrate that OCs enhance MM cell growth and survival through a cell-cell contact-mediated mechanism that is partially dependent on IL-6 and OPN. It is suggested that interactions of MM cells with OCs augment MM growth and survival and, thereby, form a vicious cycle, leading to extensive bone destruction and MM cell expansion.
(キーワード): Animals / Antibodies / Cell Adhesion / Cell Division / Cell Survival / Cells, Cultured / Coculture Techniques / Culture Media, Serum-Free / Diphosphonates / Doxorubicin / Humans / Integrin alpha4beta1 / Integrin alphaVbeta3 / Interleukin-6 / Multiple Myeloma / Osteoclasts / Osteopontin / Rabbits / Sialoglycoproteins / Stromal Cells
(出版サイトへのリンク): ● Publication site (DOI): 10.1182/blood-2003-11-3839
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15187021; ● Search Scopus @ Elsevier (PMID): 15187021; ● Search Scopus @ Elsevier (DOI): 10.1182/blood-2003-11-3839

(DOI: 10.1182/blood-2003-11-3839, PubMed: 15187021) Hirokazu Murakami, Hiroshi Fujii, Tohru Inaba, Chihiro Shimazaki, Sinichirou Okamoto, Akiyosi Miwa, Morio Sawamura, Masahiro Abe, Takaaki Chou, Hideki Asaoku, Yoshikazu Kitahara, Kunihiko Hayashi, Masaaki Kosaka, Atsushi Togawa and Kiyoshi Takatsuki :
High-dose chemotherapy and autologous peripheral blood stem cell transplantation in high-risk multiple myeloma,
European Journal of Haematology, Vol.73, No.3, 169-173, 2004.

(要約): We compared the effect of high-dose therapy together with autologous peripheral blood stem cell transplantation (autoPBSCT) in 60 patients with multiple myeloma (MM) with 90 patients who underwent conventional chemotherapy. We scored the prognostic factors according to our reported classification system that includes measurements of serum albumin, serum beta-2-microglobulin, and morphology of myeloma cells selected by multivariate analysis. We separated the patients into three risk groups at stratification level I (low, intermediate and high) and into two risk groups at stratification level II (low and high). AutoPBSCT tended to be as effective for high, as for low-risk patients in level I, and was obviously as helpful for high, as for low-risk patients in stratification II. In conclusion, high-risk patients with MM should be treated with high-dose therapy accompanied with autoPBSCT like low-risk patients.
(キーワード): myeloma / prognostic factor / stem cell transplantation / morphology / stratification
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/j.1600-0609.2004.00282.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15287913; ● Search Scopus @ Elsevier (PMID): 15287913; ● Search Scopus @ Elsevier (DOI): 10.1111/j.1600-0609.2004.00282.x

(DOI: 10.1111/j.1600-0609.2004.00282.x, PubMed: 15287913) Toshihiro Hashimoto, Masahiro Abe, Takashi Oshima, Hironobu Shibata, Shuji Ozaki, Daisuke Inoue and Toshio Matsumoto :
Ability of myeloma cells to secrete macrophage inflammatory protein (MIP)-1α and MIP-1β correlates with lytic bone lesions in patients with multiple myeloma,
British Journal of Haematology, Vol.125, No.1, 38-41, 2004.

(要約): Macrophage inflammatory protein (MIP)-1alpha and MIP-1beta have been identified as candidates for multiple myeloma (MM)-derived bone-resorbing factors. To validate the clinical relevance of these observations, we investigated correlations between the ability of MM cells to secrete these chemokines and the extent of MM bone lesions as well as levels of biochemical bone markers in patients with MM. Patients with multiple bone lesions exhibited higher MIP-1alpha and MIP-1beta secretion from MM cells along with elevated urinary deoxypyridinoline (Dpd), without significant elevation of serum bone-specific alkaline phosphatase (BALP) or osteocalcin compared with those with minimal bone lesions. MIP-1alpha and MIP-1beta levels correlated positively with urinary Dpd and serum BALP but not with serum osteocalcin. These results provide further evidence for a causal role of MIP-1alpha and MIP-1beta in the development of lytic bone lesions, and suggest that MM cells suppress osteoblastic bone formation to cause an imbalance of bone turnover and development of destructive bone lesions.
(キーワード): multiple myeloma / chemokines / bone disease
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/j.1365-2141.2004.04864.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15015966; ● Search Scopus @ Elsevier (PMID): 15015966; ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2141.2004.04864.x

(DOI: 10.1111/j.1365-2141.2004.04864.x, PubMed: 15015966) Tomoko Hara, Shingo Wakatsuki, Shuji Ozaki, Masahiro Abe and Masaaki Kosaka :
Primary adult T-cell leukemia/lymphoma of bone,
International Journal of Hematology, Vol.79, No.2, 157-160, 2004.

(要約): A 77-year-old man developed primary adult T-cell leukemia/lymphoma (ATL) of the bone with osteolytic lesions. A biopsy of the lesion revealed proliferation of atypical, large lymphoid cells with a local increase of osteoclasts. The clonal integration of human T-lymphotropic virus type I proviral DNA revealed the tumor cells to be ATL. They produced macrophage inflammatory protein 1alpha (MIP-1alpha) but not parathyroid hormone-related protein or other osteoclast-activating factors. Because MIP-1 produced by tumor cells enhances the expression of receptor activator of nuclear factor kappaB ligand (RANKL) of local osteoblasts and stromal cells, even of tumor cells, the increase of osteoclasts in the close vicinity of ATL cells was considered to result in local bone destruction.
(キーワード): adult T-cell leukemia/lymphoma / macrophage inflammatory protein 1 / local osteolysis / Bone lesion / RANKL
(出版サイトへのリンク): ● Publication site (DOI): 10.1532/IJH97.03006
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15005344; ● CiNii @ 国立情報学研究所 (CRID): 1572824499976107264; ● Search Scopus @ Elsevier (PMID): 15005344; ● Search Scopus @ Elsevier (DOI): 10.1532/IJH97.03006

(DOI: 10.1532/IJH97.03006, PubMed: 15005344, CiNii: 1572824499976107264) Mitsunori Fujimura, Masashi Akaike, Midori Kato, Nobuyuki Takamori, Masahiro Abe, Takeshi Nishiuchi, Hiroyuki Azuma and Toshio Matsumoto :
Aggressive antiplatelet therapy before coronary stent implantation in acute coronary syndrome with essential thrombocythemia--a case report,
Angiology, Vol.54, No.4, 485-490, 2003.

(要約): A 52-year-old man was admitted to the hospital because of unstable angina pectoris. Coronary angiography revealed severe stenosis at a proximal site of the left anterior descending artery. Essential thrombocythemia (ET) was diagnosed on the basis of findings of marked thrombocytosis (106 x 10(4)/microL) and an increased number of immature megakaryocytes in the bone marrow. Because hyperaggregability of platelets was demonstrated by an ex vivo platelet aggregation assay and by elevated plasma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4), antiplatelet therapy with aspirin and ticlopidine and cytoreduction therapy with hydroxyurea were started. This combination treatment resulted in a decrease in the platelet count to less than 60 x 10(4)/microL and decreases in plasma levels of both beta-TG and PF4 to almost normal values. Percutaneous coronary angioplasty and stenting were then performed successfully without thrombotic complications. These findings suggest that combination therapy with antiplatelet and cytoreduction agents before catheter intervention is useful for the prevention of thrombotic complications in patients with acute coronary syndrome associated with essential thrombocythemia.
(キーワード): Acute Disease / Angina, Unstable / Aspirin / Combined Modality Therapy / Coronary Stenosis / Humans / Hydroxyurea / Male / Middle Aged / Platelet Aggregation Inhibitors / Stents / Thrombocythemia, Essential / Ticlopidine
(出版サイトへのリンク): ● Publication site (DOI): 10.1177/000331970305400414
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12934770; ● Search Scopus @ Elsevier (PMID): 12934770; ● Search Scopus @ Elsevier (DOI): 10.1177/000331970305400414

(DOI: 10.1177/000331970305400414, PubMed: 12934770) Masahiro Abe, Kenji Hiura, Javier Wilde, Keiji Moriyama, Toshihiro Hashimoto, Shuji Ozaki, Shingo Wakatsuki, Masaaki Kosaka, Shinsuke Kido, Daisuke Inoue and Toshio Matsumoto :
Role for macrophage inflammatory protein (MIP)-1α and MIP-1β in the development of osteolytic lesions in multiple myeloma,
Blood, Vol.100, No.6, 2195-2202, 2002.

(要約): Multiple myeloma (MM) cells cause devastating bone destruction by activating osteoclasts in the bone marrow milieu. However, the mechanism of enhanced bone resorption in patients with myeloma is poorly understood. In the present study, we investigated a role of C-C chemokines, macrophage inflammatory protein (MIP)-1alpha and MIP-1beta, in MM cell-induced osteolysis. These chemokines were produced and secreted by a majority of MM cell lines as well as primary MM cells from patients. Secretion of MIP-1alpha and MIP-1beta correlated well with the ability of myeloma cells to enhance osteoclastic bone resorption both in vitro and in vivo as well as in MM patients. In osteoclastogenic cultures of rabbit bone cells, cocultures with myeloma cells as well as addition of myeloma cell-conditioned media enhanced both formation of osteoclastlike cells and resorption pits to an extent comparable to the effect of recombinant MIP-1alpha and MIP-1beta. Importantly, these effects were mostly reversed by neutralizing antibodies against MIP-1alpha and MIP-1beta, or their cognate receptor, CCR5, suggesting critical roles of these chemokines. We also demonstrated that stromal cells express CCR5 and that recombinant MIP-1alpha and MIP-1beta induce expression of receptor activator of nuclear factor-kappaB (RANK) ligand by stromal cells, thereby stimulating osteoclast differentiation of preosteoclastic cells. These results suggest that MIP-1alpha and MIP-1beta may be major osteoclast-activating factors produced by MM cells.
(キーワード): Animals / Bone Neoplasms / Bone Resorption / Carrier Proteins / Chemokine CCL3 / Chemokine CCL4 / Coculture Techniques / Culture Media, Conditioned / Humans / Macrophage Inflammatory Proteins / Membrane Glycoproteins / Multiple Myeloma / Osteoclasts / Osteolysis / Paracrine Communication / RANK Ligand / Rabbits / Receptor Activator of Nuclear Factor-kappa B / Receptors, CCR5 / Stromal Cells / Tumor Cells, Cultured
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12200385; ● Summary page in Scopus @ Elsevier: 2-s2.0-0037105599

(PubMed: 12200385, Elsevier: Scopus) Masahiro Abe, Yasumi Shintani, Yuzuru Eto, Kazuyo Harada, Masaaki Kosaka and Toshio Matsumoto :
Potent induction of activin A secretion from monocytes and bone marrow stromal fibroblasts by cognate interaction with activated T cells,
Journal of Leukocyte Biology, Vol.72, No.2, 347-352, 2002.

(要約): Activin A is a multifunctional cytokine essential for cell differentiation and apoptosis including erythroid cell differentiation in the bone marrow. In addition, activin A is induced by inflammation and exerts anti-inflammatory effects. However, the mechanism of activin A induction is still unclear, especially by inflammatory processes. Here we show that activin A secretion from monocytes and bone marrow stromal fibroblasts, its major sources in the bone marrow, is markedly enhanced by cognate interaction with activated T cells. This process is mediated by CD40/CD40 ligand interaction as well as concomitantly secreted T cell-derived cytokines, granulocyte macrophage-colony stimulating factor, and interferon-gamma. Furthermore, stromal fibroblasts as well as monocytes provide a costimulatory signal to anti-CD3-treated T cells via CD80 and CD86 to maintain the enhanced activin A production. These findings suggest that activin A is potently induced in the bone marrow and may play a role in the suppression of inflammatory or immune processes.
(キーワード): CD40 / CD28 / costimulation / GM-CSF / IFN-γ
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12149426; ● Summary page in Scopus @ Elsevier: 2-s2.0-0036698295

(PubMed: 12149426, Elsevier: Scopus) Masahiro Abe, Yasumi Shintani, Yuzuru Eto, Kazuyo Harada, Yuichi Fujinaka, Masaaki Kosaka and Toshio Matsumoto :
Interleukin-1 β enhances and interferon-γ suppresses activin A actions by reciprocally regulating activin A and follistatin secretion from bone marrow stromal fibroblasts,
Clinical and Experimental Immunology, Vol.126, No.1, 64-68, 2001.

(要約): Activin A is a multi-functional cytokine with a potent stimulation on erythroid cell differentiation in the bone marrow. The actions of activin A are determined by a balance of the levels of activin A and its inhibitor, follistatin (FS). However, the regulation of its actions in the bone marrow has been unclear. Here we show that bone marrow-derived stromal fibroblasts are the major source of activin A and FS in the bone marrow, and that the production of activin A is enhanced by interleukin-1beta (IL-1beta) and lipopolysaccharide (LPS), whereas interferon-gamma (IFN-gamma) inhibits the secretion of activin A by stromal fibroblasts. Concomitantly, IL-1beta as well as LPS inhibits and IFN-gamma stimulates FS secretion from stromal fibroblasts. Thus, these cytokines potently regulate activin A actions by reciprocal modulation of activin A and FS secretion from stromal fibroblasts. Because activin A exhibits anti-inflammatory effects in various tissues, up-regulation of activin A actions by IL-1beta and endotoxin in the bone marrow may play a protective role against inflammatory processes as well as anaemia. The present results also suggest that the inhibitory effect of IFN-gamma on erythropoiesis is mediated at least in part by a suppression of activin A actions in bone marrow.
(キーワード): activin A / フォリスタチン (follistatin) / stroma / IL-1β / IFN-γ
(出版サイトへのリンク): ● Publication site (DOI): 10.1046/j.1365-2249.2001.01644.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11678900; ● Summary page in Scopus @ Elsevier: 2-s2.0-0034781894

(DOI: 10.1046/j.1365-2249.2001.01644.x, PubMed: 11678900, Elsevier: Scopus) Masahiro Abe, Y Shintani, Y Eto, K Harada, Y Fujinaka, M Kosaka and Toshio Matsumoto :
Interleukin 1β enhances and interferon-γ suppresses activin A actions by reciprocally regulating activin A and follistatin secretion from bone marrow stromal fibroblasts,
Clinical and Experimental Immunology, Vol.126, 64-68, 2001.

(キーワード): IFN-γ / アクチビン (activin) / follistain / stroma / IL-1β

Ken-ichi Aihara, Hiroyuki Azuma, Yasumasa Ikeda, Masashi Akaike, Masahiro Abe, Takashi Sugihara and Toshio Matsumoto :
Successful combination therapy--flunarizine,pentoxifylline, and cholestyramine--for spur cell anemia,
International Journal of Hematology, Vol.73, No.3, 351-355, 2001.

(要約): Spur cell anemia, a hemolytic anemia observed in patients with alcoholic cirrhosis, is characterized by unusual erythrocyte morphology and an increased ratio of free cholesterol to phospholipid in the erythrocyte membrane. The prognosis of spur cell anemia is usually extremely poor, however, we describe here a patient with spur cell anemia who was successfully treated with combination therapy consisting of flunarizine, pentoxifylline, and cholestyramine. Initial therapy with flunarizine alone for 6 weeks did not significantly decrease the number of spur cells on peripheral blood smears. So pentoxifylline was added to the regimen. The patient recovered from the anemia, showed remarkable improvement with regard to the hyperbilirubinemia, and the changes were accompanied by a significant decrease in the number of spur cells in peripheral blood smears. To correct the hypercholesterolemia, cholestyramine was added to the regimen, which resulted in a reduction in the serum level of free cholesterol and an increase in the molar ratio of free cholesterol to phospholipid in erythrocyte membrane. However, 6 months later a skin eruption developed that was considered an adverse reaction to the drugs, so the flunarizine and pentoxifylline were discontinued. With cholestyramine therapy alone, the remission of spur cell anemia was maintained for more than 11 months. These observations suggest that non-invasive combination therapy with flunarizine, pentoxifylline, and cholestyramine is effective and valuable in the treatment of patients with spur cell anemia.
(キーワード): Spur cell anemia / Free cholesterol / Hepatosplenomegaly / Pentoxifylline / Cholestyramine
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11345202; ● Search Scopus @ Elsevier (PMID): 11345202

(PubMed: 11345202) Mototsugu Kato, Masahiro Asaka, Masao Saito, Hitoshi Sekine, Shuichi Ohara, Takayoshi Toyota, Taiji Akamatsu, Taimei Kaneko, Kendo Kiyosawa, Osamu Nishizawa, Toshiko Kumagai, Tsutomu Katsuyama, Masahiro Abe, Masaaki Kosaka, Shojiro Hariya, Kunihiro Minami, Yasuhiro Sanai, Masayuki Sawamura and Tetsuya Tachikawa :
Clinical Usefulness of Urine-based Enzyme-linked Immunosorbent Assay for Detection of Antibody to Helicobacter pylori:A Collaborative Study in Nine Medical Institutions in Japan,
Helicobacter, Vol.5, No.2, 109, 2000.

(出版サイトへのリンク): ● Publication site (DOI): 10.1046/j.1523-5378.2000.00017.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10849061; ● Summary page in Scopus @ Elsevier: 2-s2.0-0034583804

(DOI: 10.1046/j.1523-5378.2000.00017.x, PubMed: 10849061, Elsevier: Scopus) Shuji Ozaki, Masaaki Kosaka, Shingo Wakatsuki, Masahiro Abe, Yasuo Koishihara and Toshio Matsumoto :
Immunotherapy of multiple myeloma with a monoclonal antibody directed against a plasma cell-specific antigen, HM1.24,
Blood, Vol.90, No.8, 3179-3186, 1997. Zhong-Hui Liu, Yasumi Shintani, Yukihiro Sakamoto, Kazuyo Harada, Chen-Yu Zhang, Yuichi Fujinaka, Masahiro Abe, Tetsuya Goto and Shiro Saito :
Effects of LHRH, FSH and activin A on follistatin secretion from cultured rat anterior pituitary cells,
Endocrine Journal, Vol.43, No.3, 321-327, 1996.

(要約): We demonstrated the release of follistatin, an activin-binding protein, from cultured rat anterior pituitary cells by measuring immunoreactive (ir-) follistatin in a specific immunoradiometric assay. Ir-follistatin release gradually increased in cultures over 1-18 days and reached its maximal level at 12-15 days of incubation. The basal ir-follistatin levels in the culture media increased about 3- (P < 0.01) and 5-fold (P < 0.001) in 2 and 10% fetal calf serum for 6 days, respectively. LHRH and activin A caused an approximately 2.0- (P < 0.05) and 1.8-fold (P < 0.05) rise in ir-follistatin release, respectively, in contrast to the lack of significant FSH effects. The culture medium condensed on sulfate-cellulofine gel was resolved by polyacrylamide gel electrophoresis and blotted with anti-follistatin polyclonal antibody, resulting in at least three protein bands ranging from 35 to 50 kDa under non-reducing conditions. These results indicated that follistatin is produced in anterior pituitary cells and that its secretion is regulated at least in part by LHRH and activin, implying an autocrine/paracrine role of activin and follistatin in the pituitary.
(キーワード): Activins / Animals / Blotting, Western / Cells, Cultured / Female / Follicle Stimulating Hormone / Follistatin / Glycoproteins / Gonadotropin-Releasing Hormone / Growth Substances / Humans / Immunoradiometric Assay / Inhibins / Male / Pituitary Gland, Anterior / Rabbits / Random Allocation / Rats / Rats, Wistar / Time Factors
(出版サイトへのリンク): ● Publication site (DOI): 10.1507/endocrj.43.321
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 8886627; ● Search Scopus @ Elsevier (PMID): 8886627; ● Search Scopus @ Elsevier (DOI): 10.1507/endocrj.43.321

(DOI: 10.1507/endocrj.43.321, PubMed: 8886627) Hisaomi Kawai, Kenji Yokoi, Masashi Akaike, Makoto Kunishige, Masahiro Abe, Y Tanouchi, Hideki Mine, Y Mimura and Shiro Saito :
Graves' disease in HTLV-I carriers,
Journal of molecular medicine, Vol.73, No.2, 85-88, 1995.

(キーワード): human T-lymphotropic virus type I / ATL adult T-cell leukemia / HAM HTLV-I associated myelopathy / TSP tropical spastic paraparesis

安倍正博, 後藤哲也, 尾崎修治, 小阪昌明, Solomon Alan :
免疫グロブリンL鎖γ Ⅵサブグループの酵素免疫測定法:測定法と正常人，高および低ガンマグロブリン血症患者血中濃度,
日本臨床免疫学会会誌, Vol.17, No.3, 172-181, 1994年.

(キーワード): immunoglobulin / light chain / subgroup / ELISA / AL amyloidosis

Shuji Ozaki, Masahiro Abe, Dennis Wolfenbarger, Deborah T. Weiss and Alan Solomon :
Preferential Expression of Human λ-Light-Chain Variable-Region Subgroups in Multiple Myeloma, AL Amyloidosis, and Waldenström's Macroglobulinemia,
Clinical Immunology and Immunopathology, Vol.71, No.2, 183-189, 1994. 横井健治, 川井尚臣, 峯秀樹, 赤池雅史, 安倍正博, 国重誠, 三ツ井貴夫, 斎藤史郎 :
バセドウ病を発症したHTLV-Iキャリアの2家系3症例,
ホルモンと臨床, Vol.42, 94-97, 1994年. Masahiro Abe, Shuji Ozaki, Dennis Wolfenbarger, Mary deBram-Hart, Deborah T Weiss and Alan Solomon :
Variable-region subgroup distribution among lambda-type immunoglobulins in normal human serum,
Journal of Clinical Laboratory Analysis, Vol.8, No.1, 4-9, 1994.

(要約): The distribution of the major VL subgroups (V lambda I, V lambda II, V lambda III, V lambda IV, V lambda VI, and V lambda VIII) among lambda-type immunoglobulins (Igs) in normal serum was determined by a sandwich enzyme-linked immunosorbent assay (ELISA) using a panel of murine anti-human V lambda-subgroup-specific monoclonal antibodies (MoAbs) and appropriate reference standard proteins. The mean concentration of lambda I, lambda II, lambda III, lambda IV, lambda VI, and lambda VIII Igs in serum specimens obtained from 23 adults was 2158, 162, 1958, 264, 225, and 169 micrograms/mL and represented 44, 3, 40, 5, 5, and 3% of the total Ig lambda population, respectively. The low percentage of lambda II Igs in normal serum was in marked contrast to the approximately 40% incidence of this V lambda subgroup found among lambda-type Bence Jones proteins and monoclonal serum Igs obtained from patients with multiple myeloma and AL amyloidosis, or approximately 60% in Waldenström's macroglobulinemia. The non-random expression of the V lambda II subgroup in these diseases implies a relationship between V lambda-gene usage and plasma cell, as well as certain types of lymphocytic dyscrasias.
(キーワード): γ light chains / monoclonal antibodies / ELISA
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 8164110; ● Search Scopus @ Elsevier (PMID): 8164110

(PubMed: 8164110)

MISC

中村信元, 安倍正博, 松本俊夫 :
Part7. 2. 新規治療薬の開発と臨床応用の可能性を探る (抗RANKL抗体などを中心に). がん骨転移治療ビスフォスフォネート治療によるBone Management,
先端医学者高橋俊二編集, 206-214, 2012年. 遠藤逸朗, 安倍正博, 松本俊夫 :
骨転移の分子標的治療薬骨転移のバイオロジーとマネージメント,
医薬ジャーナル社米田俊之編集, 215-224, 2012年. 七條加奈, 関本悦子, 三原愛, 大田加与, 田中洋一, 大島隆志, 柴田泰伸, 橋本年弘, 尾崎修治, 安倍正博, 松本俊夫, 若槻真吾 :
Tandem transplantationが有効であった再発·難治性ホジキンリンパ腫の1例,
日本内科学会雑誌, Vol.93, No.10, 2210-2212, 2004年.

(キーワード): Hodgkin lymphoma / tandem transplantation
(出版サイトへのリンク): ● Publication site (DOI): 10.2169/naika.93.2210
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390282681418731648; ● Search Scopus @ Elsevier (DOI): 10.2169/naika.93.2210

(DOI: 10.2169/naika.93.2210, CiNii: 1390282681418731648) 安倍正博, 松本俊夫, 小阪昌明 :
骨病変に対するbisphosphonateの効果,
臨床血液, Vol.43, No.5, 349-352, 2002年.

(キーワード): Bisphosphonate / Osteolysis / 破骨細胞 (osteoclast) / Bone metabolism
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390282680010754944

(CiNii: 1390282680010754944) Yusaku Maeda, Shoichiro Takao, Shiori Morita, Shin Kondo, Michiko Yamashita, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Mamiko Takahashi, Shiroh Fujii, Takeshi Harada, Hirokazu Miki, Masahiro Abe and Shingen Nakamura :
Quality of skeletal muscles during allogeneic stem-cell transplantation: a pilot study,
BMJ Supportive & Palliative Care, 2024.

(出版サイトへのリンク): ● Publication site (DOI): 10.1136/spcare-2024-005070
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.1136/spcare-2024-005070

(DOI: 10.1136/spcare-2024-005070)

総説・解説

原田武志, 安倍正博 :
ダラツムマブ・ボルヒアルロニダーゼアルファ配合(ダラキューロ),
がん最新の薬物療法 2023-2024, 79-81, 2023年3月. 中村信元, 三木浩和, 安倍正博 :
【最新の骨粗鬆症学(第2版)-骨粗鬆症学の最新知見-】続発性骨粗鬆症の診断と治療抗悪性腫瘍薬に伴う骨粗鬆症(解説),
日本臨床(0047-1852)81巻増刊1 最新の骨粗鬆症学 Page580-584(2023.01), 2023年. 中村信元, 三木浩和, 安倍正博 :
【骨髄腫と類縁疾患-全身をみわたす診断・治療】Overview 多発性骨髄腫の発症・進展機序,
臨床雑誌内科, Vol.130, No.4, 691-694, 2022年10月.

(要約): <文献概要>▼多発性骨髄腫(MM)はゲノム不安定性や遺伝子プロモーターのメチル化などのepigeneticな制御の異常に加え多段階の分子遺伝学的異常により,意義不明の単クローン性ガンマグロブリン血症(MGUS)を経て発症・進展する.▼MMの発症原因は不明であるが,疫学調査により性差,地域差,人種差,遺伝学的要因,被曝歴,年齢との関連が示唆されている.▼全ゲノム解析やマウスモデル,腸内細菌叢の解析などからMMのさまざまな発症機序が推測されている.
(キーワード): myc遺伝子 / 骨髄腫-多発性(病理学,遺伝学) / 疾患モデル(動物) / 人種 / 性因子 / 分子生物学 (molecular biology) / 放射線障害 (radiation injury) / 有病率 / DNAメチル化 / 単クローン性免疫グロブリン血症-良性(病理学,遺伝学) / ゲノム不安定性 / 消化管微生物叢 / 全ゲノム配列分析 / ヒト (Homo sapiens) / マウス / 動物 (animal)
(出版サイトへのリンク): ● Publication site (DOI): 10.15106/j_naika130_691
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390293412208923264; ● Search Scopus @ Elsevier (DOI): 10.15106/j_naika130_691

(DOI: 10.15106/j_naika130_691, CiNii: 1390293412208923264) 中村信元, 三木浩和, 安倍正博 :
【腎臓症候群(第3版)-その他の腎臓疾患を含めて-】各種病態にみられる腎障害造血器疾患多発性骨髄腫,
日本臨牀, 124-130, 2022年10月. Takeshi Harada, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe :
Myeloma-Bone Interaction: A Vicious Cycle via TAK1-PIM2 Signaling,
Cancers, Vol.13, No.17, 4441, Sep. 2021.

(要約): Multiple myeloma (MM) has a propensity to develop preferentially in bone and form bone-destructive lesions. MM cells enhance osteoclastogenesis and bone resorption through activation of the RANKL-NF-κB signaling pathway while suppressing bone formation by inhibiting osteoblastogenesis from bone marrow stromal cells (BMSCs) by factors elaborated in the bone marrow and bone in MM, including the soluble Wnt inhibitors DKK-1 and sclerostin, activin A, and TGF-β, resulting in systemic bone destruction with loss of bone. Osteocytes have been drawn attention as multifunctional regulators in bone metabolism. MM cells induce apoptosis in osteocytes to trigger the production of factors, including RANKL, sclerostin, and DKK-1, to further exacerbate bone destruction. Bone lesions developed in MM, in turn, provide microenvironments suited for MM cell growth/survival, including niches to foster MM cells and their precursors. Thus, MM cells alter the microenvironments through bone destruction in the bone where they reside, which in turn potentiates tumor growth and survival, thereby generating a vicious loop between tumor progression and bone destruction. The serine/threonine kinases PIM2 and TAK1, an upstream mediator of PIM2, are overexpressed in bone marrow stromal cells and osteoclasts as well in MM cells in bone lesions. Upregulation of the TAK1-PIM2 pathway plays a critical role in tumor expansion and bone destruction, posing the TAK1-PIM2 pathway as a pivotal therapeutic target in MM.
(徳島大学機関リポジトリ): ● Metadata: 117425
(出版サイトへのリンク): ● Publication site (DOI): 10.3390/cancers13174441
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34503251; ● Search Scopus @ Elsevier (PMID): 34503251; ● Search Scopus @ Elsevier (DOI): 10.3390/cancers13174441

(徳島大学機関リポジトリ: 117425, DOI: 10.3390/cancers13174441, PubMed: 34503251) 中村信元, 安倍正博 :
【骨粗鬆症最新の知見に基づいた治療薬の考え方・使い方】薬剤性骨粗鬆症に対するマネジメントの勘所がん治療に伴う骨粗鬆症,
薬局, Vol.71, No.11, 3313-3321, 2020年10月.

(要約): <Key Points>◎がん治療およびがん治療の支持療法に使用する多くの薬剤が直接または間接的に骨吸収を亢進し骨喪失を来す．◎特に内分泌療法や造血幹細胞移植などのがん治療では急速に骨喪失がもたらされる．◎がん治療に伴う骨粗鬆症はQOLの低下や予後の悪化を来す．◎がんの治療と並行しがん治療に伴う骨粗鬆症に対する適切なスクリーニングと予防および治療を行う．(著者抄録)
(キーワード): コロナウイルス感染症 Diphosphonates(治療的利用) Vitamin D(治療的利用) 胃切除(有害作用) 運動療法危険因子抗腫瘍剤(毒性・副作用,治療的利用) *骨粗鬆症(薬物療法,予防,病因) *腫瘍(薬物療法,放射線療法) 食事療法食品中のカルシウム(治療的利用) 肺炎-ウイルス性放射線療法(有害作用) 早期診断 Denosumab(治療的利用) 疾病の流行 COVID-19 ヒト

安倍正博 :
多発性骨髄腫の病態解明と治療の進歩,
日本内科学会雑誌, Vol.104, No.2, 305-313, 2015年2月.

(要約): 多発性骨髄腫(multiple myeloma:MM)は，意義不明の単クローン性ガンマグロブリン血症(monoclonal gammopathy of undetermined significance:MGUS)より進展し，発症する．骨髄腫細胞内で起こるゲノム不安定性や遺伝子プロモーターのメチル化などのepigeneticな制御の異常により特定の遺伝子が活性化あるいは不活性化し，骨髄腫は多段階の発癌ステップにより進行する．また，このような骨髄腫細胞自身の細胞遺伝学的な異常に加え，本症に特徴的な病態の形成や腫瘍進展・治療耐性の獲得に骨髄腫細胞と骨髄内のみならず，骨外の微小環境との間の複雑な細胞間相互作用が注目されている．近年，MMの進展に関する分子病態の解明や新規薬剤の登場により，治療パラダイムが大きく変貌している．
(キーワード): 症候性骨髄腫 / 腫瘍クローン内不均一性 / 骨髄腫ニッチ / 新規薬剤
(出版サイトへのリンク): ● Publication site (DOI): 10.2169/naika.104.305
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26571712; ● CiNii @ 国立情報学研究所 (CRID): 1390282681426610432; ● Search Scopus @ Elsevier (PMID): 26571712; ● Search Scopus @ Elsevier (DOI): 10.2169/naika.104.305

(DOI: 10.2169/naika.104.305, PubMed: 26571712, CiNii: 1390282681426610432) 安倍正博 :
デノスマブの作用機構とその臨床応用,
化学評論社, Vol.70, No.2, 279-284, 2015年2月.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1521417755434384256

(CiNii: 1521417755434384256) 中村信元, 安倍正博 :
骨髄腫骨病変の治療,
血液内科, Vol.69, No.4, 525-533, 2014年10月. 安倍正博 :
多発性骨髄腫の骨病変,
Clinical Calcium, Vol.24, No.8, 35-44, 2014年8月. 安倍正博 :
骨髄腫の骨病変とサイトカイン,
Clinical Calcium, Vol.24, No.6, 69-76, 2014年6月. 安倍正博 :
新しい診断と治療のABC 84「多発性骨髄腫」概念:MGUS，くすぶり型から症候性骨髄腫,
最新医学, 5-23, 2014年6月. 安倍正博 :
多発性骨髄腫の骨病変形成機序とその治療,
腎と骨代謝, Vol.27, No.1, 33-40, 2014年1月. 安倍正博 :
血液学から見た骨代謝,
Clinical Calcium, Vol.23, No.9, 1271-1277, 2013年9月.

(要約): Bone marrow provides a microenvironment responsible for hematopoiesis, in which osteoclasts and osteoblasts interact with each other to maintain bone remodeling. Multiple myeloma and a portion of lymphoid tumors have a unique propensity to expand in bone. Such tumors have been demonstrated to perturb bone metabolism and skew a microenvironment in bone suited for their growth and survival. However, a bone metabolic state remains largely unknown in most of hematological disorders without apparent bone disease, although hematopoiesis and bone metabolism appear to have a link. Also, the skeletal effects of treatment for hematological disorders should be clarified further.
(キーワード): Animals / Bone Remodeling / Fractures, Bone / Hematologic Diseases / Humans / Osteoblasts / Osteoclasts / Osteoporosis
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23999362; ● Search Scopus @ Elsevier (PMID): 23999362

(PubMed: 23999362) 安倍正博 :
多発性骨髄腫の骨病変,
臨床血液, Vol.54, No.8, 696-698, 2013年8月.

(キーワード): Humans / Intercellular Signaling Peptides and Proteins / Multiple Myeloma / Osteogenesis / RANK Ligand
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24005424; ● Search Scopus @ Elsevier (PMID): 24005424

(PubMed: 24005424) 安倍正博 :
多発性骨髄腫による骨形成の抑制とWntシグナル阻害因子,
Clinical Calcium, Vol.23, No.6, 867-875, 2013年6月.

(要約): In bone destructive lesions in multiple myeloma (MM) , enhanced bone resorption is accompanied by impaired bone formation and mineralization. The overproduction of inhibitors for the canonical Wingless-type (Wnt) signaling pathway, including DKK-1, sFRP-2 and sclerostin, significantly contributes to the suppression of osteoblastogenesis and bone formation in MM. However, the source of these Wnt inhibitors and the mechanisms of their aberrant production as well as their roles in tumor growth and osteoclastogenesis in MM bone lesions still remain obscure. Better understanding of the role of the Wnt pathway in the pathogenesis of MM may offer an effective therapeutic approach in MM.
(キーワード): Animals / Cell Differentiation / Humans / Multiple Myeloma / Osteoblasts / Osteogenesis / Wnt Proteins / Wnt Signaling Pathway
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23719500; ● Search Scopus @ Elsevier (PMID): 23719500

(PubMed: 23719500) 安倍正博 :
骨髄腫細胞と骨髄微小環境の相互作用を標的とした治療法の開発,
臨床血液, Vol.54, No.6, 522-532, 2013年6月.

(キーワード): Animals / Bone Marrow Cells / Cellular Microenvironment / Cytokines / Humans / Multiple Myeloma / Osteoclasts / Stromal Cells
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23823090; ● Summary page in Scopus @ Elsevier: 2-s2.0-84892777201

(PubMed: 23823090, Elsevier: Scopus) 中村信元, 安倍正博 :
【続発性骨粗鬆症-診断と対策-】移植医療と骨粗鬆症,
THE BONE, Vol.27, No.2, 187-192, 2013年5月.

(要約): 移植医療によって臓器不全の予後は飛躍的に向上しつつあるが，その一方で移植後の合併症の予防，対策の重要性が増している．骨粗鬆症とそれによる骨折は，移植医療における頻度の高い合併症であるが，その実態の解析は十分ではない．移植前の患者個々の背景因子や原疾患の病態，治療に伴う骨障害に加え，移植医療に伴うカルシニューリン阻害薬，ステロイドなどの免疫抑制薬の長期投与など，種々の要因が影響し，移植後骨粗鬆症が発症する．ビスフォスフォネートやビタミンDなどを早期から投与することにより，骨折を防ぎ移植後のQoLを維持することが重要である．(著者抄録)
(キーワード): Diphosphonates(治療的利用) / Vitamin D(治療的利用) / 抗腫瘍剤(毒性・副作用) / 骨粗鬆症(病因,予防) / 術後合併症 / 臓器移植(有害作用) / 診療ガイドライン / 大量薬物療法(有害作用) / Calcineurin(類似体・誘導体) / ヒト (Homo sapiens)

安倍正博 :
骨粗鬆症の類縁疾患とその治療,
日本臨牀, Vol.71, No.2, 609-612, 2013年4月. Masahiro Abe :
Microenvironment for myeloma growth and drug resistance.,
International Journal of Myeloma, Vol.3, No.1, 2-11, Mar. 2013. 安倍正博 :
血液疾患と骨,
Clinical Calcium, Vol.23, No.2, 256-262, 2013年2月.

(要約): Certain types of hematological disorders show distinct bone lesions. Multiple myeloma and primary bone lymphoma develop in the bone marrow to often cause bone destruction. These tumors stimulate osteoclastogenesis and bone resorption by enhancing RANKL expression, and suppress bone formation by inhibiting osteoblast differentiation, leading to bone destruction with rapid loss of bone. Osteosclerotic lesions are manifested in POEMS syndrome and primary myelofibrosis. Hypercalcemia is often associated with aggressive types of adult T-cell leukemia/lymphoma and multiple myeloma in advanced stages.
(キーワード): Bone Neoplasms / Bone Resorption / Hematologic Diseases / Humans / Osteoclasts / RANK Ligand
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23354094; ● Search Scopus @ Elsevier (PMID): 23354094

(PubMed: 23354094) 安倍正博 :
多発性骨髄腫の骨病変に対する抗RANKL抗体denosumabの効果,
血液内科, Vol.65, No.4, 692-698, 2012年11月.

(キーワード): denosumab / 骨髄腫 (myeloma) / RANKL (RANKL) / osteoprotegerin / 破骨細胞 (osteoclast)
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1520010380317540480

(CiNii: 1520010380317540480) 藤井志朗, 安倍正博 :
腫瘍性疾患の分子標的薬多発性骨髄腫分子標的薬,
日本臨牀, Vol.70, No.8, 518-523, 2012年11月.

(キーワード): Antibodies, Monoclonal, Humanized / Antineoplastic Agents / Boron Compounds / Boronic Acids / Bortezomib / Glycine / Histone Deacetylases / Humans / Immunologic Factors / Lactones / Molecular Targeted Therapy / Multiple Myeloma / Oligopeptides / Proteasome Inhibitors / Pyrazines / Pyrroles / Thalidomide
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23513894; ● Summary page in Scopus @ Elsevier: 2-s2.0-84884374556

(PubMed: 23513894, Elsevier: Scopus) 原田武志, 安倍正博 :
プロテアソーム阻害薬の薬理作用，副作用と適応疾患,
血液内科, Vol.65, No.4, 530-537, 2012年10月. 安倍正博 :
多発性骨髄腫—現状と進歩骨髄腫の骨病変:骨破壊機序と骨病変に対する標的療法,
医学のあゆみ, Vol.242, No.13, 1068-1073, 2012年9月.

(キーワード): 骨髄腫細胞 / 破骨細胞 / 骨芽細胞 / RANKL / Wnt
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1522825130172151808

(CiNii: 1522825130172151808) 尾華絵里子, 安倍正博, 山本武範, 篠原康雄 :
ヘキソキナーゼとがんの代謝,
実験医学, Vol.30, No.15, 36-41, 2012年9月. 安倍正博 :
骨免疫学—研究最前線骨髄腫の骨破壊機序,
医学のあゆみ, Vol.242, No.9, 697-702, 2012年9月.

(キーワード): 骨髄腫 / 破骨細胞 (osteoclast) / 骨芽細胞 (osteoblast) / 骨破壊
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1520291855760299904

(CiNii: 1520291855760299904) 安倍正博 :
骨髄腫における骨破壊機構,
血液内科, Vol.64, No.4, 412-417, 2012年4月.

(キーワード): myeloma cell / 骨芽細胞 (osteoblast) / RANKL (RANKL) / Wnt
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1521136279799384832

(CiNii: 1521136279799384832) 安倍正博 :
骨髄腫の分子病態造血器腫瘍学—基礎と臨床の最新研究動向—,
日本臨牀, Vol.70, No.2, 577-583, 2012年4月.

(キーワード): paratarg-7 / gene expression profiling / MMSET / IRF4 / 骨髄腫ニッチ
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23134018; ● CiNii @ 国立情報学研究所 (CRID): 1521136280118089984; ● Summary page in Scopus @ Elsevier: 2-s2.0-84872045123

(PubMed: 23134018, CiNii: 1521136280118089984, Elsevier: Scopus) 賀川久美子, 安倍正博, 松本俊夫 :
がん治療における骨の管理の重要性がん骨転移治療ビスフォスフォネート治療によるBone Management,
先端医学者高橋俊二編集, 16-21, 2012年. 安倍正博 :
患者背景を踏まえた骨髄腫の治療戦略,
Myeloma & Lymphoma, Vol.4, 14-17, 2011年9月. 安倍正博, 松本俊夫 :
RANKLと乳癌,
Cancer Board乳癌, Vol.4, No.2, 71-74, 2011年9月. 安倍正博 :
多発性骨髄腫の骨病変とRANKLシグナル,
Clinical Calcium, Vol.21, No.8, 59-66, 2011年8月.

(要約): Multiple myeloma develops and expands almost exclusively in the bone marrow, and generates devastating bone destruction. Myeloma cells produce a variety of cytokines including MIP-1 to stimulate bone resorption by enhancing RANKL expression, and suppress bone formation by inhibiting osteoblast differentiation, leading to bone destruction and rapid loss of bone. The emerging role of the RANKL/RANK signaling axis provide a molecular rationale for consideration of targeting RANKL/RANK in a bone disease in myeloma. Given formation of vicious cycle between bone destruction and tumor progression, inhibiting RANKL signaling may also contribute to the suppression of myeloma expansion.
(キーワード): Adaptor Proteins, Signal Transducing / Antibodies, Monoclonal / Antibodies, Monoclonal, Humanized / Bone Resorption / Cell Differentiation / Humans / Macrophage Inflammatory Proteins / Molecular Targeted Therapy / Multiple Myeloma / Osteoblasts / Osteoclasts / RANK Ligand / Repressor Proteins / Signal Transduction / Transforming Growth Factor beta
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21814021; ● Search Scopus @ Elsevier (PMID): 21814021

(PubMed: 21814021) 中村信元, 安倍正博 :
骨病変/局所病変の管理 (特集多発性骨髄腫診療の新時代を迎えて--診断と治療に吹き込む「新しい風」) -- (多発性骨髄腫の合併症の管理),
内科, Vol.108, No.2, 274-281, 2011年8月.

(要約): 骨髄腫骨病変は，患者のQOLを大幅に低下させるだけでなく，放置すれば高カルシウム血症や脊髄圧迫などをきたし予後を悪化させる．・全身の骨単純X線写真(skeletal survey)で骨病変を評価する．MRIやPET/CTは病変の検出感度が高いため，これらを組み入れた評価が有用である．・骨病変の治療は，抗腫瘍療法が基本であるが，補助療法としてビスホスホネートの点滴投与を反復する．顎骨壊死や腎障害に対する予防策を行う．また，局所の疼痛に対し放射線照射や椎体形成術などが有用である．・高カルシウム血症は，進行例に出現する緊急性を要する病態である．初期には特徴的な症状がなく消化器症状や脱水症状からはじまり，腎不全や意識障害をきたす．(著者抄録)
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390001288080663552

(CiNii: 1390001288080663552) 安倍正博 :
腎障害を来す全身性疾患—最近の進歩 Ⅲパラプロテイン血症1．多発性骨髄腫,
内科学会雑誌, Vol.100, No.5, 1274-1281, 2011年5月. 安倍正博 :
多発性骨髄腫Update—診療の進歩と新規治療の展望多発性骨髄腫の骨病変,
血液内科, Vol.62, No.3, 324-331, 2011年3月. 安倍正博 :
多発性骨髄腫の骨病変のマネージメント,
日本骨髄腫研究会雑誌, Vol.1, No.1, 26-32, 2011年3月. 中村信元, 安倍正博 :
骨病変に対する薬物療法と患者予後の改善効果,
血液フロンティア, Vol.21, No.1, 43-52, 2011年1月. 安倍正博 :
多発性骨髄腫 Visual View 目でみるメカニズム,
Trands in Hematological Malignancies, Vol.2, No.4, 4-7, 2010年12月. 安倍正博 :
サイトカインと骨髄腫骨病変,
CLINICAL CALCIUM, Vol.20, No.10, 26-32, 2010年10月. 安倍正博 :
血液疾患における分子標的療法ドラッグラグ解消に向けて,
血液フロンティア, Vol.20, No.S-1, 266-267, 2010年9月. 安倍正博 :
現在開発中の多発性骨髄腫に対する治療薬,
Pharma Medica, Vol.28, No.9, 61-66, 2010年9月. 安倍正博 :
骨髄腫骨髄微小環境のマクロファージは多発性骨髄腫の治療抵抗性と関連する,
血液・腫瘍科, Vol.61, No.2, 364-368, 2010年8月.

(キーワード): myeloma / macrophage / bone marrow microenvironment / drug resistance
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1522262178395179776

(CiNii: 1522262178395179776) 安倍正博 :
MGUS 内科疾患の診断基準・病型分類・重症度,
内科, Vol.105, No.6, 1458, 2010年6月. 安倍正博, 原田武志 :
多発性骨髄腫内科疾患の診断基準・病型分類・重症度,
Vol.105, No.6, 1429-1433, 2010年6月. 安倍正博 :
多発性骨髄腫における血管新生と破骨細胞形成の促進,
細胞, Vol.42, No.2, 16-19, 2010年3月. 安倍正博 :
多発性骨髄腫造血間質(骨髄微小環境)から見た増殖動態,
カレントテラピー, Vol.28, No.3, 13-17, 2010年3月. 安倍正博 :
M蛋白と骨髄腫-診断へのステップとピットフォール <セミナー>きめ細かい最新の検査・診断とその生かし方,
Medical Practice, Vol.27, No.2, 299-302, 2010年.

講演・発表

Masahiro Abe :
Hirofumi Tenshin, Mohannad Ashtar, Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Kotaro Tanimoto, So Shimizu, Yoshiki Higa, Eiji Tanaka, Toshio Matsumoto, Masahiro Abe. European Calcified Tissue Society (ECTS) 2020. Concurrent Oral Presentation1.,
Hiroki Yamagami, Tomoyo Hara, Yukari Mitsui, Shiho Masuda, Kiyoe Kurahashi, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara :
Analysis of clinical factors involved in AGE accumulation in people with type 2 diabetes,
IDF-WPR Congress 2023/15th Scientific Meeting of AASD, Jul. 2023. Yosuke Kaneko, Saya Yasui, Minae Hosoi, Akihiro Tani, Hiroki Yamagami, Hiroyasu Mori, Tomoyo Hara, Yukari Mitsui, Kiyoe Kurahashi, Sumiko Yoshida, Shingen Nakamura, Akio Kuroda, Toshiki Otoda, Tomoyuki Yuasa, Itsuro Endo, Takeshi Soeki, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara :
Dehydroepiandrosterone sulfate and skeletal muscle disorders in patients with type 2 diabetes,
IDF-WPR Congress 2023/15th Scientific Meeting of AASD, Tokyo, Jul. 2023. Tomoyo Hara, Hiroki Yamagami, Yukari Mitsui, Shiho Masuda, Kiyoe Kurahashi, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara :
Clinical factors and glycemic control in Japanese people with type 2 diabetes treated with weekly Dulaglutide at a dose of 0.75 mg,
IDF-WPR Congress 2023/15th Scientific Meeting of AASD, Jul. 2023. Minae Hosoki, Hiroki Yamagami, Taiki Hori, Saya Yasui, Tomoyo Hara, Kiyoe Kurahashi, Sumiko Yoshida, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa, Itsuro Endo, Masahiro Abe and Ken-ichi Aihara :
Pharmaceutical Influences on In-hospital Death in Patients with and Those without Diabetes at a Japanese General Hospital,
The 29th Scientific Meeting of the International Society of Hypertension, Oct. 2022. Shiho Masuda, Tomoyo Hara, Hiroki Yamagami, Mitsui Yukari, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Shingen Nakamura, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara :
Evaluation of Vascular Function for Prediction of Renal Prognosis in Japanese Patients with Lifestyle-Related Diseases,
The 29th Scientific Meeting of the International Society of Hypertension, Oct. 2022. Takeshi Harada, Asuka Oda, Yosuke Matsushita, Ryohei Sumitani, Yusuke Inoue, Tomoyo Hara, Masahiro Oura, Kimiko Sogabe, Tomoko Maruhashi, Mamiko Takahashi, Kiyoe Kurahashi, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Masahiro Hiasa, Jumpei Teramachi, Toyomasa Katagiri and Masahiro Abe :
ADAR1-dsRNA metabolism in myeloma cells with 1q amplification: a novel therapeutic target,
19th International Myeloma Society Annual Meeting, Aug. 2022. Tomoyo Hara, Mitsui Yukari, Masuda Shiho, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara :
Plasma heparin cofactor activity is inversely associated with the development NAFLD in patients with diabetes,
American Diabetes Association 82nd Scientific Sessions, Jun. 2022. Hiroki Yamagami, Yasui Saya, Hosoki Minae, Hori Taiki, Tomoyo Hara, Kiyoe Kurahashi, Sumiko Yoshida, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa, Itsuro Endo, Masahiro Abe and Ken-ichi Aihara :
Skin autofluorescence is associated with tubular injury represented by urinary excretion of liver-type fatty acid-binding protein in patients with diabetes,
American Diabetes Association 82nd Scientific Sessions, Jun. 2022. Yamagami Hiroki, Yasui Saya, Hosoki Minae, Hori Taiki, Hara Tomoyo, Kurahashi Kiyoe, Yoshida Sumiko, Nakamura Shingen, Otoda Toshiki, Yuasa Tomoyuki, Endo Itsuro, Abe Masahiro and Masahiro Abe :
Skin autofluorescence is associated with tubular injury represented by urinary excretion of liver-type fatty acid-binding protein in patients with diabetes.,
The American Diabetes Association's 82nd Scientific Sessions, New Orleans, Louisiana., Jun. 2022. Kotaro Tanimoto, Masahiro Hiasa, Hirofumi Tenshin, Jumpei Teramachi, Asuka Oda, Takeshi Harada, Yoshiki Higa, Kimiko Sogabe, Masahiro Oura, Ryohei Sumitani, Tomoyo Hara, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe :
Mechanical unloading promotes bone destruction and myeloma tumor expansion,
Cancer and bone society young investigator symposium, Online, Feb. 2022. Hirofumi Tenshin, Takeshi Harada, Yusuke Inoue, Jumpei Teramachi, Masahiro Hiasa, Sou Shimizu, Emiko Nakaue, Kotaro Tanimoto, Yoshiki Higa, Masahiro Oura, Kimiko Sogabe, Tomoyo Hara, Ryohei Sumitani, Tomoko Maruhashi, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
Targeting SLAMF7 to disrupt myeloma-osteoclast interaction: elotuzumabs ADCC activity with Th1-like gamma delta T cells towards osteoclasts and myeloma cells.,
Cancer and bone society young investigator symposium, Feb. 2022. Tomoyo Hara, Mitsui Yukari, Masuda Shiho, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara :
Heparin cofactor II prevents the development of albuminuria in patients with diabetes,
EASD 2021 57th Annual Meeting, Sep. 2021. Takeshi Harada, Yusuke Inoue, Hirofumi Tenshin, Asuka Oda, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe :
Novel strategy of elotuzumab and zoledronic acid with Th1-like T cells against myeloma,
18th International Myeloma Workshop, Wien, Sep. 2021. Takeshi Harada, Yusuke Inoue, Hirofumi Tenshin, Asuka Oda, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe :
Induction of elotuzumabs ADCC activity by Th1-like T cells towards osteoclasts as well as myeloma cells,
EHA2021 Virtual Congress, Jun. 2021. Takeshi Harada and Masahiro Abe :
Targeting osteoclasts and myeloma cells by CELMoDs plus zoledronic acid-inducible Th1-like γδT cells in combination with elotuzumab,
The 12th JSH International Symposium 2021, May 2021. Hirokazu Miki, Shingen Nakamura, Masafumi Nakamura, Makiko Mizuguchi, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Mamiko Takahasi, Tomoko Maruhashi, Takeshi Harada, Shiro Fujii, Kumiko Kagawa, Hirofumi Hamano, Masateru Kondou, Naoto Okada, Yoshimi Bando, Itsuro Endo and Masahiro Abe :
The importance of retaining physical functions to prevent skeletal-related events in multiple myeloma patients with bone disease.,
The 48th annual meeting of European Calcified Tissue Society (ECTS), Online, May 2021. Hirofumi Tenshin, Takeshi Harada, 井上雄介, Jumpei Teramachi, Masahiro Hiasa, 小田明日香, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Masahiro Oura, Kimiko Sogabe, Tomoyo Hara, Tomoko Maruhashi, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
The anti-SLAMF7 elotuzumab enhances ADCC activity with Th1-like γδT cells towards osteoclasts and myeloma cells.,
The European Calcified Tissue Society 2021 Digital Congress 2021, web, Mar. 2021. Yuka Sogawa, Makoto Fukui, Shingen Nakamura, Kimiko Sogabe, Ryohei Sumitani, Masami Yoshioka, Masahiro Abe and Daisuke Hinode :
Risk factors for chemotherapy-induced febrile neutropenia in hematological cancer patients,
106th Annual Meeting of American Academy of Periodontology, Honolulu, Nov. 2020.

(要約): 1

Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Takeshi Harada, Eiji Tanaka, Kotaro Tanimoto, Sou Shimizu, Masahiro Oura, Kimiko Sogabe, Masahiro Abe, Toshio Matsumoto and Itsuro Endo :
The novel therapeutic approaches with TAK1 inhibition against the aberrant NLRP3 inflammasome activation in rheumatoid arthritis,
ECTS 2020 Digital Congress, Oct. 2020. Kotaro Tanimoto, Masahiro Hiasa, Hirofumi Tenshin, Masahiro Abe and Eiji Tanaka :
Immobilization accelerates bone loss and myeloma tumor expansion.,
9th IOC, Yokohama, Oct. 2020. Mohannad Ashtar, Hirofumi Tenshin, Masahiro Abe and Eiji Tanaka :
The effects of Febuxostat on RANKL-induced bone resorption.,
9th IOC, Yokohama, Oct. 2020. Tomoyo Hara, H Yamagami, Y Mitsui, S Masuda, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara :
Plasma heparin cofactor activity is inversely associated with the development NAFLD in patients with diabetes,
American Diabetes Association 80th Scientific Session, Chicago, Jun. 2020. Takeshi Harada, Asuka Oda, Hiroto Ohguchi, Yohann Grondin, Hirofumi Tenshin, Masahiro Hiasa, Jumpei Teramachi, Masahiro Oura, Kimiko Sogabe, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Hirokazu Miki, Kumiko Kagawa, Shuji Ozaki, Teru Hideshima, Kenneth C. Anderson and Masahiro Abe :
Novel therapeutic rationale for targeting HDAC1 and PIM2 in multiple myeloma,
61th ASH Annual Meeting & Exposition, Orlando, Dec. 2019.

(出版サイトへのリンク): ● Publication site (DOI): 10.1182/blood-2019-127679
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.1182/blood-2019-127679

(DOI: 10.1182/blood-2019-127679) Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Ashtar Mohannad, Kotaro Tanimoto, Soh Shimizu, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
The role of NLRP3 inflammasome activation in joint inflammation and destruction in rheumatoid arthritis: novel therapeutic approaches with TAK1 inhibition.,
29th Australian and New Zealand Bone and Mineral Society Annual Scientific Meeting, Oct. 2019. Mai Kanai, Itsuro Endo, Yasuko Takahashi, Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Seiji Fukumoto, Masahiro Abe and Toshio Matsumoto :
Establishment of model mice of FGF23-related hypophosphatemia induced by iron solution administration,
ASBMR 2019, Orlando, Sep. 2019. Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Ashtar Mohannad, Kotaro Tanimoto, Masami Iwasa, Bat-Erdene Ariunzaya, Takeshi Harada, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
TAK1 inhibition effectively alleviates joint inflammation as well as bone destruction in rheumatoid arthritis: Suppression of NLRP3 inflammasome-mediated inflammation and osteoclastic bone resorption,
American Society for Bone and Mineral Society Annual meeting 2019, Orlando, Florida, USA,, Sep. 2019. Jumpei Teramachi, Soh Shimizu, Hirofumi Tenshin, Bat-Erdene Ariunzaya, Masahiro Hiasa, Kotaro Tanimoto, Oda Asuka, Takeshi Harada, Mohannad Ashtar, Kotaro Tanimoto, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe :
A progressive auto-amplification loop in TAK1 expression and activation in MM cells.,
ASBMR 2019,, Orlando, Florida, USA., Sep. 2019. Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Oda Asuka, Ashtar Mohannad, Kotaro Tanimoto, Masami Iwasa, Bat-Erdene Ariunzaya, Takeshi Harada, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
TAK1 inhibition effectively alleviates joint inflammation as well as bone destruction in rheumatoid arthritis: Suppression of NLRP3 inflammasome-mediated inflammation and osteoclastic bone resorption.,
ASBMR 2019,, Orlando, Florida, USA., Sep. 2019. Takeshi Harada, Asuka Oda, Hirofumi Tenshin, Jumpei Teramachi, Masahiro Oura, Kimiko Sogabe, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Shuji Ozaki, Teru Hideshima, C. Kenneth Anderson and Masahiro Abe :
Targeting myeloma metabolisms regulated by HDAC1-IRF4 axis can be a novel therapeutic strategy,
17th International Myeloma Workshop, Sep. 2019. Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Masahiro Abe and Eiji Tanaka :
Effective suppression of inflammasome-mediated joints destruction by TAK1 inhibition,
第97回IADR学術大会, Vancouver, Jun. 2019. Sumiko Yoshida, Ken-ichi Aihara and Masahiro Abe :
Eicosapentaenoic acid administration ameliorates cardiac remodeling in humans and protects against Ang II-induced cardiovascular remodeling via attenuation of oxidative stress in mice.,
Endocrine Society's Annual Meeting 2019, Mar. 2019. Mohannad Ashtar, Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Kotaro Tanimoto, Oda Asuka, Iwasa Masami, Takeshi Harada, Bat-Erdene Ariunzaya, Kimiko Sogabe, Masahiro Oura, Shiroh Fujii, Kumiko Kagawa, Shingen Nakamura, Hirokazu Miki, Toshio Matsumoto, Masahiro Abe and Eiji Tanaka :
Peri-implantitis and the role of Febuxostat in osteoclast differentiation.,
AEEDC Dubai World Orthodontic Conference, Dubai, UAE, Feb. 2019. Takeshi Harada, Asuka Oda, Yohann Grondin, Jumpei Teramachi, Ariunzaya Bat-Erdene, Masami Iwasa, Masahiro Oura, Shingen Nakamura, Kumiko Kagawa, Yasunobu Okamoto, Kimiko Sogabe, Shiroh Fujii, Hirokazu Miki, Shuji Ozaki, Teru Hideshima, Kenneth C. Anderson and Masahiro Abe :
The critical role of the HDAC1-IRF4-Pim-2 axis in myeloma cell growth and survival: therapeutic impacts of targeting the HDAC1-IRF4-Pim-2 axis,
60th ASH Annual Meeting & Exposition, San Diego, Dec. 2018. Shingen Nakamura, Hirokazu Miki, Ariunzaya Bat-Erdene, Yasunobu Okamoto, Kimiko Sogabe, Masahiro Oura, Mamiko Takahashi, Masami Iwasa, Takeshi Harada, Shiroh Fujii, Kumiko Kagawa and Masahiro Abe :
Alteration of muscle mass after chemotherapy in patients with newly diagnosed multiple myeloma.,
Esmo asia 2018, Nov. 2018. Yuichi Takashi, Yuka Kinoshita, Nobuaki Ito, Shun Sawatsubashi, Hidetaka Kosako, Masahiro Abe, Munehide Matsuhisa, Toshio Matsumoto and Seiji Fukumoto :
FGF receptor 1c works as a phosphate-sensor to regulate FGF23 production,
ASBMR 2018 Annual Meeting Registration Confirmation, Sep. 2018. Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Oda Asuka, Bat-Erdene Ariunzaya, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Toshio Matsumoto and Masahiro Abe :
Disruption of a progressive vicious cycle between myeloma tumor growth and bone destruction by TAK1 inhibition,
ASBMR 2018 Annual Meeting, Montreal, Sep. 2018. Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Oda Asuka, Ashtar Mohannad, Kotaro Tanimoto, Iwasa Masami, Bat-Erdene Ariunzaya, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
Opposite effects of TRAIL on the Sp-1-c-FLIP survival pathway in myeloma cells and osteoclasts.,
ASBMR 2018 Annual Meeting, Montreal, Sep. 2018. Takeshi Harada, Oda Asuka, Jumpei Teramachi, Bat-Erdene Ariunzaya, Iwasa Masami, Oura Masahiro, Shingen Nakamura, Kumiko Kagawa, Okamoto Yasunobu, Kimiko Sogabe, Shiroh Fujii, Hirokazu Miki, Hideshima Teru, Anderson C. Kenneth and Masahiro Abe :
Selective inhibition of class-I HDAC induces myeloma cell death through targeting IRF4-Pim-2 axis,
The 9th JSH International Symposium 2018 in Kyoto, Jul. 2018.

(キーワード): Multiple myeloma / Class-I HDAC / IRF4 / Pim2

Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Oda Asuka, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Tatsuji Haneji, Itsuro Endo, Toshio Matsumoto and Masahiro Abe :
Therapeutic impact of TAK1 inhibition on myeloma tumor progression and bone destruction,
8th International Workshop on Advances in the Molecular Pharmacology and Therapeutics of Bone and other Musculoskeletal Diseases and Cancer and Bone Society 2018 Meeting, Oxford, Jun. 2018. Akio Kuroda, Misuzu Yamada, Yukari Tominaga, Reiko Suzuki, Motoyuki Tamaki, Yuko Akehi, Yuichi Takashi, Daisuke Otsuka, Eisuke Shimokita, Fuminori Tanihara, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Masahiro Abe, Kevin Ferreri and Munehide Matsuhisa :
Detection of pancreatic beta cell DNA in the circulation using the amplification refractory mustation system PCR,
American Diabetes Association 78th Scientific Sessions, Orlando, Jun. 2018. Hirofumi Tenshin, Jumpei Teramachi, Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, Toshio Matsumoto, Masahiro Abe and Eiji Tanaka :
Apoptosis inducer TRAIL stimulates osteoclast differentiation and survival via TAK1 activation.,
1st International Conference of Biophysical Technology in Dentistry (+10th International Scientific Meeting in Dentistry),, Makassar, Indonesia., Apr. 2018. Sumiko Yoshida, Kiyoe Kurahashi, Akio Kuroda, Itsuro Endo, Ken-ichi Aihara, Seiji Fukumoto, Munehide Matsuhisa and Masahiro Abe :
Changes of oxidative stress markers in patient of diabetes educational hospitalization.,
The Endocrine Society's Annual Meeting 2018, Chicago, Mar. 2018. Noboru Niki, Yoshiki Kawata, Hidenobu Suzuki, Mitsuo Shimada, Masafumi Harada, Issei Imoto, Masahiro Abe, Keiji Umetani, Masahiko Kusumoto, Keiju Aokage, Genichirou Ishii, Gen Iinuma, Yuuji Matsumoto, Yasutaka Nakano and Hiroaki Sakai :
Cancer diagnosis and prognosis assistance based on multidisciplinary computational anatomy - progress overview FY2017 -,
The 4nd International Symposium on Multidisciplinary Computational Anatomy, 107-114, Mar. 2018. Hirofumi Tenshin, Jumpei Teramachi, Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, Toshio Matsumoto, Masahiro Abe and Eiji Tanaka :
Apoptosis inducer TRAIL stimulates osteoclast differentiation and survival via TAK1 activation.,
The 4th ASEAN plus Tokushima Joint International Conference, Bali, Indonesia, Dec. 2017. Ken-ichi Aihara, Uemoto Ryoko, Ishikawa Kazue, Kana Morimoto, Kiyoe Kurahashi, Sumiko Yoshida, Tomoyuki Yuasa and Masahiro Abe :
Heparin cofactor II, a serine protease inhibitor, is associated with albuminuria in humans and mice.,
International Conference on Diabetes and Its Complications 2017, Baltimore, Nov. 2017.

(キーワード): heparin cofactor II / albuminuria

Itsuro Endo, Dong Bingzi, Ohnishi Yukiyo, Kondo Takeshi, Masahiro Hiasa, Jumpei Teramachi, Toshio Matsumoto, Masahiro Abe, Seiji Fukumoto and Tatsuji Haneji :
Decreased bone strength induced by persistent activation of calcium-sensing receptor,
American Society for Bone and Mineral Research (ASBMR) 2017 Annual Meeting, Denver, Sep. 2017. Jumpei Teramachi, Masahiro Hiasa, Oda Asuka, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe :
TAK1 inhibition impairs myeloma cell-bone marrow interaction to reduce myeloma tumor growth and bone destruction,
American Society for Bone and Mineral Research (ASBMR) 2017 Annual Meeting, Denver, Sep. 2017. Jumpei Teramachi, Masahiro Hiasa, Oda Asuka, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe :
Therapeutic impact of TAK1 inhibition on myeloma tumor progression and bone destruction,
International Society for Experimental Hematology 46th Annual Scientific Meeting, Frankfurt, Aug. 2017. Masahiro Abe :
Novel targets of treatment for myeloma-bone interaction,
Australian New Zealand Bone Mineral Society (ANZBMS)-IFMRS-JSBMR 2017, Brisbane, Jun. 2017. Hirofumi Tenshin, Jumpei Teramachi, A Oda, Ryota Amachi, Masahiro Hiasa, A Baterdene, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
Osteoclasts utilize TRAIL for their NF-B activation, but TAK1 inhibition resumes TRAIL-induced apoptosis in osteoclasts.,
Australian and New Zealand Bone and Mineral Society 2017, Brisbane, Australia., Jun. 2017. Jumpei Teramachi, Masahiro Hiasa, Oda Asuka, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Akihito Yamamoto, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe :
Therapeutic impact of TAK1 inhibition on myeloma tumor progression and bone destruction,
Cancer and Bone Society Conference 2017, Indianapolis, May 2017. Ryota Amachi, Masahiro Hiasa, Oda Asuka, Bat-Erdene Ariunzaya, Jumpei Teramachi, Hirofumi Tenshin, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Shiroh Fujii, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe :
Osteoblast Creates a Non-permissive Niche for Myeloma Cells,
95th General Session & Exhibition of the IADR program book, San Francisco, Mar. 2017. Hirofumi Tenshin, Jumpei Teramachi, Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, Toshio Matsumoto, Masahiro Abe and Eiji Tanaka :
TRAIL Stimulates Osteoclast Differentiation and Survival via TAK1 Activation.,
95th General Session & Exhibition of the IADR program book, San Francisco, Mar. 2017. Noboru Niki, Yoshiki Kawata, Hidenobu Suzuki, Mitsuo Shimada, Masafumi Harada, Issei Imoto, Masahiro Abe, Keiji Umetani, Masahiko Kusumoto, Keiju Aokage, Genichirou Ishii, Gen Iinuma, Yuuji Matsumoto, Yasutaka Nakano and Hiroaki Sakai :
Cancer diagnosis and prognosis assistance based on multidisciplinary computational anatomy - Progress Overview FY2016 -,
The 3nd International Symposium on Multidisciplinary Computational Anatomy, 87-94, Mar. 2017. Kiyoe Kurahashi, Itsuro Endo, Nakamura Maiko, Ohnishi Yukiyo, Takeshi Kondo, Aizawa Shinichi, Toshio Matsumoto, Seiji Fukumoto and Masahiro Abe :
Glucose intolerance induced by persistent activation of calcium-sensing receptor,
American Society for Bone and Mineral Research 2016 Annual Meeting, Atlanta, Sep. 2016. Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Kiyoe Kurahashi, Takeshi Kondo, Hirokazu Miki, Itsuro Endo, Toshio Matsumoto and Masahiro Abe :
TAK-1 inhibition disrupts Pim-2-associated and Pim-2-independent key signaling pathways to effectively suppress tumor growth and restore bone formation in myeloma,
American Society for Bone and Mineral Research 2016 Annual Meeting, Atlanta, Sep. 2016. Hirofumi Tenshin, Jumpei Teramachi, A Oda, Ryota Amachi, Bingzi Dong, Masahiro Hiasa, Keiichiro Watanabe, Ryota Amachi, S Nakamura, H Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
Osteoclasts utilize an apoptosis-inducer TRAIL as a stimulator for osteoclastogenesis Critical roles of the TAK-1-Pim-2 signaling induced by RANK ligand and TRAIL.,
ANZBMS 2016 Annual Meeting, Gold Coast, Aug. 2016. Ken-ichi Aihara, Masashi Akaike, Sumiko Yoshida, Yasumasa Ikeda, Shusuke Yagi and Masahiro Abe :
Pleiotropic Effects of Pitavastatin against Vascular Stress in eNOS-deficient Mice,
The 10th Congress of the Asian-Pacific Society of Atherosclerosis and Vascular Diseases, Tokyo, Jul. 2016. Kana Morimoto, Kiyoe Kurahashi, Takeshi Kondo, Sumiko Yoshida, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara :
Analysis of sodium restriction-induced blood pressure reduction in hospitalized patients with type 2 diabetes mellitus,
The 10th Congress of the Asian-Pacific Society of Atherosclerosis and Vascular Diseases, Tokyo, Jul. 2016. Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe :
Therapeutic impact of TAK-1 inhibition on tumor growth and bone destruction in myeloma,
21st Congress European Hematology Association, Copenhagen, Jun. 2016. Noboru Niki, Yoshiki Kawata, Hidenobu Suzuki, Mitsuo Shimada, Masafumi Harada, Issei Imoto, Masahiro Abe, Keiji Umetani, Hironobu Ohmatsu, Genichirou Ishii, Gen Iinuma, Keiji Aokage, Yuuji Matsumoto, Yasutaka Nakano, Michiaki Mishima and Hiroaki Sakai :
Cancer diagnosis and prognosis assistance based on multidisciplinary computational anatomy - Progress Overview FY2015 -,
The 2nd International Symposium on Multidisciplinary Computational Anatomy, 83-89, Feb. 2016. Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Derek Hanson, Keiichiro Watanabe, Shiroh Fujii, Kumiko Kagawa, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe :
Pim inhibition suppresses osteoclastogenesis and tumor growth in myeloma,
57th ASH Annual Meeting and Exposition, Orlando, Dec. 2015. Hirofumi Tenshin, Jumpei Teramachi, A Oda, Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, S Nakamura, H Miki, I Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
TRAIL is not a proapoptotic but rather anti-apoptotic mediator for osteoclasts to stimulate their differentiation and survival,
ASBMR 2015 Annual Meeting, Seattle, Oct. 2015. Ryota Amachi, Masahiro Hiasa, Jumpei Teramachi, Asuka Oda, Hirofumi Tenshin, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Shiroh Fujii, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
Up-regulation of the pH sensor TRPV1 in myeloma cells and their adaption to an acidic microenvironment,
ASBMR 2015 Annual Meeting, Seattle, Oct. 2015. Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Keiichiro Watanabe, Shiroh Fujii, Kumiko Kagawa, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe :
Pivotal role of TAK-1 in tumor growth and bone destruction in myeloma: Therapeutic impact of TAK-1 inhibition,
American Society for Bone and Mineral Research 2015 Annual Meeting, Oct. 2015. Hirokazu Miki, Shingen Nakamura, Hirofumi Tenshin, Ryota Amachi, Keiichiro Watanabe, Jumpei Teramachi, Shiroh Fujii, Kumiko Kagawa and Masahiro Abe :
Effective impairment of myeloma progenitors by hyperthermia: augmentation with bortezomib and Pim inhibition in combination,
Clinical Lymphoma, Myeloma & Leukemia, Vol.15, No.S3, e217-e218, Sep. 2015.

(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.clml.2015.07.470
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.1016/j.clml.2015.07.470

(DOI: 10.1016/j.clml.2015.07.470) Shingen Nakamura, Hirokazu Miki, Hirofumi Tenshin, Ryota Amachi, Keiichiro Watanabe, Jumpei Teramachi, Shiroh Fujii, Kumiko Kagawa and Masahiro Abe :
Alteration of Pim-2 expression by clinically available anti-myeloma agents: combinatory anti-myeloma effects with Pim inhibition,
Clinical Lymphoma, Myeloma & Leukemia, Vol.15, No.S3, e243, Sep. 2015.

(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.clml.2015.07.517
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.1016/j.clml.2015.07.517

(DOI: 10.1016/j.clml.2015.07.517) Takeshi Kondo, Itsuro Endo, Ken-ichi Aihara, nishi Oh Yukiyo, Bingzi Dong, Kiyoe Kurahashi, Sumiko Yoshida, Ryota Amachi, Masahiro Hiasa, Jumpei Teramachi, Masahiro Abe, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
Serum carboxy-terminal telopeptide of type I collagen, as a marker for systemic atherosclerosis,
ANZBMS 2015 Annual Meeting, Hobart, Sep. 2015. Noboru Niki, Yoshiki Kawata, Hidenobu Suzuki, Mitsuo Shimada, Masafumi Harada, Issei Imoto, Masahiro Abe, Keiji Umetani, Hironobu Ohmatsu, Genichirou Ishii, Gen Iinuma, Keiju Aokage, Yuji Matsumoto, Yasutaka Nakano, Michiaki Mishima and Hiroaki Sakai :
Cancer diagnosis and prognosis assistance based on multidisciplinary computational anatomy -Plan of five years and progress overview FY2014-,
he First International Symposium on the Project ``Multidisciplinary Computational Anatomy'', 40-44, Fukuoka, Feb. 2015. Jumpei Teramachi, Masahiro Hiasa, 小田明日香, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Kumiko Kagawa, Hirokazu Miki, Shiroh Fujii, Keiichiro Watanabe, Itsuro Endo, Toshio Matsumoto and Masahiro Abe :
Critical role of Pim-2 in NF-B-mediated suppression of osteoblastogenesis and stimulation of osteoclastogenesis: Therapeutic impact of Pim inhibition on myeloma bone disease.,
2014 ASBMR Annual Meeting, Houston, Sep. 2014. Dong Bingzi, Takeshi Kondo, Itsuro Endo, 大西幸代, 尾松卓, Masahiro Abe, 相澤慎一 and Toshio Matsumoto :
educed bone formation and increased adiposity with insulin resistance in interleukin-11 deficient mice,
European Calcified Tissue Society Annual Meeting 2014, Prague, May 2014. Noboru Niki, Yoshiki Kawata, Hidenobu Suzuki, Masafumi Harada, Hideki Otsuka, Junji Ueno, Mitsuo Shimada, Tetsuji Takayama, Masahiro Abe, Haruimi Itoh, Kenji Eguchi, Masahiko Kusumoto, Takaaki Tsuchida, Hironobu Ohmatsu, Masashi Takahashi, Yasutaka Nakano, Hiroaki Sakai and Yuichi Takiguchi :
Computer-aided diagnosis based on computational anatomical models:Progress overview FY2009-2013,
The 5th International Symposium on the Project ``Computational Anatomy'', 39-43, Mar. 2014. Ryota Amachi, Masahiro Abe, Masahiro Hiasa, Keiichiro Watanabe, S Fujii, T Harada, H Miki, S Nakamura, I Endo, Eiji Tanaka and Toshio Matsumoto :
Acidic conditions epigenetically repress the TRAIL receptor DR4 in myeloma cells to confer their resistance to TRAIL,
ASBMR 2013 Annual Meeting,, Baltimore, Oct. 2013. Keiichiro Watanabe, Masahiro Abe, H Mori, Ryota Amachi, Masahiro Hiasa, T Harada, S Fujii, S Nakamura, H Miki, K Kagawa, I Endo, Eiji Tanaka and Toshio Matsumoto :
Potent induction of bone formation in myeloma bone lesions by the cathepsin K inhibitor KK1-300-01 in combination with the proteasome inhibitor bortezomib,
ASBMR 2013 Annual Meeting,, Baltimore, Oct. 2013. Masahiro Abe :
Overview of the pathophysiology of MBD and acquired genetic events: Bench work for the targeted therapy to the microenvironment of MBD,
The 14th International Myeloma Workshop, Apr. 2013. Keiichiro Watanabe, Masahiro Abe, Ryota Amachi, Masahiro Hiasa, T Harada, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, H Mori, Itsuro Endo, Eiji Tanaka and Toshio Matsumoto :
Induction of bone formation in myeloma osteolytic lesions by cathepsinK inhibition,
Kyoto, Apr. 2013. Ryota Amachi, Keiichiro Watanabe, Shiroh Fujii, T Harada, Hirokazu Miki, Shingen Nakamura, A Oda, Masahiro Hiasa, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
An acidic milieu suppersses histone acetylation in myeloma cells to down-regulate the TRAIL receptor DR4 expression.,
Kyoto, Apr. 2013. Noboru Niki, Yoshiki Kawata, Hidenobu Suzuki, Masafumi Harada, Hideki Otsuka, Junji Ueno, Mitsuo Shimada, Tetsuji Takayama, Masahiro Abe, Harumi Itoh, Masahiro Kaneko, Kenji Eguchi, Masahiko Kusumoto, Takaaki Tsuchida, Hironobu Ohmatsu, Masashi Takahashi, Yasutaka Nakano, Hiroaki Sakai and Yuichi Takiguchi :
Computer-Aided Diagnosis Based on Computational Anatomical Models: Progress Overview FY2012,
he 4th International Symposium on the Project ``Computational Anatomy'', 45-51, Feb. 2013. Harada Takeshi, Ozaki Shuji, Oda Asuka, Iwasa Masami, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Masahiro Abe, Shibata Hironobu, Akishige Ikegame, Daisuke Tsuji, Ito Kohji, Ri Masaki, Iida Shinsuke, Shiotsu Yukimasa, Kawai Shigeto, Yamada-Okabe Hisafumi and Toshio Matsumoto :
Combination therapy of a defucosylated anti-HM1.24 monoclonal antibody plus Ienalidomide induces marked antibody-dependent cellular cytotoxicity and inhibits the clonogenic potential of myeloma cancer stem-like cells. Atlanta, Dec. 2012.,
The 54th Annual Meeting of the American Society of Hamatology, Dec. 2012. T Harada, Shuji Ozaki, A Oda, M Iwasa, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Masahiro Abe, Hirofumi Shibata, Akishige Ikegame, Daisuke Tsuji, Kouji Itou, M Ri, S Iida, Y Shiotsu, S Kawai, H Yamada-Okabe and Toshio Matsumoto :
Combination Therapy of a Defucosylated Anti-HM1.24 Monoclonal Antibody Plus Lenalidomide Induces Marked Antibody-Dependent Cellular Cytotoxicity and Inhibits the Clonogenic Potential of Myeloma Cancer Stem-Like Cells.,
54th ASH Annual Meeting and Exposition, USA, Atlanta, Dec. 2012. Ryota Amachi, Masahiro Abe, Ryota Amachi, Keiichiro Watanabe, S Fujii, T Harada, H Miki, S Nakamura, A Oda, Masahiro Hiasa, Eiji Tanaka and Toshio Matsumoto :
An acidic milieu suppresses DR4 editing to cause myeloma resistance to TRAIL,
ASEAN plus and Tokushima Joint International Conference, Yogjakarta, Indonesia, Dec. 2012. Masahiro Abe, Masahiro Hiasa, Watanabe ken-ichiro, Nakamura Shingen, Harada Takeshi, Itsuro Endo and Toshio Matsumoto :
Prevention of tumor growth and bone destruction in myeloma by Pim kinase inhibition,
12th CIBD International Meeting on Cancer Induced Bone Disease (CIBD) Lyon, Nov. 2012, Nov. 2012. Masahiro Hiasa, Keiichiro Watanabe, Shingen Nakamura, Harada Takeshi, Itsuro Endo, Toshio Matsumoto and Masahiro Abe :
Prevention of tumor growth and bone destruction in myeloma by Pim kinase inhibition,
12th Int'l Meeting on Cancer Induced Bone Disease, Lyon, Nov. 2012. Masahiro Hiasa, Ryota Amachi, Keiichiro Watanabe, Harada Takeshi, Fujii Shirou, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Itsuro Endo, Toshio Matsumoto and Masahiro Abe :
Pim-2 suppresses BMP-2 signaling as a common inhibitory mediator of osteoblastogenesis in myeloma,
ASBMR 2012 Anuual Meeting, Minneapolis, Oct. 2012. Keiichiro Watanabe, Masahiro Abe, Ryota Amachi, Masahiro Hiasa, T Harada, S Fujii, S Nakamura, H Miki, K Kagawa, H Mori, I Endo, Eiji Tanaka and Toshio Matsumoto :
Restoration of bone formation in myeloma osteolytic lesions by the cathepsin K inhibitor KK1-300-01,
34th ASBMR meeting, Minneapolis, MN, USA., Oct. 2012. Masahiro Hiasa, Masahiro Abe and Toshio Matsumoto :
RelB attenuates the activation of the classical NF-kB pathway to facilitate osteoblastogenesis,
Sep. 2012. Masahiro Hiasa, Masahiro Abe, Rieko Arakaki, Akiko Yamada, Kenzo Asaoka, Toshio Matsumoto, Yoshio Hayashi and Naozumi Ishimaru :
RelB attenuates the activation of the classical NF-κB pathway to facilitate osteoblastogenesis,
ANZBMS Annual Scientific Meeting, Perth, Sep. 2012. Keiichiro Watanabe, Masahiro Abe, Hiroyo Mori, Ryota Amachi, Masahiro Hiasa, T Harada, S Fujii, S Nakamura, H Miki, K Kagawa, I Endo, Eiji Tanaka and Toshio Matsumoto :
The cathepsin K inhibitor KK1-300-01 prevents bone destruction and resumes bone formation in myeloma osteolytic lesions,
Australian & New Zealand Bone & Mineral Society 22th Annual Scientific Meeting with 1st Asia-Pacific Bone and Mineral Research meeting, Perth, Australia., Sep. 2012. Noboru Niki, Yoshiki Kawata, Hidenobu Suzuki, Masafumi Harada, Hideki Otsuka, Junji Ueno, Mitsuo Shimada, Tetsuji Takayama, Masahiro Abe, Harumi Itoh, Masahiro Kaneko, Kenji Eguchi, Masahiko Kusumoto, Takaaki Tsuchida, Hironobu Ohmatsu, Masashi Takahashi, Yasutaka Nakano, Hiroaki Sakai and Yuichi Takiguchi :
Computer-aided diagnosis based on computational anatomical models: progress overview FY2011,
The 3rd International Symposium on the Project ``Computational Anatomy'', 35-42, Mar. 2012. Ayako Nakano and Masahiro Abe :
Inactivation of ABC transporters to restore drug sensitivity in myeloma cells by inhibition of hexokinase II,
53th Annual Meeting of the American Society of Hematology, Dec. 2011. Masahiro Abe :
An Acidic Milieu Aggravates Myeloma Growth And Drug Resistance But Triggers Anti-myeloma Activity Of Reveromycin A, A Novel Anti-resorptive Agent,
11th International Meeting on Cancer Induced Bone Disease, Dec. 2011. Keiichiro Watanabe, Masahiro Abe, M Kawatani, Masahiro Hiasa, A Kawano, T Jinno, T Harada, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki, Eiji Tanaka, H Osada and Toshio Matsumoto :
Aggravation of myeloma growth and drug resistance by an acidic created in myeloma-osteoclast interaction.,
ASBMR 2011 Annual Meeting, San Diego, Sep. 2011. Masahiro Hiasa, nakano ayako, Keiichiro Watanabe, C Qu, T Harada, Shiroh Fujii, Hirokazu Miki, Shingen Nakamura, Kumiko Kagawa, Kyoko Takeuchi, Eiji Tanaka, Kenzo Asaoka, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe :
Prevention of tumor growth and bone destruction in myeloma by Pim kinase inhibition.,
ASBMR 2011 Annual Meeting, San Diego, Sep. 2011. Masahiro Hiasa, nakano ayako, Keiichiro Watanabe, C Qu, T Harada, Shiroh Fujii, Hirokazu Miki, Shingen Nakamura, Kumiko Kagawa, Kyoko Takeuchi, Eiji Tanaka, Kenzo Asaoka, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe :
Dual effects of Pim inhibition on myeloma: induction of bone formation and tumor suppression.,
IOF-ANZBMS 2011 Annual Meeting, Gold Coast, Sep. 2011. Masahiro Abe :
An acidic microenvironment enhances myeloma growth but triggers anti-tumor and anti-resorptive activity of reveromycin A,
European Congress on Osteoporosis & Osteoarthritis ECCEO11-IOF, Mar. 2011. Noboru Niki, Yoshiki Kawata, Hidenobu Suzuki, Masafumi Harada, Hideki Otsuka, Junji Ueno, Mitsuo Shimada, Tetsuji Takayama, Masahiro Abe, Harumi Itoh, Masahiro Kaneko, kenji Eguchi, Masahiko Kusumoto, Takaaki Tsuchida, Hironobu Ohmatsu, Masashi Takahashi, Yasutaka Nakano and Hiroaki Sakai :
Computer-aided diagnosis based on computational anatomical models: progress overview FY2010,
The 2nd International Symposium on the Project ``Computational Anatomy'', 95-100, Mar. 2011. Keiichiro Watanabe, Masahiro Abe, Cui Qu, Kawatani Makoto, Masahiro Hiasa, Nakano Ayako, Jinno Tadashi, Harada Takeshi, Shiroh Fujii, Shingen Nakamura, Miki Hirokazu, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki, Eiji Tanaka, Osada Hiroyuki and Toshio Matsumoto :
An Acidic Mileu Created In Myeloma-Osteoclast Interaction Enhances Tumor Growth, but Triggers Anti-Myeloma Activity of Reveromycin A, a Novel Anti-Resorptive Agent,
52th American Society of Hematology, Orlando, Dec. 2010. Cui Qu, Masahiro Abe, Miki Hirokazu, Shingen Nakamura, Keiichiro Watanabe, Akishige Ikegame, Masahiro Hiasa, Nakano Ayako, Harada Takeshi, Shiroh Fujii, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki and Toshio Matsumoto :
Lenalidomide In Combination with Zoledronic Acid Restores the Activation and Anti-Myeloma Effects of γδT Cells Attenuated by the Bone Marrow Microenvironment,
52th American Society of Hematology, Orlando, Dec. 2010. Keiichiro Watanabe, Masahiro Abe, Cui Qu, Kawatani Makoto, Masahiro Hiasa, Nakano Ayako, Jinno Tadashi, Harada Takeshi, Shiroh Fujii, Shingen Nakamura, Miki Hirokazu, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki, Eiji Tanaka, Osada Hiroyuki and Toshio Matsumoto :
A Novel Anti-resorptive Agent, Reveromycin A, Ameliorates Bone Destruction and Tumor Growth in Myeloma,
ASBMR 2010 Annual Meeting, Toronto, Oct. 2010. Masahiro Hiasa, Masahiro Abe, nakano ayako, oda aska, amo hiroe, Keiichiro Watanabe, Shingen Nakamura, miki hirokazu, Kyoko Takeuchi, Kumiko Kagawa, Shuji Ozaki, Eiji Tanaka, Kenzo Asaoka and Toshio Matsumoto :
Bone Marrow Stromal Cells Suppress TACE-mediated M-CSFR and RANK Shedding to Facilitate Osteoclastogenesis and Suppress DC Differentiation from Monocytes.,
ASBMR 2010 Annual Meeting, Toronto, Oct. 2010. Masahiro Abe, Masahiro Hiasa, Nakano A, Shingen Nakamura, Miki H, Qu C, Keiichiro Watanabe, Harada T, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki and Toshio Matsumoto :
TIMP-3 up-regulation facilitates osteoclastogenesis and suppresses DC differentiation from monocytes in the bone marrow microenvironment in myeloma,
10th International Conference Cancer-induced Bone Disease, Sep. 2010.

(キーワード): Sheffield (United Kingdom)

Keiichiro Watanabe, Masahiro Abe, Cui Qu, Kawatani Makoto, Masahiro Hiasa, Nakano Ayako, Jinno Tadashi, Harada Takeshi, Shiroh Fujii, Shingen Nakamura, Miki Hirokazu, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki, Eiji Tanaka, Osada Hiroyuki and Toshio Matsumoto :
The novel anti-resorptive agent reveromycin A ameliorates bone destruction and tumor growth in myeloma,
10th International Conference Cancer-induced Bone Disease, Sheffield (United Kingdom), Sep. 2010. Masahiro Hiasa, Masahiro Abe, Eiji Tanaka, Kenzo Asaoka and Toshio Matsumoto :
Stroma inhibit DC differentiation through the suppression of M-CSFR shedding,
88th IADR, Barcelona, Jul. 2010. Masahiro Hiasa, Masahiro Abe, I Endo, A Nakano, Shuji Ozaki, Eiji Tanaka, Kenzo Asaoka and Toshio Matsumoto :
Myeloma-bone marrow stromal cell interaction enhances osteoclastogenesis and suppresses dendritic cell differentiation from monocytes,
14th International Congress of Endocrinology, Kyoto, Mar. 2010. Noboru Niki, Yoshiki Kawata, Hiromu Nishitani, Mitsuo Shimada, Junji Ueno, Masafumi Harada, Masahiro Abe, Hideki Otsuka, Harumi Itoh, Masahiro Kaneko, Takaaki Tuchida, Kenji Eguchi, Hironobu Ohmatsu, Masashi Takahashi and Yasutaka Nakano :
Computer-aided diagnosis based on computational anatomical models,
The First International Symposium on the Project ``Computational Anatomy'', 65-71, Tokyo, Feb. 2010. Akishige Ikegame, Shuji Ozaki, Daisuke Tsuji, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Ayako Nakano, Kumiko Kagawa, Kyoko Takeuchi, Ken-ichiro Yata, Masahiro Abe, Kouji Itou and Toshio Matsumoto :
A recombinant HLA class I-specifi single-chain Fv diabody can target cancer stem cell-like side population cells in multiple myeloma,
51th Annual Meeting of the American Society of Hematolog, New Orleans, Louisiana, USA, Dec. 2009. Masahiro Hiasa, Masahiro Abe, A Nakano, Kyoko Takeuchi, K Watanabe, Kumiko Kagawa, Ken-ichiro Yata, Kenzo Asaoka, Eiji Tanaka and Toshio Matsumoto :
Bone marrow stromal cells inhibit dendritic cell differentiation and facilitate osteoclastogenesis in myeloma through the suppression of M-CSF receptor shedding in monocytes,
第26回内藤コンファレンス, Nov. 2009. S Nakamura, Masahiro Abe, Cui Qui, A Nakano, Oda A., Amou H., Ikegame A., Harada T., Masahiro Hiasa, H Miki, Kumiko Kagawa, Kyoko Takeuchi, Ken-ichiro Yata, Shuji Ozaki and Toshio Matsumoto :
Facilitation of Osteoblast Differentiation by ATF-4 Accumulation through Proteasome Inhibition.,
ASH Annual Meeting, Nov. 2009. Itsuro Endo, Onishi Yukiyo, Kido Rika, Kurahashi Kiyoe, Ito Yuuji, Yuichi Fujinaka, Ken-ichi Aihara, Sumiko Yoshida, Masahiro Abe, Fukumoto S and Toshio Matsumoto :
A new calcilytic compound,JTT-305,inhibits enhanced signaling by activating mutations of calcium-sensing receptor in autosomal dominant hypocalcemia (ADH),
ASBMR 31st Annual Meeting, Denver, Sep. 2009. A Nakano, Asano J., Masahiro Abe, Masahiro Hiasa, S Nakamura, H Miki, Kumiko Kagawa, Kyoko Takeuchi, Ken-ichiro Yata, Itsuro Endo, Shuji Ozaki and Toshio Matsumoto :
Up-regulation of Pim-2 in myeloma cells by an interaction with bone marrow microenvironment enhances myeloma cell survival via stimulating Bad phosphorylation,
ASBMR Annual Meeting, Denver, Sep. 2009. Masahiro Abe, A Oda, Shinsuke Kido, A Nakano, Masahiro Hiasa, H Amou, S Nakamura, Kyoko Takeuchi, H Miki, Kumiko Kagawa, Ken-ichiro Yata, Shuji Ozaki, Itsuro Endo and Toshio Matsumoto :
Bortezomib, a proteasome inhibitor with anti-myeloma activity, stimulates osteoblast differentiation by enhancing ATF4 accumulation in osteoblastic cells.,
ASBMR Annual Meeting, Denver, Sep. 2009. Ken-ichiro Yata, Masahiro Abe, Oda A., Amou H., takeuchi K., Masahiro Hiasa, Nakano A., Miki H., Nakamura S., Tanaka O., Kumiko Kagawa, Shuji Ozaki and Toshio Matsumoto :
Anti-myeloma effects of γδ T cells are hampered by bone marrow stromal cells but resumed by stromal cell-derived osteoblasts,
Annual Meeting of the American Society of Hematology, San Francisco, Dec. 2008. Takashi Iwase, Hirotsugu Kurobe, Masashi Akaike, Shunji Nakano, Sumiko Yoshida, Sumitomo Yuka, Shusuke Yagi, Ken-ichi Aihara, Shuji Ozaki, Masahiro Abe, Natsuo Yasui, Toshio Matsumoto, Tetsuya Kitagawa and Masataka Sata :
Erythropoietin administration with autologous blood donation - a novel strategy to enhance mobilization of circulating progenitor cells,
American Heart Association Sessions 2008, New Orleans, Nov. 2008. Masahiro Abe, Masahiro Hiasa, Oda A., Amou H., takeuchi K., Tanaka O., Nakamura S., Miki H., Kumiko Kagawa, Ken-ichiro Yata, Shuji Ozaki, Kido S. and Toshio Matsumoto :
Bone marrow stromal cells up-regulate M-CSF receptor in monocytes to disrupt dendritic cell differentiation while facilitating osteoclastogenesis in myeloma,
ASBMR, Montreal, Sep. 2008. Takeuchi K., Masahiro Abe, Oda A., Amou H., Masahiro Hiasa, Tanaka O., Nakamura S., Miki H., Kumiko Kagawa, Ken-ichiro Yata, Hashimoto T., Shuji Ozaki, Kido S. and Toshio Matsumoto :
TGF-β Suppresses Adipocytic Differentiation and Enhances Accumulation of Stromal Cells in Myeloma Bone Lesions,
ASBMR, Montreal, Sep. 2008. Masahiro Abe, Masahiro Hiasa, Kido S., Oda A., Amou H., takeuchi K., Ken-ichiro Yata, Shuji Ozaki and Toshio Matsumoto :
TACE up-regulation in monocytes by GM-CSF and IL-4 disrupts myeloma cell-induced osteoclastogenesis while inducing dendritic cell differentiation,
International Meeting on Cancer Induced Bone Disease, Scotland, Jun. 2008. Takako Miyamoto, Shinsuke Kido, Masahiro Abe, Toshio Matsumoto and Hisaaki Taniguchi :
Expression Profiling by Quantitative and Large-scale Proteomics in Differentiating Osteoblasts,
HUPO 5th Annual World Congress, Los Angeles, Nov. 2006. Ali Jalili, Shuji Ozaki, Tomoko Hara, Etsuko Sekimoto, Yoichi Tanaka, Takashi Ohshima, Hironobu Shibata, Toshihiro Hashimoto, Masahiro Abe, Yasuhiko Nishioka and Toshio Matsumoto :
Generation of HM1.24-specific cytotoxic T lymphocytes from peripheral blood stem cell harvests of patients with multiple myeloma,
46th Annual Meeting: American Society of Hematology, San Francisco, Dec. 2004. Atsushi Shioyasono, Yasuo Oba, Hiura Kenji, Masahiro Abe, Toshio Matsumoto and Keiji Moriyama :
MIP-1alpha is upregulated during experimental tooth movement,
IADR 82nd General Session, Honolulu, Mar. 2004. 菅菜奈子, 安藤英紀, 松尾アモリムクリスティーナ菜々, 角南尚哉, 土井祐輔, 髙田春風, 安倍正博, 石田竜弘 :
ヒト悪性リンパ腫細胞の異種移植モデルに対するオキサリプラチン封入リポソームの単独あるいは抗体医薬との併用における抗腫瘍効果の検討,
日本薬剤学会第39年会, 2024年5月. 住谷龍平, 三木浩和, 岡村和美, 前田悠作, 大浦雅博, 曽我部公子, 八木ひかる, 高橋真美子, 丸橋朋子, 原田武志, 藤井志朗, 中村信元, 尾矢剛志, 安倍正博, 佐藤亜紀 :
KRAS変異を認めた治療抵抗性Rosai-Dorfman病の1例,
臨床血液, Vol.65, No.5, 473, 2024年5月. 中上絵美子, 寺町順平, 日浅雅博, 清水宗, 比嘉佳基, 田中茉里子, 金秀河, 中川宗純, 田中栄二, 安倍正博 :
プロテアソーム阻害薬による骨髄腫骨病変部における骨形成のメカニズム,
第82回日本矯正歯科学会学術大会抄録集, 192, 2023年11月. 比嘉佳基, 日浅雅博, 中川宗純, 金秀河, 田中茉里子, 中上絵美子, 清水宗, 天眞寛文, 田中栄二, 安倍正博 :
KEAP1-NRF2軸を介した脂肪細胞分化と骨芽細胞分化の制御機構,
第82回日本矯正歯科学会学術大会抄録集, 194, 2023年11月. 金秀河, 寺町順平, 日浅雅博, 天眞寛文, 中上絵美子, 田中茉里子, 中川宗純, 遠藤逸朗, 原田武志, 田中栄二, 安倍正博 :
骨形成誘導による骨髄腫排他的ニッチ形成の分子機序の探索,
日本骨代謝学会学術集会プログラム抄録集, 173, 2023年7月. 住谷龍平, 中村信元, 大浦雅博, 曽我部公子, 髙橋真美子, 藤井志朗, 原田武志, 三木浩和, 安倍正博 :
周期的な発熱，血小板減少，高LDH血症で発症したびまん性大細胞型B細胞リンパ腫の1例,
第128回日本内科学会四国地方会, 2023年7月. 山上紘規, 原倫世, 答島悠貴, 浅井孝仁, 三井由加里, 倉橋清衛, 乙田敏城, 湯浅智之, 黒田暁生, 遠藤逸朗, 松久宗英, 安倍正博, 粟飯原賢一 :
2型糖尿病患者のSkin autofluorscenceを規定する因子の検討,
第96回日本内分泌学会学術総会, 2023年6月. 山上紘規, 原倫世, 答島悠, 浅井孝, 三井由加里, 倉橋清衛, 乙田敏城, 湯浅智之, 黒田暁生, 遠藤逸朗, 松久宗英, 安倍正博, 粟飯原賢一 :
2型糖尿病患者のAGEs蓄積に関わる臨床的因子の解析,
第66回日本糖尿病学会年次学術集会, 2023年5月. 答島悠貴, 原倫世, 浅井孝仁, 山上紘規, 三井由加里, 倉橋清衛, 吉田守美子, 黒田暁生, 松久宗英, 福本誠二, 松久宗英, 安倍正博 :
首下がりを契機に診断に至ったCushing病の一例,
内科学会第127回四国地方会, 2022年12月. 林成樹, 住谷龍平, 大浦雅博, 原田武志, 中村信元, 森彩花, 田蒔昌憲, 安倍正博 :
ITP，自己免疫性出血病F13に続発しTAFRO症候群を発症した1例,
第127回日本内科学会四国地方会, 2022年12月. 佃恵里加, 李悦子, 瀧本朋美, 小田直輝, 原田武志, 藤井志朗, 中村信元, 三木浩和, 安倍正博 :
ダラツムマブ投与患者における間接抗グロブリン試験干渉期間の検討,
日本輸血細胞治療学会誌, Vol.68, No.6, 582-583, 2022年12月. 答島悠貴, 三井由加里, 浅井孝仁, 原倫世, 山上紘規, 倉橋清衛, 吉田守美子, 遠藤逸朗, 黒田暁生, 安倍正博, 松久宗英 :
レパグリニドとクロピドグレルの併用による遷延性低血糖を認めた一例,
日本糖尿病学会中国四国地方会第60回総会, 2022年11月. Mamiko Takahashi, Shingen Nakamura, Shin Kondo, Masafuumi Nakamura, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Takeshi Harada, Shiroh Fujii, Hirokazu Miki and Masahiro Abe :
Importance of skeletal muscle mass during chemotherapies in patients with hematological malignancies,
JSH2022, Oct. 2022. Takeshi Harada, Ryohei Sumitani, Asuka Oda, Yusuke Inoue, Masahiro Oura, Kimiko Sogabe, Tomoko Maruhashi, Mamiko Takahashi, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Shuji Ozaki, Hirofumi Tenshin, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe :
The therapeutic potential targeting ADAR1-dsRNA metabolism in myeloma cells with 1q amplification,
The 84th Annual Meeting of the Japanese Society of Hematology, Oct. 2022. 比嘉佳基, 日浅雅博, 金秀河, 田中茉里子, 中上絵美子, 清水宗, 谷本幸多朗, 天眞寛文, 田中栄二, 安倍正博 :
キサンチンオキシダーゼ阻害薬febuxostatはKEAP1-NRF2軸を介し脂肪細胞分化と骨芽細胞分化を制御する,
第81回日本矯正歯科学会学術大会, 2022年10月. 清水宗, 寺町順平, 日浅雅博, 天眞寛文, 比嘉佳基, 中上絵美子, 安倍正博, 田中栄二 :
骨髄腫細胞の生存・増殖におけるTAK1-CIP2A経路の重要な役割,
第81回日本矯正歯科学会学術大会, 2022年10月. 谷口元基, 本田剛士, 柳谷伸一郎, 髙成広起, 南康夫, 中村信元, 三木浩和, 安倍正博, 坂東良美, 常山幸一 :
ALアミロイドーシス無染色標本のラマン分光顕微観察,
2022年第83回応用物理学会秋季学術講演会, 20p-C301-12, 2022年9月.

(キーワード): ラマン分光 / アミロイドーシス

角南尚哉, 安藤英紀, 土井祐輔, 清水太郎, 異島優, 安倍正博, 石田竜弘 :
オキサリプラチン封入PEG修飾リポソームの悪性リンパ腫治療への展開,
第27回創剤フォーラム若手研究会, 2022年9月. 三井由加里, 黒田暁生, 原倫世, 山上紘規, 倉橋清衛, 吉田守美子, 遠藤逸朗, 安倍正博, 松久宗英 :
持続皮下インスリン注入療法下 1 型糖尿病合併妊娠における分娩直後のインスリン投与設定変更の提案,
第22回日本糖尿病インフォマティクス学会年次学術集会, 2022年8月. 新居寛子, 髙橋真美子, 藤井志朗, 曽我部公子, 林成樹, 住谷龍平, 大浦雅博, 原田武志, 中村信元, 安積麻衣, 湊将典, 三木浩和, 安倍正博 :
ループス腎炎に対してミコフェノール酸モフェチル投与中に発症した他の医原性免疫不全関連リンパ増殖性疾患の1例,
第265回徳島医学会学術集会, 2022年7月. 中上絵美子, 天眞寛文, 日浅雅博, 寺町順平, 原田武志, 井上雄介, 谷本幸多朗, 清水宗, 比嘉佳基, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 :
プロテアソーム阻害薬による骨髄腫骨病変部選択的骨形成誘導活性の検討,
第40回日本骨代謝学会学術集会, 141, 2022年7月. 比嘉佳基, 日浅雅博, 天眞寛文, 寺町順平, 原田武志, 小田明日香, 遠藤逸朗, 松本俊夫, 田中栄二, 安倍正博 :
キサンチンオキシダーゼ(XO)阻害薬febuxostatによる脂肪細胞分化と骨芽細胞分化の制御機構,
第40回日本骨代謝学会学術集会, 2022年7月. 田中茉里子, 日浅雅博, 谷本幸多朗, 天眞寛文, 清水宗, 比嘉佳基, 中上絵美子, 金秀河, 寺町順平, 原田武志, 中村信元, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 :
不動は骨髄腫骨病変部DPP-4発現増加と骨髄腫の腫瘍進展・髄外播種を加速させる,
第40回日本骨代謝学会学術集会, 2022年7月. 原田武志, 天眞寛文, 井上雄介, 住谷龍平, 中上絵美子, 寺町順平, 日浅雅博, 田中栄二, 松本俊夫, 安倍正博 :
破骨細胞によるSLAMF7の産生と骨髄腫関連骨病変に対するSLAMF7標的療法の開発,
第40回日本骨代謝学会学術集会, 2022年7月. 角南尚哉, 安藤英紀, 清水太郎, 異島優, 安倍正博, 石田竜弘 :
オキサリプラチン封入PEG修飾リポソームの悪性リンパ腫に対する治療効果の検討,
第38回日本DDS学会学術集会, 2022年6月. Ryohei Sumitani, Makiko Mizuguchi, Masahiro Oura, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Toshihiro Hashimoto, Takeshi Harada and Masahiro Abe :
126,
第126回日本内科学会四国地方会, Jun. 2022. 本田壮一, 中村信元, 高橋啓輝, 堀太貴, 安倍正博 :
地域での造血腫瘍の診療を考える,
第126回日本内科学会四国地方会, 2022年6月. 中村昌史, 三木浩和, 住谷龍平, 大浦雅博, 曽我部公子, 丸橋朋子, 高橋真美子, 原田武志, 藤井志朗, 中村信元, 西尾進, 友成哲, 安倍正博 :
ALアミロイドーシスの肝病変の評価における超音波エラストグラフィの有用性,
臨床血液, Vol.63, No.6, 685-686, 2022年6月.

(キーワード): *肝臓疾患(超音波診断,薬物療法) *組織弾性イメージング *アミロイドーシス-免疫グロブリン軽鎖(超音波診断,薬物療法) ヒト中年(45∼64) 男女

Shingen Nakamura, HORI Taiki, Masafumi Nakamura, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Tomoko Maruhashi, 高橋真美子, Shiroh Fujii, Hirokazu Miki, Takeshi Harada and Masahiro Abe :
Humoral response of the mRNA vaccine against SARS-CoV-2 in patients with plasma cell dyscrasia,
The 47th annual meeting of Japanese Society of Myeloma, May 2022. 天眞寛文, 原田武志, 井上雄介, 菊池次郎, 小田明日香, 住谷龍平, 大浦雅博, 曽我部公子, 丸橋朋子, 高橋真美子, 藤井志朗, 中村信元, 三木浩和, 日浅雅博, 寺町順平, 鈴木敦, 角川学士, 峯畑健一, 古川雄祐, 安倍正博 :
破骨細胞はSLAMF7を強発現し可溶性SLAMF7を産生する,
第47回日本骨髄腫学会学術集会, 2022年5月. 井上雄介, 原田武志, 天眞寛文, 小田明日香, 住谷龍平, 大浦雅博, 曽我部公子, 丸橋朋子, 高橋真美子, 藤井志朗, 三木浩和, 中村信元, 日浅雅博, 寺町順平, 安倍正博 :
骨髄腫に対する抗体免疫療法へのTh1様γδT細胞の応用,
第47回日本骨髄腫学会学術集会, 2022年5月. 原田武志, 住谷龍平, 小田明日香, 井上雄介, 大浦雅博, 曽我部公子, 丸橋朋子, 高橋真美子, 藤井志朗, 中村信元, 三木浩和, 天眞寛文, 日浅雅博, 寺町順平, 安倍正博 :
RNA編集酵素ADAR1を標的にする1q増幅骨髄腫細胞に対する治療法の開発,
第47回日本骨髄腫学会学術集会, 2022年5月. 寺町順平, 天眞寛文, 日浅雅博, 小田明日香, 清水宗, 住谷龍平, 大浦雅博, 曽我部公子, 丸橋朋子, 藤井志朗, 中村信元, 三木浩和, 遠藤逸朗, 原田武志, 安倍正博 :
TAK1 阻害は骨髄腫の細胞間相互作用による骨破壊と薬剤耐性を改善する,
第47回日本骨髄腫学会学術集会, 2022年5月. 丸橋朋子, 三木浩和, 曽我部公子, 原田武志, 小田明日香, 中村信元, 中村昌史, 住谷龍平, 大浦雅博, 高橋真美子, 藤井志朗, 安倍正博 :
骨髄腫細胞のプロテアソーム阻害薬への抵抗性の機序と温熱療法によるその克服の可能性,
第47回日本骨髄腫学会学術集会, 2022年5月. 中村信元, 堀太貴, 中村昌史, 住谷龍平, 大浦雅博, 曽我部公子, 丸橋朋子, 髙橋真美子, 藤井志朗, 三木浩和, 原田武志, 安倍正博 :
形質細胞疾患における新型コロナワクチンの有効性,
第47回日本骨髄腫学会学術集会, 2022年5月. 三木浩和, 中村信元, 中村昌史, 住谷龍平, 大浦雅博, 曽我部公子, 髙橋真美子, 丸橋朋子, 原田武志, 藤井志朗, 西尾進, 友成哲, 安倍正博 :
肝臓アミロイドーシスに対する超音波エラストグラフィを用いた非侵襲的診断法の有用性,
第47回日本骨髄腫学会学術集会, 2022年5月. 吉田守美子, 辻誠一郎, 倉橋清衛, 宮恵子, 島久登, 田代学, 井上朋子, 水口潤, 中村信元, 黒田暁生, 遠藤逸朗, 安倍正博, 松久宗英 :
透析患者における新型コロナワクチン抗体と糖尿病の関連の検討,
第 65 回日本糖尿病学会年次学術集会, 2022年5月. 比嘉佳基, 日浅雅博, 天眞寛文, 谷本幸多朗, 清水宗, 寺町順平, 原田武志, 小田明日香, 遠藤逸朗, 松本俊夫, 田中栄二, 安倍正博 :
骨髄腫骨髄微小環境の変容におけるキサンチンオキシダーゼ-ROS経路の重要な役割,
International Journal of Myeloma, Vol.12, No.3, 149, 2022年5月. 中村信元, 堀太貴, 中村昌史, 住谷龍平, 大浦雅博, 曽我部公子, 丸橋朋子, 高橋真美子, 藤井志朗, 三木浩和, 原田武志, 粟飯原賢一, 安倍正博 :
形質細胞異常症患者におけるSARS-CoV-2に対するmRNAワクチンの液性免疫応答の評価(Humoral response of the mRNA vaccine against SARS-CoV-2 in patients with plasma cell dyscrasia),
International Journal of Myeloma, Vol.12, No.3, 199, 2022年5月.

(キーワード): *予防接種 *単クローン性免疫グロブリン血症-良性(免疫学) *液性免疫 *アミロイドーシス-免疫グロブリン軽鎖(免疫学) *COVID-19ワクチン(治療的利用,薬理学)

中上絵美子, 天眞寛文, 寺町順平, 日浅雅博, 原田武志, 谷本幸多朗, 清水宗, 比嘉佳基, 住谷龍平, 丸橋朋子, 大浦雅博, 曽我部公子, 中村信元, 三木浩和, 遠藤逸朗, 田中栄二, 安倍正博 :
プロテアソーム阻害薬のパルス投与の骨代謝への影響,
International Journal of Myeloma, Vol.12, No.3, 152, 2022年5月.

(キーワード): 骨髄腫-多発性(薬物療法,病理学) / 骨組織リモデリング / パルス療法(薬物療法) / Proteasome Inhibitors(治療的利用,薬理学) / ヒト (Homo sapiens)

天眞寛文, 原田武志, 井上雄介, 菊池次郎, 小田明日香, 住谷龍平, 大浦雅博, 曽我部公子, 丸橋朋子, 高橋真美子, 藤井志朗, 中村信元, 三木浩和, 日浅雅博, 寺町順平, 鈴木敦, 角川学士, 峯畑健一, 古川雄祐, 安倍正博 :
破骨細胞はSLAMF7を強発現し可溶性SLAMF7を産生する(Osteoclasts robustly express SLAMF7 and secrete soluble SLAMF7),
International Journal of Myeloma, Vol.12, No.3, 150, 2022年5月.

(キーワード): *骨髄腫-多発性(遺伝学,病理学) *破骨細胞 *Signaling Lymphocytic Activation Molecule Family(血液) *SLAMF7 Protein(血液) ヒト

吉田守美子, 辻誠士郎, 宮恵子, 島久登, 田代学, 井上朋子, 水口潤, 岡田一義, 中村信元, 安倍正博 :
高齢者透析患者における新型コロナワクチン抗体価に影響する因子の検討,
日本老年医学会雑誌, Vol.59, No.Suppl., 107, 2022年5月.

(キーワード): *IgG *血液透析 *ウイルス抗体 *腎不全-慢性(治療) 予防接種年齢因子 *COVID-19(免疫学) COVID-19ワクチン(治療的利用) ヒト成人(19∼44) 中年(45∼64) 高齢者(65∼79) 高齢者(80∼) 男女

吉田守美子, 辻誠士郎, 倉橋清衛, 宮恵子, 島久登, 田代学, 井上朋子, 水口潤, 中村信元, 黒田暁生, 遠藤逸朗, 安倍正博, 松久宗英 :
透析患者における新型コロナワクチン抗体と糖尿病の関連の検討,
糖尿病, Vol.65, No.Suppl.1, S-165, 2022年4月.

(キーワード): *血液透析ウイルス抗体腎不全-慢性(治療) *糖尿病性腎症(治療) 予防接種 COVID-19ワクチン(治療的利用) *Tozinameran(治療的利用) ヒト男女

高原由実子, 三木浩和, 中村信元, 中村昌史, 住谷龍平, 大浦雅博, 曽我部公子, 高橋真美子, 丸橋朋子, 原田武志, 藤井志朗, 安倍正博, 岡本秀樹, 岡田直人, 矢野由美子, 高橋真理, 青田桂子, 尾崎修治 :
HIV感染症および後天性免疫不全症候群患者の臨床的特徴と今後の課題,
四国医学雑誌, Vol.78, No.1-2, 89, 2022年4月. 吉田守美子, 辻誠士郎, 金子遥祐, 森建介, 河田沙紀, 川原綾香, 遠藤ふうり, 原倫世, 倉橋清衛, 黒田暁生, 明比祐子, 遠藤逸朗, 安倍正博, 松久宗英 :
精神疾患とうつ尺度が減量入院効果に及ぼす影響,
第41回日本肥満学会・第38回日本肥満症治療学会, 2022年3月. 辻誠士郎, 吉田守美子, 金子遥祐, 森建介, 河田沙紀, 川原綾香, 遠藤ふうり, 原倫世, 倉橋清衛, 黒田暁生, 明比祐子, 遠藤逸朗, 安倍正博, 松久宗英 :
行動療法を重視した2週間の減量入院後の減量効果の検討,
第41回日本肥満学会・第38回日本肥満症治療学会, 2022年3月. 辻誠士郎, 吉田守美子, 金子遥祐, 森建介, 河田沙紀, 川原綾香, 遠藤ふうり, 原倫世, 倉橋清衛, 黒田暁生, 明比祐子, 遠藤逸朗, 安倍正博, 松久宗英 :
行動療法を重視した2週間の減量入院後の減量効果の検討,
第42回日本肥満学会第39回日本肥満症治療学会学術集会, 2022年3月. 吉田守美子, 辻誠士郎, 金子遥祐, 森建介, 河田沙紀, 川原綾香, 遠藤ふうり, 原倫世, 倉橋清衛, 明比祐子, 遠藤逸朗, 安倍正博, 松久宗英 :
精神疾患とうつ尺度が減量入院効果に及ぼす影響,
第42回日本肥満学会第39回日本肥満症治療学会学術集会, 2022年3月. 中村昌史, 三木浩和, 住谷龍平, 大浦雅博, 曽我部公子, 丸橋朋子, 髙橋真美子, 原田武志, 藤井志朗, 中村信元, 西尾進, 友成哲, 安倍正博 :
ALアミロイドーシスの肝病変の評価における超音波エラストグラフィの有用性.,
第61回日本血液学会中国四国地方会, 2022年3月. 住谷龍平, 原田武志, 中村昌史, 水口槙子, 大浦雅博, 曽我部公子, 丸橋朋子, 髙橋真美子, 藤井志朗, 中村信元, 三木浩和, 賀川久美子, 矢田未央, 松立吉弘, 上原久典, 安倍正博 :
少量methotrexate療法が有効であった進行期原発性皮膚未分化大細胞型リンパ腫.,
臨床血液, Vol.63, No.6, 536-543, 2022年3月.

(要約): 進行期の原発性皮膚未分化大細胞リンパ腫(pcALCL)に対する標準治療は定まっていない．症例は71歳,男性．多発性の皮膚紅斑と結節病変を認め,左耳介後部からの生検でリンパ腫性丘疹症(LyP)と診断された．局所電子線照射にて全ての病変は消退したが,5ヵ月後に両内眼角に結節病変が出現し,同部位の生検ではCD30陽性大型細胞が大部分を占めpcALCLと診断された．PET/CTにて右口蓋扁桃腫大,頸部,鼠径部の表在リンパ節腫大およびFDG集積を認め,TNM分類T3bN3M0であった．慢性閉塞性肺疾患による呼吸機能低下と肺炎を反復していたため,多剤併用化学療法ではなくmethotrexate(MTX)15mg/週の内服療法を選択した．皮膚,リンパ節病変は縮小し,副作用なく長期間病勢コントロールが可能であった．pcALCLの標準治療は確立されていないが様々な治療法が開発されてきており,少量MTX療法は呼吸器感染症を繰り返すフレイルな患者に有用であった．LyPにpcALCLが続発する機序や本疾患群に対する少量MTX療法の作用機序の解明が望まれる．(著者抄録)
(キーワード): Etoposid / Methotrexate / 顔面腫瘍 / 肺疾患 (lung disease) / 皮膚疾患-顔面 / 皮膚腫瘍 / 扁桃腫瘍 / 放射線療法 / Folic Acid / リンパ腫-未分化大細胞 / 心筋症-たこつぼ型 / PET-CT検査 / フレイル / ヒト (Homo sapiens) / 高齢者
(出版サイトへのリンク): ● Publication site (DOI): 10.11406/rinketsu.63.536
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.11406/rinketsu.63.536

(DOI: 10.11406/rinketsu.63.536) 高原由実子, 三木浩和, 中村信元, 中村昌史, 住谷龍平, 大浦雅博, 曽我部公子, 髙橋真美子, 丸橋朋子, 岡本秀樹, 岡田直人, 矢野由美子, 高橋真理, 原田武志, 藤井志朗, 青田桂子, 尾崎修治, 安倍正博 :
HIV感染症および後天性免疫不全症候群患者の臨床的特徴と今後の課題.,
第264回徳島医学会学術集会(令和3年度冬期), 2022年2月20日(Web開催), 2022年2月. 原倫世, 河田沙紀, 川原綾香, 金子遥祐, 森建介, 三井由加里, 倉橋清衛, 吉田守美子, 遠藤逸朗, 福本誠二, 安倍正博 :
低Mg血症によるPTH分泌不全により著明な低Ca血症を来した一例,
第33回日本老年医学会四国地方会, 2022年1月.

(キーワード): 副甲状腺

森建介, 倉橋清衛, 河田沙紀, 川原綾香, 金子遥祐, 高丸利加子, 吉田守美子, 遠藤逸朗, 西岡安彦, 安倍正博 :
失語症のため治療説明に難渋し方針決定が遅れた異所性ACTH症候群の1例,
第33回日本老年医学会四国地方会, 2022年1月. 辻誠士郎, 吉田守美子, 宮恵子, 島久登, 田代学, 井上朋子, 水口潤, 中村信元, 遠藤逸朗, 安倍正博 :
65歳以上の透析患者における新型コロナワクチン抗体価の検討,
第33回日本老年医学会四国地方会, 2022年1月. 青山理央, 川原綾香, 倉橋清衛, 原倫世, 吉田守美子, 黒田暁生, 松久宗英, 松久宗英, 福本誠二, 遠藤逸朗, 安倍正博 :
1型糖尿病とバセドウ病を同時に診断した1例,
日本内科学会第125回四国地方会, 2021年12月. 高岡俊, 金子遥祐, 辻誠士郎, 倉橋清衛, 吉田守美子, 明比祐子, 遠藤逸朗, 安倍正博, 福本誠二 :
レンバチニブで破壊性甲状腺炎をきたし，医原性副腎皮質機能低下症による副腎不全が顕在化した一例,
日本内科学会第125回四国地方会, 2021年12月. 西條早希, 三木浩和, 中村昌史, 大浦雅博, 曽我部公子, 髙橋真美子, 原田武志, 藤井志朗, 中村信元, 安倍正博 :
超音波エラストグラフィが肝病変の評価に有用であった全身性ALアミロイドーシスの1例.,
第125回日本内科学会四国地方会, 2021年12月. 山田博貴, 大森理央, 岡田直人, 中村信元, 賀川久美子, 藤井志朗, 三木浩和, 石澤啓介, 安倍正博, 佐藤陽一 :
ゲノムワイド関連解析によるビンクリスチン副作用発現関連遺伝子の同定と機械学習を用いた副作用発現予測モデルの構築,
第60回日本薬学会中国四国支部学術大会, 2021年11月. 河田沙紀, 原倫世, 吉田守美子, 川原綾香, 金子遥祐, 森建介, 遠藤ふうり, 辻誠士郎, 三井由加里, 倉橋清衛, 明比祐子, 遠藤逸朗, 安倍正博, 福本誠二 :
アルドステロンを含む3種のホルモン産生副腎皮質癌の一例,
第32回臨床内分泌代謝Update, 2021年11月. 河田沙紀, 原倫世, 吉田守美子, 川原綾香, 金子遥祐, 森建介, 遠藤ふうり, 辻誠士郎, 三井由加里, 倉橋清衛, 明比祐子, 遠藤逸朗, 安倍正博, 福本誠二 :
アルドステロンを含む3種のホルモン産生性副腎皮質癌の一例,
第31回臨床内分泌代謝Update, 2021年11月. 森建介, 辻誠士郎, 吉田守美子, 河田沙紀, 川原綾香, 金子遥祐, 細木美苗, 遠藤ふうり, 原倫世, 三井由加里, 倉橋清衛, 遠藤逸朗, 福本誠二, 安倍正博 :
10cmの右大腿部腫瘤を原因とする腫瘍性骨軟化症の1例,
第31回臨床内分泌Update, 2021年11月. 吉田守美子, 河田沙紀, 川原綾香, 金子遥祐, 森建介, 遠藤ふうり, 辻誠士郎, 原倫世, 倉橋清衛, 明比祐子, 遠藤逸朗, 安倍正博, 福本誠二 :
新型コロナワクチン投与後に発症した亜急性甲状腺炎の1例,
第64回日本甲状腺学会学術集会, 2021年11月. Sou Shimizu, Jumpei Teramachi, Takeshi Harada, 小田明日香, Hirofumi Tenshin, Masahiro Hiasa, Kotaro Tanimoto, Yoshiki Higa, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
The critical roles of the TAK1-CIP2A axis in MM cell growth and survival and osteoclastogensis,
第83回日本血液学会学術集会, BPA-3-3, Sep. 2021. 曽我部公子, 原田武志, 中村信元, 三木浩和, 小田明日香, 井上雄介, 住谷龍平, 丸橋朋子, 大浦雅博, 藤井志朗, 賀川久美子, 天眞寛文, 日浅雅博, 寺町順平, 安倍正博 :
PIMとAkt阻害は骨髄腫細胞におけるプロテアソーム阻害薬感受性を増強する,
The 83rd Annual Meeting of the Japanese Society of Hematology, 2021年9月. Yoshiki Higa, Masahiro Hiasa, Hirofumi Tenshin, Jumpei Teramachi, Takeshi Harada, 小田明日香, 大浦雅弘, Kimiko Sogabe, Itsuro Endo, Toshio Matsumoto, Masahiro Abe and Eiji Tanaka :
Critical roles of the XO-ROS axis in the pathology of bone loss in myeloma,
第83回日本血液学会学術集会, BPA-3-4, Sep. 2021. Hirofumi Tenshin, 寺町順平日浅雅博小田明日香原田武志, Masahiro Hiasa, 小田明日香, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Eiji Tanaka, Itsuro Endo, Toshio Matsumoto and Masahiro Abe :
NLRP3 inflammasome aggravates osteoclastic bone destruction in myeloma,
日本血液学会学術集会83回 Page 83回 Page OS2-4B-4(2021.09), Sep. 2021. Kotaro Tanimoto, Masahiro Hiasa, Hirofumi Tenshin, Jumpei Teramachi, Takeshi Harada, 小田明日香, Masahiro Oura, Kimiko Sogabe, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe :
Extraosseous dissemination of myeloma by mechanical unloading,
日本血液学会学術集会83回 Page 83回 Page OS2-11C-3(2021.09), Sep. 2021. 原田武志, 井上雄介, 天眞寛文, 小田明日香, 住谷龍平, 大浦雅博, 曽我部公子, 藤井志朗, 中村信元, 三木浩和, 賀川久美子, 日浅雅博, 寺町順平, 安倍正博 :
CELMoDsを用いたγδT細胞増幅法とエロツズマブによるγδT細胞の抗骨髄腫作用の増強法の開発,
第83回日本血液学会学術集会, 2021年9月. 川原綾香, 原倫世, 平岡栞名, 辻誠士郎, 三井由加里, 倉橋清衛, 吉田守美子, 遠藤逸朗, 安倍正博, 福本誠二 :
前立腺癌の副腎転移が123I-MIBGシンチグラフィ陽性を示した1例,
第21回日本内分泌学会四国支部学術集会, 2021年9月. 中村信元, 上野宜久, 吉田守美子, 中村昌史, 水口槙子, 住谷龍平, 大浦雅博, 曽我部公子, 高橋真美子, 丸橋朋子, 原田武志, 藤井志朗, 三木浩和, 賀川久美子, 広津崇亮, 安倍正博 :
血液がんにおける線虫がん検査 N-NOSEの検討(Detection of hematological malignancies using N-NOSE(Nematode-NOSE)),
日本血液学会学術集会, OS1-11B-2, 2021年9月.

(キーワード): *検尿走化性 Caenorhabditis elegans *造血器腫瘍(診断) ヒト男女

三木浩和, 中村信元, 藤井志朗, 中村昌史, 水口槙子, 住谷龍平, 大浦雅博, 曽我部公子, 髙橋真美子, 丸橋朋子, 原田武志, 賀川久美子, Nishio Susumu, 友成哲, 安倍正博 :
肝臓アミロイドーシスに対する超音波エラストグラフィの診断的有用性.,
第83回日本血液学会学術集会, OS1-8D-2, 2021年9月. 曽我部公子, 原田武志, 中村信元, 三木浩和, 小田明日香, 井上雄介, 住谷龍平, 丸橋朋子, 大浦雅博, 藤井志朗, 賀川久美子, 天眞寛文, 日浅雅博, 寺町順平, 安倍正博 :
PIMとAkt阻害による骨髄腫細胞のプロテアソーム阻害薬感受性の増強(Sensitization of myeloma cells to proteasome inhibitors by PIM and Akt inhibition),
日本血液学会学術集会, OS2-11D-3, 2021年9月. 吉川紘平, 金子遥祐, 辻誠士郎, 河田沙紀, 川原綾香, 森健介, 遠藤ふうり, 原倫世, 倉橋清衛, 吉田守美子, 黒田暁生, 明比祐子, 遠藤逸朗, 松久宗英, 安倍正博, 福本誠二 :
TIA様発作を契機に診断されたインスリノーマの一例,
第263回徳島医学会, 2021年8月. 西條早希, 中村信元, 三木浩和, 谷口早紀, 岡本秀樹, 岡田直人, 矢野由美子, 高橋真理, 青田桂子, 菅俊行, 渡邊浩良, 大坂朱美, 安倍正博 :
当院における先天性血友病患者(成人例)の実態調査∼移行期医療の重要性∼,
第263回徳島医学会学術集会(令和3年度夏期), 2021年8月. 安倍正博 :
骨髄腫骨病変の病態解明と治療の進歩と展望.,
第46回日本骨髄腫学会学術集, 2021年5月. 原田武志, 井上雄介, 天眞寛文, 小田明日香, 住谷龍平, 大浦雅博, 曽我部公子, 藤井志朗, 中村信元, 三木浩和, 賀川久美子, 日浅雅博, 寺町順平, 安倍正博 :
Development of combinatory treatment of Th1-like γδT cells with elotuzumab against osteoclasts as well as myeloma cells,
第46回日本骨髄腫学会学術集会, 2021年5月. 粟飯原賢一, 堀太貴, 山上紘規, 安井沙耶, 金子遥祐, 中村信元, 谷口達哉, 乙田敏城, 湯浅智之, 添木武, 安倍正博 :
生体電気インピーダンス法による細胞外水分比および位相角と糖尿病患者における血中HbおよびHtレベルの連関解析,
第64回日本糖尿病学会年次学術集会, 2021年5月. 辻誠士郎, 吉田守美子, 平岡栞名, 宮高紘輔, 細木美苗, 原倫世, 三井由加里, 倉橋清衛, 黒田暁生, 明比祐子, 遠藤逸朗, 船木真理, 福本誠二, 安倍正博, 松久宗英 :
行動療法を中心とした2週間の減量入院プログラムの退院後の減量効果,
第64回日本糖尿病学会年次学術集会, 2021年5月. 遠藤理子, 倉橋清衛, 平岡栞名, 細木美苗, 宮高紘輔, 辻誠士郎, 吉田守美子, 遠藤逸朗, 松久宗英, 安倍正博 :
慢性膵炎の急性増悪を繰り返し，仮性脾動脈瘤の急速な増大を認めた一例,
第124回日本内科学会四国地方会(WEB開催), 2021年5月. 三木浩和, 中村信元, 中村昌史, 水口槙子, 住谷龍平, 大浦雅博, 曽我部公子, 髙橋真美子, 丸橋朋子, 原田武志, 藤井志朗, 賀川久美子, 近藤正輝, 岡田直人, 坂東良美, 遠藤逸朗, 安倍正博 :
骨髄腫骨関連事象の発生予防における身体機能維持の重要性,
第46回日本骨髄腫学会学術集会, 2021年5月. 曽我部公子, 原田武志, 中村信元, 三木浩和, 小田明日香, 井上雄介, 住谷龍平, 大浦雅博, 藤井志朗, 賀川久美子, 天眞寛文, 日浅雅博, 寺町順平, 李政樹, 飯田真介, 安倍正博 :
骨髄腫細胞のプロテアソーム阻害薬の耐性機序におけるPIM2とAkt活性およびNRF2蓄積の役割(Mechanisms for the resistance to proteasome inhibitors in myeloma cells: the role of PIM2 and Akt kinase activation and NRF2 accumulation),
International Journal of Myeloma, Vol.11, No.2, 85, 2021年5月.

(キーワード): *癌原遺伝子タンパク質 *骨髄腫-多発性(遺伝学,実験的) *Protein-Serine-Threonine Kinases *抗腫瘍剤耐性 c-akt癌原遺伝子タンパク質 *NF-E2-Related Factor 2 *Proteasome Inhibitors(薬理学) *PIM2 Protein

金井麻衣, 大西幸代, 原倫世, 遠藤逸朗, 安倍正博, 福本誠二, 松本俊夫 :
TAK1 阻害による炎症性サイトカイン誘導性筋萎縮の改善,
第94回日本内分泌学会学術総会, 2021年4月. 堀太貴, 山上紘規, 安井沙耶, 金子遥祐, 中村信元, 谷口達哉, 乙田敏城, 湯浅智之, 添木武, 安倍正博, 粟飯原賢一 :
生体電気インピーダンス法による細胞外水分比および位相角は糖尿病患者の血中HbおよびHtレベルを規定する,
第94回日本内分泌学会学術総会, 2021年4月. 石田卓也, 三木浩和, 髙橋真美子, 中村昌史, 水口槙子, 住谷龍平, 大浦雅博, 曽我部公子, 丸橋朋子, 岡本秀樹, 岡田直人, 矢野由美子, 高橋真理, 友成哲, 原田武志, 藤井志朗, 中村信元, 賀川久美子, 青田桂子, 渡邊浩良, 安倍正博 :
HIV感染血友病患者における臨床的特徴と今後の課題,
第262回徳島医学会学術集会, 2021年3月. 木村蘭子, 倉橋清衛, 細木美, 辻誠司郎, 三井由加里, 吉田守美子, 明比祐子, 遠藤逸朗, 福本誠二, 安倍正博 :
繰り返す脆弱性骨折を契機に発見されたクッシング症候群の一例,
第262回徳島医学会学術集会, 2021年3月. 丸橋朋子, 藤井志朗, 賀川久美子, 中村昌史, 川田知代, 水口槇子, 住谷龍平, 大浦雅博, 曽我部公子, 高橋真美子, 原田武志, 中村信元, 三木浩和, 安倍正博 :
造血幹細胞移植(allo-SCT)が奏効したMLL遺伝子変異合併CML急性転化(CML-BP)の2例,
第43回日本造血細胞移植学会総会, 2021年3月. 細木美苗, 吉田守美子, 平岡栞名, 宮高紘輔, 辻誠士郎, 原倫世, 三井由加里, 倉橋清衛, 遠藤逸朗, 安倍正博 :
持続血糖モニタリングシステムを使用した遠隔診療が有効であった高齢1型糖尿病の2症例,
第32回日本老年医学会四国地方会, 2021年2月. 吉本ちひろ, 相原苑果, 長井輝幸, 松田和子, 大西幸代, 原倫世, 中村信元, 賀川久美子, 三木浩和, 安倍正博, 櫻井明子, 金井麻衣, 遠藤逸朗 :
血液悪性腫瘍化学療法入院中の骨格筋量の減少ビタミンD充足との関連,
第44回徳島県医学検査学会, 2020年12月. 長井輝幸, 吉本ちひろ, 松田和子, 相原苑果, 大西幸代, 原倫世, 倉橋清衛, 安倍正博, 金井麻衣, 遠藤逸朗 :
TAK1阻害による炎症性サイトカイン誘導性筋萎縮の改善,
第44回徳島県医学検査学会, 2020年12月. 武井みのり, 岡田直人, 中村信元, 賀川久美子, 藤井志朗, 三木浩和, 石澤啓介, 安倍正博, 佐藤陽一 :
機械学習による遺伝情報を用いた抗がん剤投与の味覚障害発現予測モデルの構築,
第59回中国四国支部学術大会, 2020年12月. 遠藤優香, 田島穂澄, 岡田直人, 中村信元, 賀川久美子, 藤井志朗, 三木浩和, 石澤啓介, 安倍正博, 佐藤陽一 :
ゲノム情報を用いた機械学習によるシタラビン投与後の副作用発現予測モデルの構築,
第59回中国四国支部学術大会, 2020年12月. 清重尚希, 住谷龍平, 水口槙子, 中村昌史, 大浦雅博, 曽我部公子, 高橋真美子, 原田武志, 藤井志朗, 賀川久美子, 安倍正博, 中村信元, 三木浩和, 曽賀愛未, 一宮由貴, 山本由理 :
急性転化をきたしたAYA世代慢性骨髄性白血病の1例,
四国医学雑誌, Vol.76, No.5-6, 354-355, 2020年12月.

(キーワード): 同種移植抗腫瘍剤(治療的利用) *白血病-BCR-ABL陽性慢性骨髄性(診断,治療,薬物療法) 急性転化(白血病) 障害者の子供造血幹細胞移植家族介護者ヒト青年期(13~18) 女

高原実香, 山本伸昭, 宮本亮介, 藤田浩司, 和泉唯信, 住谷龍平, 中村信元, 安倍正博, 島津秀紀, 西田善彦 :
意識障害，高アンモニア血症を呈した78歳男性,
四国医学雑誌, Vol.76, No.5-6, 346, 2020年12月.

(キーワード): Dexamethasone(治療的利用) / 意識障害(病因) / 腫瘍多剤併用療法 / 骨髄腫-多発性(合併症,病理学,薬物療法) / 高アンモニア血症(病因,診断) / Bortezomib(治療的利用) / BD Protocol (Bortezomib-Dexamethasone) / ヒト / 高齢者(65~79) / 男

三木浩和, 李悦子, 佃恵里加, 小田直輝, 瀧本朋美, 中村昌史, 水口槙子, 住谷龍平, 大浦雅博, 曽我部公子, 高橋真美子, 原田武志, 藤井志朗, 賀川久美子, 安倍正博, 中村信元 :
Daratumumab投与による輸血関連検査への影響とその対策,
四国医学雑誌, Vol.76, No.5-6, 341, 2020年12月.

(キーワード): Coombsテスト / 骨髄腫-多発性(診断,薬物療法) / Daratumumab(治療的利用) / ヒト / 中年(45~64) / 高齢者(65~79) / 高齢者(80~) / 男 / 女

中村昌史, 藤井志朗, 三木浩和, 細木美苗, 曽我部公子, 髙橋真美子, 丸橋朋子, 大櫛祐一郎, 安倍正博 :
ACE阻害薬による血管性浮腫が原因と考えられた喉頭浮腫の一例,
第123回日本内科学会四国地方会, 2020年11月. 丸橋朋子, 三木浩和, 中村昌史, 高橋真美子, 藤井志朗, 中野綾子, 安倍正博 :
Evans症候群に合併した自己免疫性骨髄線維症の1例,
第123回日本内科学会四国地方会, 2020年11月. 市原聖也, 住谷龍平, 中村昌史, 水口槙子, 原田武志, 藤井志朗, 中村信元, 三木浩和, 賀川久美子, 安倍正博 :
ウイルス関連血球貪食症候群が疑われたアグレッシブNK細胞白血病の1例,
第123回日本内科学会四国地方会, 2020年11月. 金山涼加, 倉橋清衛, 明比祐子, 岡本耕一, 中村信元, 吉田守美子, 遠藤逸朗, 高山哲治, 安倍正博 :
潰瘍性大腸炎とバセドウ病の治療中に汎血球減少を契機に自己免疫性胃炎が判明した一例,
第123回日本内科学会四国地方会, 2020年11月. 細木美苗, 遠藤ふうり, 三井由加里, 平岡栞名, 宮髙紘輔, 辻誠士郎, 倉橋清衛, 吉田守美子, 遠藤逸朗, 安倍正博 :
推奨量のヒドロコルチゾン補充で症状が改善しなかった中枢性副腎不全の一例,
第123回日本内科学会四国地方会, 2020年11月. 辻誠士郎, 吉田守美子, 遠藤ふうり, 平岡栞名, 細木美苗, 宮髙紘輔, 三井由加里, 倉橋清衛, 明比祐子, 遠藤逸朗, 安倍正博, 福本誠二 :
副腎皮質癌と舌癌を合併しがんゲノム検査を施行した一例,
第30回臨床内分泌代謝Update, 2020年11月. 宮髙紘輔, 倉橋清衛, 吉田守美子, 平岡栞名, 細木美苗, 遠藤ふうり, 辻誠士郎, 三井由加里, 明比祐子, 遠藤逸朗, 安倍正博, 福本誠二 :
glioblastomaを発症した神経線維腫症1型の1例,
第30回臨床内分泌代謝Update, 2020年11月. 細木美苗, 三井由加里, 平岡栞名, 宮髙紘輔, 辻誠士郎, 原倫世, 桝田志保, 倉橋清衛, 吉田守美子, 明比祐子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 福本誠二 :
顕性Cushing症候群を示し片側副腎切除を施行したBMAHの一例,
第30回臨床内分泌代謝update, 2020年11月. 平岡栞名, 三井由加里, 細木美苗, 宮高紘輔, 辻誠士朗, 三井由加里, 倉橋清衛, 吉田守美子, 遠藤逸朗, 黒田暁生, 安倍正博, 松久宗英 :
原田病，重症筋無力症を合併した1型糖尿病の1例,
日本糖尿病学会中国四国地方会第58総会, 2020年10月. 辻誠士朗, 倉橋清衛, 平岡栞名, 細木美苗, 宮高紘輔, 三井由加里, 吉田守美子, 黒田暁生, 遠藤逸朗, 安倍正博, 松久宗英 :
びまん性膵腫大を契機に膵癌再発と診断したGAD抗体陽性の糖尿病の一例,
日本糖尿病学会中国四国地方会第58総会, 2020年10月. 曽我部公子, 中村信元, 藤井志朗, 三木浩和, 小田明日香, 原田武志, 住谷龍平, 大浦雅博, 賀川久美子, 天眞寛文, 寺町順平, Masaki Ri, Shinsuke Iida, 安倍正博 :
プロテアソーム阻害薬による骨髄腫細胞の抗アポトーシス因子PIM2の急速な蓄積,
第82回日本血液学会学術集会, 2020年10月. 大浦雅博, 原田武志, 寺町順平, 小田明日香, 井上雄介, 曽我部公子, 住谷龍平, 藤井志朗, 中村信元, 三木浩和, 賀川久美子, Hasegawa Hiroo, Fujiwara Hiroshi, 安倍正博 :
ATL新規治療標的としてのTAK1-c-Myc相互連関の重要な役割,
第82回日本血液学会学術集会, 2020年10月. 井上雄介, 原田武志, Asuka Oda, Masahiro Oura, 曽我部公子, 住谷龍平, Shiro Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Shuji Ozaki, Jumpei Teramachi, 安倍正博 :
骨髄腫細胞のBlimp-1非依存的なBCMA発現亢進: IRF4の重要な関与,
第82回日本血液学会学術集会, 2020年10月. 清水宗, 寺町順平, 原田武志, 小田明日香, 天眞寛文, 日浅雅博, 谷本幸多朗, 比嘉佳基, 田中栄二, 松本俊夫, 安倍正博 :
骨髄腫細胞のPP2A阻害因子CIP2A発現誘導を介するTAK1活性化増強機構,
日本骨代謝学会学術集会プログラム抄録集, 149, 2020年10月. 谷本幸多朗, 日浅雅博, 天眞寛文, ASHTAR MOHANNAD, 清水宗, 比嘉佳基, 寺町順平, 原田武志, 中村信元, 三木浩和, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 :
不動は骨吸収と骨髄腫進展を促進させる,
日本骨代謝学会学術集会プログラム抄録集, 149, 2020年10月. 天眞寛文, ASHTAR MOHANNAD, 寺町順平, 日浅雅博, 谷本幸多朗, 清水宗, 比嘉佳基, 原田武志, 大浦雅博, 曽我部公子, 中村信元, 三木浩和, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 :
抗腫瘍薬が誘導するROSは破骨細胞分化を促進する:Xanthine oxidase阻害剤febuxostatの治療効果．,
日本骨代謝学会学術集会プログラム抄録集, 148, 2020年10月. Takeshi Harada, Yusuke Inoue, Hirofumi Tenshin, Asuka Oda, Masahiro Oura, Kimiko Sogabe, Ryohei Sumitani, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe :
Versatile anti-myeloma effects by elotuzumab: impact on γδT cells and osteoclasts,
The 82nd Annual Meeting of Japanese Soceity of Hematology, Oct. 2020. 安倍正博 :
教育講演:多発性骨髄腫に対する治療の進歩と分子標的療法の開発,
第24回日本がん分子標的治療学会学術集会, 2020年10月. Tania Afroj, 荻野広和, 三橋惇志, 米田浩人, 香西博之, 大塚憲司, 軒原浩, 安倍正博, 西岡安彦 :
腫瘍免疫における線維細胞の免疫調節機能の検討,
第24回日本がん分子標的治療学会学術集会, 2020年10月. 吉田守美子, 工藤千晶, 辻本賀美, 安井沙耶, 遠藤ふうり, 桝田志保, 三井由加里, 倉橋清衛, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 船木真理, 福本誠二, 安倍正博, 松久宗英 :
血糖管理入院でのテストステロン値の変化の検討,
第63回日本糖尿病学会年次学術集会, 2020年10月. 遠藤逸朗, 近藤剛史, 倉橋清衛, 松本俊夫, 安倍正博, 福本誠二 :
家族歴を有するFGF23関連低リン血症性骨軟化症の一例,
日本骨代謝学会学術集会プログラム抄録集, 150, 2020年10月. 倉橋清衛, 村井純平, 堀太貴, 住谷龍平, 原田武志, 中村信元, 金井麻衣, 櫻井明子, 原倫世, 桝田志保, 吉田守美子, 遠藤逸朗, 松本俊夫, 安倍正博, 福本誠二 :
高1,25(OH)2D血症による高Ca血症を来したホジキンリンパ腫の一例,
日本骨代謝学会学術集会プログラム抄録集, 150, 2020年10月.

(キーワード): *Calcitriol Dacarbazine(治療的利用) Doxorubicin(治療的利用) *Hodgkin病(合併症,病理学,薬物療法) Vinblastine(治療的利用) *高カルシウム血症(病因,病理学,薬物療法) 免疫組織化学 Brentuximab Vedotin(治療的利用) ヒト高齢者(65~79) 男

Hirofumi Tenshin, アシテルモハナッド, Jumpei Teramachi, Masahiro Hiasa, Kotaro Tanimoto, Sou Shimizu, 比嘉佳基, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
抗腫瘍薬が誘導するROSは破骨細胞分化を促進する Xanthine oxidase阻害剤febuxostatの治療効果,
The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 148, Oct. 2020.

(キーワード): Xanthine Oxidase(拮抗物質・阻害物質) / 活性酸素 (reactive oxygen species) / 抗腫瘍剤(毒性・副作用) / 骨吸収(化学的誘発,薬物療法,実験的) / 細胞分化 (cell differentiation) / 破骨細胞 (osteoclast) / 破骨細胞分化因子 / Febuxostat(治療的利用) / RAW264.7細胞 / マウス / 動物 (animal)

大浦雅博, 中村信元, 堀太貴, 曽我部公子, 原田武志, 藤井志朗, 三木浩和, 賀川久美子, 小林智子, 尾矢剛志, 安倍正博 :
結節性紅斑と悪性腫瘍関連血球貪食症候群を惹起した骨髄異形成症候群の1例,
臨床血液, Vol.61, No.10, 1542, 2020年10月.

(キーワード): *骨髄異形成症候群(合併症) *紅斑-結節性(病因) *血球貪食性リンパ組織球症(病因) ヒト中年(45~64) 男

中村昌史, 三木浩和, 大浦雅博, 川田知代, 堀太貴, 村井純平, 住谷龍平, 曽我部公子, 高橋真美子, 原田武志, 藤井志朗, 中村信元, 賀川久美子, 菅崎幹樹, 徳永尚樹, 池亀彰茂, 森下英理子, 安倍正博 :
クロスミキシングテストの特徴的な所見が診断の契機となったプレカリクレイン欠乏症の1例,
臨床血液, Vol.61, No.10, 1537-1538, 2020年10月.

(キーワード): *Prekallikrein(欠損・欠乏) *血液凝固異常(診断) *血液凝固検査ヒト中年(45~64) 男

岩佐みゆき, 西京子, 佐藤功志, 浅井孝仁, 前田拓也, 中村昌史, 門田宗之, 田中久美子, 河北直也, 武田美佐, 藤永裕之, 近藤明男, 木下倫子, 酒井陽子, 田中克哉, 安倍正博, 西村匡司, 香美祥二 :
メディカルゾーン(MZ)重点研修プログラムにおける麻酔化融合研修,
第261回徳島医学会学術集会, 2020年8月. 川原綾香, 倉橋清衛, 工藤千晶, 鎌田基夢, 加藤真介, 富岡有紀子, 辻本賀美, 安井沙耶, 遠藤ふうり, 桝田志保, 三井由加里, 吉田守美子, 粟飯原賢一, 遠藤逸朗, 福本誠二, 松久宗英, 安倍正博 :
歩行不能だったが，多職種の高度な連携と患者特性に配慮したケアにより自宅生活可能となった高度肥満症の一例,
第261回徳島医学会学術集会, 2020年8月. 平岡栞名, 三井由加里, 三木浩和, 佐藤正大, 東桃代, 遠藤ふうり, 宮髙紘輔, 辻誠士郎, 桝田志保, 倉橋清衛, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 福本誠二, 松久宗英, 安倍正博 :
発熱・全身リンパ節腫脹で発症し，リンパ節生検で診断しえた結核性リンパ節炎の一例,
第261回徳島医学会学術集会, 2020年8月. 吉田守美子, 工藤千晶, 辻本賀美, 安井沙耶, 遠藤ふうり, 桝田志保, 三井由香里, 倉橋清衛, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 松久宗英, 安倍正博, 福本誠二 :
糖尿病教育入院でのテストステロン値の変化の検討,
第93回日本内分泌学会学術総会, Vol.96, No.1, 287, 2020年7月. 堀大貴, 中村信元, 原田武志, 住谷龍平, 村井純平, 高松信敏, 手束文威, 安倍正博 :
若年で発症しアトピー性皮膚炎に合併した化膿性脊椎炎の1例,
第123回日本内科学会四国地方会, 2020年7月. 岡田直人, 神農麻里奈, 中村信元, 三木浩和, 渡邊浩良, 合田光寛, 中馬真幸, 武智研志, 座間味義人, 桐野靖, 中村敏己, 寺岡和彦, 安倍正博, 石澤啓介 :
血液凝固因子製剤の在庫適正化に向けた取り組みによる薬剤廃棄額の削減効果,
日本病院薬剤師会雑誌, Vol.56, No.7, 803-808, 2020年7月.

(要約): 血友病治療に用いる血液凝固因子製剤(coagulation factor:以下，CF)は高価である一方で，在庫流動性が低いという製剤的性質を有するが，これまで適切な在庫管理法の報告はない．徳島大学病院は2017年4月から，診療科と連携したCFの在庫適正化の取り組みを開始した．取り組み開始前である2015年4月~2017年3月の期間と，取り組み開始後である2017年4月~2019年3月の期間における血友病患者数，CF調剤薬剤数に差はなかったが，取り組み開始後のCF廃棄額は取り組み開始前と比較して78.4
(キーワード): 血液凝固因子(治療的利用) / 血友病A(薬物療法) / 病院在庫管理 / ヒト / 新生児 / 乳児(1~23ヶ月) / 幼児(2~5) / 小児(6~12) / 青年期(13~18) / 成人(19~44) / 中年(45~64) / 高齢者(65~79) / 男 / 女

原田武志, 天眞寛文, 谷本幸多朗, 清水宗, 安倍正博 :
骨髄腫細胞はHDAC1とIRF4を介しSLAMF7を過剰発現する,
第24回日本がん分子標的治療学会学術集会, 2020年6月. 秦真公人, 菅崎幹樹, 井上雄介, 多田智紀, 吉田裕子, 中尾隆之, 住谷龍平, 中村信元, 安倍正博, 高山哲治 :
特徴的な形態像を呈し鑑別に苦慮したIgDκ型多発性骨髄腫の一症例,
日本検査血液学会雑誌, Vol.21, S244, 2020年6月.

(キーワード): *IgD(血液) *骨髄腫-多発性(診断,免疫学) ヒト高齢者(65~79) 男

村井純平, 堀太貴, 川田知代, Ryohei Sumitani, 宇高憲吾, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, Kumiko Kagawa, Masahiro Abe, Hirokazu Miki, 桝田志保, Itsuro Endo and Seiji Fukumoto :
高ビタミンD血症による高Ca血症を来したホジキンリンパ腫の一例,
Shikoku Acta Medica, Vol.76, No.1-2, 124, Apr. 2020.

(キーワード): Calcitriol(毒性・副作用,血液) / Hodgkin病(合併症,薬物療法) / Vitamin D(毒性・副作用,血液) / 高カルシウム血症(化学的誘発) / 腫瘍多剤併用療法 / ヒト / 高齢者(65~79) / 男

遠藤優香, 田島穂澄, 岡田直人, 中村信元, 賀川久美子, 藤井志朗, 三木浩和, 石澤啓介, 安倍正博, 佐藤陽一 :
機械学習を用いたゲノム情報によるシタラビン投与の副作用発現予測モデルの構築,
日本薬学会第140年会, 2020年3月. 武井みのり, 岡田直人, 中村信元, 賀川久美子, 藤井志朗, 三木浩和, 石澤啓介, 安倍正博, 佐藤陽一 :
遺伝情報を用いた機械学習による抗がん剤投与の味覚障害発現予測モデルの構築,
日本薬学会第140年会, 2020年3月. 遠藤優香, 田島穂澄, 岡田直人, 中村信元, 賀川久美子, 藤井志朗, 三木浩和, 石澤啓介, 安倍正博, 佐藤陽一 :
機械学習を用いたゲノム情報によるシタラビン投与の副作用発現予測モデルの構築,
日本薬学会年会要旨集, 26M-am07S, 2020年3月.

(キーワード): Cytarabine(毒性・副作用) / 皮膚疾患(化学的誘発) / リスク評価 / 機械学習 / ヒト

桝田志保, 吉田守美子, 工藤千晶, 辻本賀美, 安井沙耶, 遠藤ふうり, 三井由加里, 倉橋清衛, 遠藤逸朗, 安倍正博 :
診断に時間を要したバセドウ病による甲状腺クリーゼの一例,
第31回日本老年医学会四国地方会, 2020年2月. 川原綾香, 倉橋清衛, 工藤千晶, 鎌田基夢, 加藤真介, 富岡有紀子, 辻本賀美, 安井沙耶, 遠藤ふうり, 桝田志保, 三井由加里, 吉田守美子, 粟飯原賢一, 遠藤逸朗, 福本誠二, 松久宗英, 安倍正博 :
歩行不能だったが，多職種の密な連携と患者特性に配慮したケアにより自宅生活可能となった高度肥満症の一例,
第260回徳島医学会学術集会大塚講堂, 2020年2月. 菊池結愛, 坂井ちか, 櫻井明子, 金井麻衣, 大西幸代, 安倍正博, 遠藤逸朗 :
TAK1阻害による炎症性サイトカイン誘導性筋萎縮の改善,
第43回徳島県医学検査学会, 2019年12月. 毛利咲恵, 鶴尾美穂, 坂東佐知子, 添木武, 松本直也, 湯浅智之, 黒田暁生, 佐田政隆, 安倍正博, 寺澤敏秀, 松久宗英 :
発熱，高血糖，低K血症を契機に一時的にBrugada型心電図を呈した糖尿病の1例,
日本糖尿病学会中国四国地方会第57回総会, 2019年12月. 奥村慈子, 鶴尾美穂, 湯浅智之, 瀬尾浩二, 木内美瑞穂, 金川泰彦, 黒田暁生, 松本俊夫, 安倍正博, 寺澤敏秀, 松久宗英 :
急激にせん妄状態が悪化した高齢2型糖尿病の1例,
日本糖尿病学会中国四国地方会第57回総会, 2019年12月. 上野裕子, 鶴尾美穂, 湯浅智之, 黒田暁生, 木内美瑞穂, 西正晴, 安井沙耶, 安倍正博, 寺澤敏秀, 松久宗英 :
高齢者糖尿病患者に対するLCDEと徳島市糖尿病サポーター(TCDS)の連携した取り組み,
日本糖尿病学会中国四国地方会第57回総会, 2019年12月. 三井由加里, 黒田暁生, 石津将, 桝田志保, 倉橋清衛, 吉田守美子, 明比祐子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 松久宗英 :
頻回インスリン注射療法下の1型糖尿病患者における基礎インスリン比率の検討,
日本糖尿病学会中国四国地方会第57回総会, 2019年12月. 鶴尾美穂, 黒田暁生, 湯浅智之, 木内美瑞穂, 安井沙耶, 松本俊夫, 安倍正博, 寺澤敏秀, 松久宗英 :
TIR(Time-In-Range)とHbA1cとの関連∼HbA1cと組み合わせる血糖管理方法∼,
日本糖尿病学会中国四国地方会第57回総会, 2019年12月. 森岡隆子, 黒田暁生, 鶴尾美穂, 堀筋冨士子, 秋田賢子, 松本幸恵, 湯浅智之, 松本俊夫, 安倍正博, 寺澤敏秀, 松久宗英 :
予測低血糖自動注入停止型インスリンポンプが有効だった高齢1型糖尿病例,
日本糖尿病学会中国四国地方会第57回総会, 2019年12月. 斎村玉緒, 黒田暁生, 鶴尾美穂, 福井健壮, 掘貫理恵, 藤原敏孝, 湯浅智之, 松本俊夫, 安倍正博, 寺澤敏秀, 松久宗英 :
脳悪性リンパ腫を発症した2がた糖尿病の1例,
日本糖尿病学会中国四国地方会第57回総会, 2019年12月. 三井由加里, 黒田暁生, 石津将, 倉橋清衛, 吉田守美子, 明比祐子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 松久宗英 :
頻回インスリン注射療法下の1型糖尿病患者における基礎インスリン比率の検討,
第19回日本先進糖尿病治療研究会・第17回1型糖尿病研究会, 2019年11月. 髙士祐一, 沢津橋俊, 遠藤逸朗, 安倍正博, 松久宗英, 松本俊夫, 福本誠二 :
FGFR1は血中FGF23濃度を制御するリン感知受容体である,
第38回日本骨代謝学会学術集会, 2019年10月. 天眞寛文, 寺町順平, 日浅雅博, 谷本幸多朗, ASHTAR MOHANNAD, Bat-Erdene Ariunzaya, 岩佐昌美, 原田武志, 中村信元, 三木浩和, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 :
TAK1阻害は関節リウマチにおけるNLRP3インフラマソーム誘導性の炎症および骨破壊を抑制する,
日本骨代謝学会学術集会プログラム抄録集, 190, 2019年10月. 谷本幸多朗, 日浅雅博, 岩浅亮彦, 天眞寛文, 寺町順平, ASHTAR MOHANNAD, 岩佐昌美, 小田明日香, 曾我部公子, 大浦雅博, 原田武志, 中村信元, 三木浩和, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 :
不動性骨吸収の亢進は骨髄内の骨髄腫進展を促進させる．,
日本骨代謝学会学術集会プログラム抄録集, 2019年10月. 天眞寛文, 寺町順平, 日浅雅博, 谷本幸多朗, ASHTAR MOHANNAD, Ariunzaya Bat-Erdene, 岩佐昌美, 原田武志, 中村信元, 三木浩和, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 :
TAK1阻害は関節リウマチにおけるNLRP3インフラマソーム誘導性の炎症および骨破壊を抑制する．,
第37回日本骨代謝学会学術集会, 2019年10月. 谷本幸太朗, 日浅雅博, 天眞寛文, 寺町順平, ASHTAR MOHANNAD, 岩佐昌美, 小田明日香, 曽我部公子, 大浦雅博, 原田武志, 中村信元, 三木浩和, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 :
不動性骨吸収の亢進は骨髄内の骨髄腫進展を促進させる,
第37回日本骨代謝学会学術集会, 2019年10月. 吉田守美子, 池田康将, 粟飯原賢一, 安倍正博 :
心血管病におけるアンドロゲン受容体の意義,
第30回日本性機能学会学術総会, 2019年9月. 辻本賀美, 三井由加里, 工藤千晶, 安井沙耶, 遠藤ふうり, 桝田志保, 倉橋清衛, 吉田守美子, 明比祐子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 福本誠二 :
勤務時間の影響で副腎皮質機能異常が疑われた2例,
日本内分泌学会第19回四国支部学術集会, 2019年9月. 工藤千晶, 枡田志保, 辻本賀美, 安井沙耶, 遠藤ふうり, 三井由加里, 倉橋清衛, 吉田守美子, 明比祐子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 新谷保実, 福本誠二 :
両側副腎偶発腫瘍で発見された123I-MIBGシンチ陰性の褐色細胞腫の一例,
日本内分泌学会第19回四国支部学術集会, 2019年9月. Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, 小田明日香, Kotaro Tanimoto, Soh Shimizu, Ashtar Mohannad, Takeshi Harada, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
NLRP3 inflammasome-mediated inflammation and osteoclastic bone resorption in rheumatoid arthritis : the therapeutic roles of TAK1 inhibition,
16th Meeting of Bone Biology Forum, Aug. 2019. 安井沙耶, 桝田志保, 吉田守美子, 辻本賀美, 工藤千晶, 遠藤ふうり, 三井由加里, 倉橋清衛, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 船木真理, 松久宗英, 安倍正博, 福本誠二 :
成長ホルモン分泌不全症と甲状腺機能低下症を呈した小児がん経験者の一例,
第259回徳島医学会学術集会(令和元年度夏期), 2019年8月. 吉田守美子, 粟飯原賢一, 安倍正博 :
エイコサペントエン酸は酸化ストレス抑制を介してアンジオテンシンII刺激による心血管リモデリングを抑制する,
第37回内分泌代謝学サマーセミナー, 2019年7月. 吉田守美子, 粟飯原賢一, 安倍正博 :
心血管病と性差 ∼アンドロゲンを中心に∼,
第61回日本老年医学会学術集会, 2019年6月. 宮高絋輔, 吉田守美子, 遠藤ふうり, 枡田志保, 三井由加里, 倉橋清衛, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 福本誠二, 船木真理, 松立吉弘, 軒原浩, 西岡安彦, 安倍正博, 松久宗英 :
免疫チェックポイント阻害薬投与後に1型糖尿病を発症した2例,
第62回日本糖尿病学会年次学術集会, 2019年5月. 十川悠香, 吉岡昌美, 南明香, 福井誠, 日野出大輔, 中村信元, 安倍正博 :
自家末梢血幹細胞移植患者の口腔ケアによる口腔粘膜炎障害の低減効果,
第68回日本口腔衛生学会総会, 2019年5月. 安宅克博, 中村信元, 大浦雅博, 曽我部公子, 原田武志, 藤井志朗, 三木浩和, 賀川久美子, 西岡安彦, 安倍正博 :
長期にわたる血小板減少が先行した芽球性形質細胞様樹状細胞腫瘍の1例,
第120回日本内科学会四国地方会, 2019年5月. 原田武志, Oda Asuka, 天眞寛文, 寺町順平, 大浦雅博, 曽我部公子, 岩佐昌美, 藤井志朗, 三木浩和, 賀川久美子, 秀島輝, Anderson C. Kenneth, 安倍正博 :
The novel therapeutic strategy targeting the HDAC1-IRF4-PIM2 pathway in myeloma cells,
The 44th Annual Meeting of the Japanese Society of Myeloma, 2019年5月.

(キーワード): Multiple myeloma / Class-I HDAC / IRF4 / Pim-2

金井麻衣, 松岡飛翔, 遠藤逸朗, 大西幸代, 髙士祐一, 倉橋清衛, 吉田守美子, 粟飯原賢一, 安倍正博, 福本誠二, 松本俊夫 :
鉄製剤投与によるFGF23関連低リン血症モデル作成の試み,
第92回日本内分泌学会学術総会, Vol.95, No.1, 422, 2019年5月. 髙士祐一, 小迫英尊, 沢津橋俊, 木下祐加, 伊東伸朗, 安倍正博, 松久宗英, 加藤茂明, 松本俊夫, 福本誠二 :
FGFR1はFGF23濃度調節を媒介するリン感知受容体である,
第92回日本内分泌学会学術総会, Vol.95, No.1, 333, 2019年5月. 吉田守美子, 粟飯原賢一, 安倍正博 :
骨格筋アンドロゲン受容体と耐糖能異常の検討,
第92回日本内分泌学会総会, 2019年5月. 寺町順平, 天眞寛文, 日浅雅博, 安倍正博 :
TAK1阻害は腫瘍と微小環境との相互作用を遮断し腫瘍進展・骨破壊病変形成を抑制する,
第124回日本解剖学会総会・全国学術集会, 2019年3月. 谷垣雄都, 山口裕大, 岡田直人, 中村信元, 賀川久美子, 藤井志朗, 三木浩和, 石澤啓介, 安倍正博, 佐藤陽一 :
ゲノムワイド関連解析を用いたテイコプラニン・バンコマイシン投与による皮疹発現および血中濃度関連遺伝子座の同定,
日本薬学会第139年会, 2019年3月. 宮高紘輔, 遠藤ふうり, 三井由加里, 枡田志保, 倉橋清衛, 吉田守美子, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 船木真理, 福本誠二, 軒原浩, 西岡安彦, 安倍正博, 松久宗英 :
抗PD-1抗体投与後に1型糖尿病を発症した1例,
第258回徳島医学会学術集会ポスターセッション, 2019年2月. 金子遥祐, 近藤真代, 髙橋直希, 飛梅亮, 荻野広和, 佐藤正大, 三木浩和, 後東久嗣, 安倍正博, 西岡安彦 :
多発小結節影を認めたHIV陽性ニューモシスチス肺炎の1例,
第119回日本内科学会四国地方会, 2018年12月. 大森理央, 岡田直人, 中村信元, 賀川久美子, 藤井志朗, 三木浩和, 石澤啓介, 安倍正博, 佐藤陽一 :
ゲノムワイド関連解析を用いたビンクリスチンによる末梢神経障害発現関連遺伝子の同定,
第57回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, 2018年11月. 山口裕大, 谷垣雄都, 岡田直人, 中村信元, 賀川久美子, 藤井志朗, 三木浩和, 石澤啓介, 安倍正博, 佐藤陽一 :
CYP遺伝子多型とバンコマイシンの副作用発現及び血中濃度との関連解析,
第57回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, 2018年11月. 吉田守美子, 原倫世, 山口佑樹, 近藤剛史, 遠藤ふうり, 筒井康継, 桝田志保, 倉橋清衛, 明比祐子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 中島公平, 福本誠二 :
急速に腫瘍が増大し悪性転化が疑われたCushing病の1例,
第28回臨床内分泌代謝Update, 2018年11月. 鶴尾美穂, 黒田暁生, 湯浅智之, 木内美瑞穂, 曽我部公子, 加部一行, 瀬尾浩二, 西正晴, 松本直也, 金川泰彦, 安倍正博, 松本俊夫, 寺澤敏秀, 松久宗英 :
リブレ使用糖尿病患者の検討,
日本糖尿病学会中国四国地方会第56回総会, 2018年10月. 原倫世, 吉田守美子, 細井美希, 遠藤ふうり, 筒井康継, 桝田志保, 倉橋清衛, 明比祐子, 遠藤逸朗, 粟飯原賢一, 中島公平, 坂東良美, 安倍正博, 福本誠二 :
脳内，副鼻腔，下垂体に炎症を認めステロイドが著効した1例,
第22回日本臨床内分泌病理学会学術総会, 2018年10月. Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Oda Asuka, Bat-Erdene Ariunzaya, Takeshi Harada, Iwasa Masami, Shiroh Fujii, Kimiko Sogabe, Shingen Nakamura, Hirokazu Miki, Masahiro Oura, Kumiko Kagawa, Itsuro Endo, Toshio Matsumoto and Masahiro Abe :
Mechanisms of TAK1 over-activation in myeloma cells and TAK1-mediated myeloma growth and bone destruction,
第80回日本血液学会学術集会, Oct. 2018. 岩佐昌美, 原田武志, Ariunzaya Bat-Erdene, 小田明日香, 曽我部公子, 大浦雅博, 寺町順平, 藤井志朗, 中村信元, 三木浩和, 賀川久美子, 安倍正博 :
HDAC阻害による骨髄腫細胞のIFN-γ-STAT1- PD-L1経路の増強効果,
第80回日本血液学会学術集会, 2018年10月.

(キーワード): Multiple myeloma

Ashtar Mohannad, Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Kotaro Tanimoto, Oda Asuka, Iwasa Masami, Takeshi Harada, Ariunzaya Erdene Bat, Kimiko Sogabe, Oura Masahiro, Shiroh Fujii, Kumiko Kagawa, Shingen Nakamura, Hirokazu Miki, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
Roles of ROS in induction of bone disease and cancer treatment-induced bone loss in myeloma.,
The 80th Annual Meeting of the Japanese Society of Hematology, Oct. 2018. Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Kotaro Tanimoto, Mohannad Ashtar, Ariunzaya Bat-Erdene, Iwasa Masami, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Kimiko Sogabe, Oura Masahiro, Shiroh Fujii, Kumiko Kagawa, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
Inverse regulation of c-FLIP-mediated survival in myeloma cells and osteoclasts by TRAIL.,
The 80th Annual Meeting of the Japanese Society of Hematology, Oct. 2018. Kotaro Tanimoto, Masahiro Hiasa, Hirofumi Tenshin, Jumpei Teramachi, Oda Asuka, Mohannad Ashtar, Ariunzaya Bat-Erdene, Iwasa Masami, Kimiko Sogabe, Oura Masahiro, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
Impact of denervation-induced paralysis and mechanical unloading on tumor expansion in myeloma.,
The 80th Annual Meeting of the Japanese Society of Hematology, Oct. 2018. Masahiro Hiasa, Jumpei Teramachi, Hirofumi Tenshin, Kotaro Tanimoto, Ariunzaya Bat-Erdene, Mohannad Ashtar, Masami Iwasa, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Kimiko Sogabe, Oura Masahiro, Shiroh Fujii, Kumiko Kagawa, Oda Asuka, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
The effects of cathepsin K inhibition on osteocytes: its role in bone restoration in MM bone disease.,
The 80th Annual Meeting of the Japanese Society of Hematology, Oct. 2018. 幾尾真理子, 杉崎圭, 寺町順平, 田原栄俊, 安倍正博, 伊藤孝司 :
骨芽前駆細胞の骨分化経路BMP/Smadは，核内DNA結合Smadを標的とする多発性骨髄腫由来分泌小胞exosomeによって抑制される,
第91回日本生化学会大会, 2018年9月. 倉橋清衛, 遠藤逸朗, 近藤剛史, 遠藤ふうり, 原倫世, 桝田志保, 吉田守美子, 明比祐子, 坂東良美, 粟飯原賢一, 安倍正博, 福本誠二 :
ソマトスタチンアナログ製剤にて著明な縮小がみられたGH産生マクロアデノーマの1例,
第22回日本臨床内分泌病理学会, 2018年9月. 粟飯原賢一, 吉田守美子, 遠藤ふうり, 筒井康継, 原倫世, 桝田志保, 倉橋清衛, 乙田敏城, 湯浅智之, 遠藤逸朗, 森本佳奈, 黒田暁生, 明比祐子, 船木真理, 松久宗英, 福本誠二, 安倍正博 :
原発性アルドステロン症におけるミネラルコルチコイド受容体拮抗薬の血管機能への影響,
第18回日本内分泌学会四国支部学術集会, 2018年9月. 山上紘規, 吉田守美子, 遠藤ふうり, 原倫世, 筒井康継, 桝田志保, 倉橋清衛, 明比祐子, 遠藤逸朗, 粟飯原賢一, 大崎裕亮, 梶龍兒, 髙士祐一, 安倍正博, 福本誠二 :
壊死性ミオパチーを合併したX連鎖性低リン血症性くる病・骨軟化症の一例,
第18回日本内分泌学会四国支部学術集会, 2018年9月. 遠藤逸朗, 大西幸代, 倉橋清衛, 寺町順平, 日浅雅博, 天眞寛文, 福本誠二, 安倍正博, 松本俊夫 :
カルシウム感知受容体活性型変異マウスにおける骨強度の低下,
第36回日本骨粗鬆症学会各術集会, 2018年7月. 寺町順平, 天眞寛文, 日浅雅博, 遠藤逸朗, 松本俊夫, 安倍正博 :
TAK1 inhibition impairs myeloma cell-bone marrow interaction to reduce myeloma growth and bone destruction,
日本骨代謝学会学術集会プログラム抄録集, 2018年7月. 日浅雅博, 寺町順平, 天眞寛文, 谷本幸多朗, ASHTAR MOHANNAD, Ariunzaya Bat-Erdene, 岩佐昌美, 原田武志, 中村信元, 三木浩和, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 :
カテプシンK阻害による多発性骨髄腫骨病変部の骨量回復プロセスにおける骨細胞の役割．,
第36回日本骨代謝学会学術集会, 2018年7月. 天眞寛文, 寺町順平, 日浅雅博, 谷本幸多朗, ASHTAR MOHANNAD, Ariunzaya Bat-Erdene, 岩佐昌美, 原田武志, 中村信元, 三木浩和, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 :
TAK1阻害はTRAILによる破骨細胞活性化作用を遮断させると同時にTRAILの抗骨髄腫作用を増強する,
第36回日本骨代謝学会学術集会, 2018年7月. 天眞寛文, 寺町順平, 日浅雅博, 小田明日香, 谷本幸多朗, ASHTAR MOHANNAD, Ariunzaya Bat-Erdene, 岩佐昌美, 原田武志, 中村信元, 三木浩和, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 :
TAK1による破骨細胞に対するTRAILの生存・細胞死シグナル制御機構．,
第4回日本骨免疫学会, 2018年6月. 谷本幸多朗, 日浅雅博, 天眞寛文, 寺町順平, 小田明日香, ASHTAR MOHANNAD, Ariunzaya Bat-Erdene, 岩佐昌美, 曽我部公子, 大浦雅弘, 原田武志, 中村信元, 三木浩和, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 :
神経切断による麻痺と免荷の骨髄腫の進展への影響．,
第4回日本骨免疫学会, 2018年6月. 吉田守美子, 原倫世, 桝田志保, 倉橋清衛, 黒田暁生, 遠藤逸朗, 粟飯原賢一, 安倍正博, 松久宗英 :
高齢者における糖尿病教育入院中の体組成の変化,
第60回日本老年医学会学術集会, 2018年6月. 黒田暁生, 山田美鈴, 冨永ゆかり, 鈴木麗子, 田蒔基行, 明比祐子, 髙士祐一, 石津将, 古賀大輔, 井本逸勢, 倉橋清衛, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 安倍正博, Kevin Ferreri, 松久宗英 :
膵β細胞特異的PCRによる膵β細胞死の検出,
第61回日本糖尿病学会年次学術集会, 2018年5月. 吉田守美子, 原倫世, 細井美希, 山上紘規, 山口佑樹, 桝田志保, 倉橋清衛, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 船木真理, 福本誠二, 安倍正博, 松久宗英 :
糖尿病教育入院における筋肉量の変化,
第61回日本糖尿病学会年次学術集会, 2018年5月. 山上紘規, 吉田守美子, 原倫世, 細井美希, 山口佑樹, 桝田志保, 倉橋清衛, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 船木真理, 福本誠二, 安倍正博, 松立吉弘, 松久宗英 :
免疫チェックポイント阻害薬投与後に甲状腺機能異常と劇症1型糖尿病を発症した1例,
第61回日本糖尿病学会年次学術集会, 2018年5月. 粟飯原賢一, 上元良子, 石川カズ江, 森本佳奈, 桝田志保, 山上綋規, 山口佑樹, 原倫世, 細井美希, 倉橋清衛, 吉田守美子, 乙田敏城, 湯浅智之, 黒田暁生, 明比祐子, 遠藤逸朗, 船木真理, 福本誠二, 松久宗英, 東博之, 安倍正博 :
生活習慣病患者の尿中酸化ストレス指標における糖尿病および薬物療法の影響,
第61回日本糖尿病学会年次学術集会, 2018年5月. 岩佐昌美, 原田武志, Ariunzaya Bat-Erdene, 小田明日香, 前田悠作, 高橋真美子, 大浦雅博, 寺町順平, 藤井志朗, 中村信元, 三木浩和, 賀川久美子, 安倍正博 :
パノビスタットによる骨髄腫細胞のIFN-γ-STAT1- PD-L1経路の増強,
The 43rd Annual Meeting of the Japanese Society of Myeloma, 2018年5月.

(キーワード): Multiple myeloma

原田武志, Oda Asuka, 寺町順平, Bat-Erdene Ariunzaya, 岩佐昌美, Maeda Yusaku, 中村信元, Oura Masahiro, 藤井志朗, 三木浩和, 賀川久美子, Hideshima Teru, Anderson C. Kenneth, 安倍正博 :
HDAC1/3 inhibition disrupts the IRF4-Pim-2 pathway to induce effective myeloma cell death,
The 43rd Annual Meeting of the Japanese Society of Myeloma, 2018年5月.

(キーワード): Multiple myeloma / Class-I HDAC / IRF4 / Pim-2

遠藤逸朗, Dong Bingzi, 大西幸代, 吉田守美子, 粟飯原賢一, 相澤慎一, 福本誠二, 安倍正博, 松本俊夫 :
常染色体優性低Ca血症1型モデルマウスにおける骨強度の低下,
第91回日本内分泌学会学術総会, 2018年4月. 吉田守美子, 原倫世, 細井美希, 山上紘規, 山口佑樹, 桝田志保, 倉橋清衛, 黒田暁生, 遠藤逸朗, 粟飯原賢一, 船木真理, 福本誠二, 浜田大輔, 松久宗英, 安倍正博 :
待機的高リスク整形外科手術における血糖管理の効果,
第91回日本内分泌学会学術総会, 2018年4月. 原倫世, 桝田志保, 吉田守美子, 細井美希, 山上紘規, 山口佑樹, 倉橋清衛, 黒田暁生, 遠藤逸朗, 松久宗英, 安倍正博 :
急性合併症を来した高齢1型糖尿病の2症例,
第29回日本老年医学会四国地方会, 2018年2月. 斎村玉緒, 鶴尾美穂, 黒田暁生, 湯浅智之, 加部一行, 木内美瑞穂, 吉田守美子, 山上紘規, 近藤剛史, 西正晴, 松本直也, 松本俊夫, 安倍正博, 寺澤敏秀, 松久宗英 :
フラッシュグルコースモニタリングシステムにより施設入所可能となった高齢1型糖尿病の一例,
日本糖尿病学会中国四国地方会第55回総会抄録集, 2017年11月. 山口佑樹, 吉田守美子, 原倫世, 細井美希, 山上紘規, 桝田志保, 倉橋清衛, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 船木真理, 福本誠ニ, 安倍正博, 柏原秀也, 吉川幸造, 松久宗英 :
高度肥満症に対するスリーブ状胃切除術の長期の耐糖能異常改善効果の検討,
日本糖尿病学会中国四国地方会第55回総会抄録集, 2017年11月. 國方脩登, 吉田守美子, 原倫世, 細井美希, 山上紘規, 山口佑樹, 桝田志保, 倉橋清衛, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 船木真理, 福本誠ニ, 安倍正博, 浜田大輔, 松久宗英 :
待機的整形外科手術の術後経過における糖尿病の影響,
日本糖尿病学会中国四国地方会第55回総会抄録集, 2017年11月. 鶴尾美穂, 松本俊夫, 黒田暁生, 湯浅智之, 加部一行, 近藤剛史, 木内美瑞穂, 井野口卓, 山上紘規, 松本直也, 西正晴, 寺澤敏秀, 安倍正博, 松久宗英 :
SLADHを発症した高齢1型糖尿病の一例,
日本糖尿病学会中国四国地方会第55回総会抄録集, 2017年11月. 谷垣雄都, 佐藤陽一, 山口裕大, 岡田直人, 中村信元, 賀川久美子, 藤井志朗, 三木浩和, 石澤啓介, 安倍正博, 山内あい子 :
テイコプラニン投与による副作用発現および血中濃度とCYP遺伝子多型との関連解析,
第56回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, 2017年10月. 田島穂澄, 佐藤陽一, 岡田直人, 中村信元, 賀川久美子, 藤井志朗, 三木浩和, 石澤啓介, 安倍正博, 山内あい子 :
シタラビン投与による副作用発現と代謝経路関連遺伝子多型の関連解析,
第56回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, 2017年10月. Jumpei Teramachi, Masahiro Hiasa, Oda Asuka, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Masami Iwasa, Masahiro Oura, Yusaku Maeda, Shiroh Fujii, Kumiko Kagawa, Hirokazu Miki, Itsuro Endo, Toshio Matsumoto and Masahiro Abe :
Disruption of myeloma cell-bone marrow interaction by TAK-1 inhibition,
第80回日本血液学会学術集会, Oct. 2017. 原倫世, 吉田守美子, 山口佑樹, 細井美希, 山上紘規, 桝田志保, 倉橋清衛, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 松久宗英, 船木真理, 福本誠ニ, 安倍正博 :
当院での免疫チェックポイント阻害薬による下垂体機能低下症の5例,
第17回日本内分泌学会四国支部学術集会抄録集, 2017年9月. 西京子, 安倍正博, 田中久美子, 西野豪志, 飛梅威 :
徳島大学病院の多職種連携による若手教育ー院内ネットワーク研修を地域包括ケアシステムにおける医療従事者の確保・養成につなぐー,
第1回徳島県地域包括ケアシステム学会, 2017年8月. 天眞寛文, 寺町順平, 小田明日香, 天知良太, 日浅雅博, 渡邉佳一郎, Ariunzaya Baterdene, 岩佐昌美, 藤井志朗, 賀川久美子, 中村信元, 三木浩和, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 :
TRAILは破骨細胞を活性化させるが，TAK1阻害により骨髄腫細胞とともに破骨細胞にもTRAILのアポトーシス誘導活性が惹起できる,
第35回日本骨代謝学会学術集会, 2017年7月. 吉田守美子, 粟飯原賢一, 倉橋清衛, 遠藤逸朗, 安倍正博 :
骨格筋のアンドロゲン受容体と耐糖能異常,
第35回内分泌代謝学サマーセミナー, 2017年7月. 大森理央, 佐藤陽一, 木口美沙妃, 岡田直人, 中村信元, 賀川久美子, 藤井志朗, 三木浩和, 石澤啓介, 安倍正博, 山内あい子 :
ビンクリスチンによる副作用発現とMDR1遺伝子多型との関連性,
第20回日本医薬品情報学会総会・学術大会, 2017年7月. 山口裕大, 佐藤陽一, 谷垣雄都, 岡田直人, 中村信元, 賀川久美子, 藤井志朗, 三木浩和, 石澤啓介, 安倍正博, 山内あい子 :
バンコマイシン投与による副作用発現及び血中濃度とCYP遺伝子多型との関連解析,
第20回日本医薬品情報学会総会・学術大会, 2017年7月. 森本佳奈, 桝田志保, 倉橋清衛, 田蒔基行, 近藤剛史, 吉田守美子, 湯浅智之, 黒田暁生, 遠藤逸朗, 福本誠二, 松久宗英, 安倍正博, 東博之, 粟飯原賢一 :
生活習慣病患者における血管内皮機能制御に関わる臨床指標の検討,
第49回日本動脈硬化学会総会・学術集会, 2017年7月. 李悦子, 瀧本朋美, 小田直輝, 仁木恵里加, 伊藤正一, 荻山佳子, 須賀健一, 中川竜二, 三木浩和, 安倍正博 :
抗Jra保有妊婦に重症胎児貧血を認め，児のJra抗原発現抑制が疑われた1症例,
第65回日本輸血細胞治療学会総会, 2017年6月. 天眞寛文, 寺町順平, 小田明日香, 天知良太, 日浅雅博, Baterdene Ariunzaya, 渡邉佳一郎, 中村信元, 三木浩和, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 :
TAK1阻害はTRAILの抗骨髄腫作用を増強するともに骨吸収促進活性を抑制活性に変換する．,
第42回日本骨髄腫学会, 2017年5月. 天知良太, 中村信元, 日浅雅博, 小田明日香, バットエルデネアリウンザヤ, 寺町順平, 天眞寛文, 渡邉佳一郎, 三木浩和, 賀川久美子, 藤井志朗, 田中栄二, 松本俊夫, 安倍正博 :
骨形成誘導による骨髄腫細胞のエネルギー代謝の抑制,
第42回日本骨髄腫学会学術集会, 2017年5月. 西山美月, 倉橋清衛, 桝田志保, 近藤剛史, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 小松まち子, 福本誠二, 安倍正博 :
維持透析中に管理困難な高Ca血症を契機に診断されたサルコイドーシスの一例,
第116回日本内科学会四国地方会, 2017年5月. 森本佳奈, 桝田志保, 倉橋清衛, 田蒔基行, 近藤剛史, 吉田守美子, 湯浅智之, 黒田暁生, 明比祐子, 遠藤逸朗, 船木真理, 福本誠ニ, 松久宗英, 安倍正博, 粟飯原賢一 :
糖尿病患者における自律神経機能をアルブミン尿の相互関連および各病態に影響を及ぼす因子解析,
第60回日本糖尿病学会年次学術集会, 2017年5月. 吉田守美子, 粟飯原賢一, 倉橋清衛, 近藤剛史, 遠藤逸朗, 湯浅智之, 福本誠二, 安倍正博 :
骨格筋におけるアンドロゲン受容体の耐糖能への影響,
第90回日本内分泌学会学術総会, 2017年4月. 森本佳奈, 高橋優花, 山下沙織, 上元良子, 石川カズ江, 倉橋清衛, 近藤剛史, 吉田守美子, 黒田暁生, 遠藤逸朗, 湯浅智之, 松久宗英, 東博之, 安倍正博, 粟飯原賢一 :
生活習慣病患者の血管内皮機能に関わる因子の臨床的検討,
第90回日本内分泌学会学術集会抄録集, 2017年4月. 寺町順平, 日浅雅博, 天眞寛文, 岡村裕彦, 安倍正博, 羽地達次 :
骨髄腫腫瘍進展と骨破壊病変形成におけるTAK-1の枢軸的役割,
第122回日本解剖学会総会・全国学術集会, 2017年3月. 岡本恵暢, 中村信元, 上村宗範, 住谷龍平, 高橋真美子, 藤井志朗, 賀川久美子, 安倍正博, 三木浩和 :
発熱と下肢対麻痺で発症した血管内大細胞型B細胞性リンパ腫の2例,
四国医学雑誌, Vol.72, No.5-6, 236-237, 2016年12月.

(キーワード): 下肢 / 発熱(病因) / 対麻痺(病因) / リンパ腫 / びまん性大細胞型B細胞性(合併症,薬物療法,病理学) / 血管腫瘍(合併症,薬物療法,病理学) / 血管内(合併症,薬物療法,病理学) / ヒト (Homo sapiens) / 中年(45∼64) / 高齢者(65∼79) / 女性 (female)

桝田志保, 吉田守美子, 倉橋清衛, 近藤剛史, 遠藤逸朗, 安倍正博, 黒田暁生, 松久宗英, 粟飯原賢一, 福本誠二 :
メーグルコシダーゼ阻害薬による腸管気腫症の一例,
第115回日本内科学会四国地方会, 2016年11月. 上田浩之, 遠藤逸朗, 近藤剛史, 倉橋清衛, 吉田守美子, 安倍正博, 黒田暁生, 松久宗英, 粟飯原賢一, 福本誠二 :
デノスマブによる耐糖能改善,
第115回日本内科学会四国地方会, 2016年11月. 近藤剛史, 遠藤逸朗, 明比祐子, 倉橋清衛, 田蒔基行, 吉田守美子, 黒田暁生, 粟飯原賢一, 松久宗英, 安倍正博, 福本誠二 :
免疫チェックポイント阻害剤で中枢性副腎不全を来した2例,
第26回臨床内分泌代謝Update, 2016年11月. 山下沙織, 吉田守美子, 高橋優花, 粟飯原賢一, 倉橋清衛, 近藤剛史, 森本佳奈, 田蒔基行, 湯浅智之, 黒田暁生, 明比祐子, 遠藤逸朗, 船木真理, 福本誠二, 松久宗英, 安倍正博 :
糖尿病教育入院における酸化ストレス減少に影響を及ぼす因子の検討,
日本糖尿病学会中国四国地方会第54回総会, 2016年11月. 鶴尾美穂, 黒田暁生, 湯浅智之, 近藤剛史, 木内美瑞穂, 松井尚子, 細井恵美子, 安倍正博, 松本俊夫, 松久宗英, 寺澤敏秀 :
γグロブリン療養後に一過性のGAD抗体価上昇がみられた糖尿病の一例,
日本糖尿病学会中国四国地方会第54回総会, 2016年11月. 天眞寛文, 寺町順平, 小田明日香, 天知良太, 日浅雅博, 渡邉佳一郎, 中村信元, 三木浩和, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 :
30. 天真寛文, 寺町順平, 小田明日香, 天知良太, , ,破骨細胞系細胞はアポトーシス誘引因子TRAILを生存促進・破骨細胞形成誘導因子として利用する:TAK1-Pim-2経路の役割,
第19回日本癌と骨病変研究会, 2016年11月. 斎村玉緒, 鶴尾美穂, 黒田暁生, 近藤剛史, 湯浅智之, 木内美瑞穂, 安倍正博, 松本俊夫, 寺澤敏秀, 松久宗英 :
インスリンポンプの院内検定の試み,
日本糖尿病学会中国四国地方会第54回総会, 2016年11月. 荒瀬美晴, 近藤剛史, 黒田暁生, 倉橋清衛, 田蒔基行, 吉田守美子, 明比祐子, 遠藤逸朗, 粟飯原賢一, 福本誠二, 安倍正博, 松久宗英 :
術前後で持続血糖モニター(CGM)を比較したアドレナリン優位褐色細胞腫の二例,
日本糖尿病学会中国四国地方会第54回総会, 2016年11月. 上田浩之, 近藤剛史, 黒田暁生, 倉橋清衛, 田蒔基行, 吉田守美子, 明比祐子, 遠藤逸朗, 粟飯原賢一, 福本誠二, 安倍正博, 松久宗英 :
基礎インスリンが不要であった膵性糖尿病の一例,
日本糖尿病学会中国四国地方会第54回総会, 2016年11月. 森本佳奈, 桝田志保, 倉橋清衛, 田蒔基行, 近藤剛史, 吉田守美子, 湯浅智之, 黒田暁生, 明比祐子, 遠藤逸朗, 船木真理, 福本誠二, 松久宗英, 安倍正博, 粟飯原賢一 :
糖尿病患者における心電図R-R間隔変動係数に影響を及ぼす因子の検討,
日本糖尿病学会中国四国地方会第54回総会, 2016年11月. 日浅雅博, 天知良太, 天眞寛文, 堀内信也, 安倍正博, 石丸直澄, 田中栄二 :
RelBは古典的NF-κB経路の活性化を阻害し骨癒合不全と偽関節形成を予防する,
日本矯正歯科学会大会プログラム・抄録集., 192., 2016年11月. 寺町順平, 日浅雅博, 岡村裕彦, 安倍正博, 羽地達次 :
骨髄腫の腫瘍進展と骨破壊病変形成におけるTAK1の枢軸的な役割,
日本解剖学会第71回中国・四国支部学術集会, 2016年10月. 寺町順平, 森裕史, 越智保夫, 天知良太, 小田明日香, 日浅雅博, 原田武志, 藤井志朗, 中村信元, 三木浩和, 賀川久美子, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 :
Potent induction of bone formation by anti-resorptive cathepsin K inhibitor in myeloma.,
第77回日本血液学会学術集会,, 2016年10月. 天眞寛文, 寺町順平, 小田明日香, 天知良太, 日浅雅博, 渡邉佳一郎, 中村信元, 三木浩和, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 :
TAK1 inhibition subverts TRAIL-mediated osteoclastogenesis.,
第77回日本血液学会学術集会,, 2016年10月. 天知良太, 日浅雅博, 寺町順平, 小田明日香, 天眞寛文, 渡邉佳一郎, 中村信元, 三木浩和, 賀川久美子, 藤井志朗, 遠藤逸郎, 田中栄二, 松本俊夫, 安倍正博 :
Mechanism of the TRPV1 up-regulatation in myeloma cells and adaptation to an acidic microenvironment.,
第77回日本血液学会学術集会,, 2016年10月. 渡邉佳一郎, 寺町順平, 天知良太, 小田明日香, 天眞寛文, 岩浅正美, 日浅雅博, 中村信元, 遠藤逸郎, 川谷誠, 長田裕之, 田中栄二, 松本俊夫, 安倍正博 :
Amelotin gene expression is temporarily being upregulated at the initiation of apoptosis induced by TGFb1 in mouse gingival epithelial cells,
第77回日本血液学会学術集会,, 2016年10月. Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Kiyoe Kurahashi, Takeshi Kondo, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe :
TAK-1 inhibition disrupts Pim-2-associated and Pim-2-independent key signaling pathways to effectively suppress tumor growth and restore bone formation in myeloma,
第78回日本血液学会学術集会, Oct. 2016. 高橋優花, 山下沙織, 吉田守美子, 桝田志保, 森本佳奈, 倉橋清衛, 田蒔基行, 近藤剛史, 黒田暁生, 湯浅智之, 遠藤逸朗, 松久宗英, 福本誠二, 東博之, 安倍正博, 粟飯原賢一 :
生活習慣病患者における血管内皮機能正常群および低下群の臨床指標に関する検討,
第16回日本内分泌学会四国支部学術集会, 2016年9月. 山上紘規, 倉橋清衛, 森本佳奈, 近藤剛史, 遠藤逸朗, 明比祐子, 吉田守美子, 黒田暁生, 粟飯原賢一, 松久宗英, 福本誠二, 安倍正博 :
バセドウ病を合併したTSH産生下垂体腺腫の一例,
第16回日本内分泌学会四国支部学術集会, 2016年9月. 遠藤ふうり, 倉橋清衛, 森本佳奈, 近藤剛史, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 黒田暁生, 明比祐子, 船木真理, 松久宗英, 福本誠二, 安倍正博 :
日和見感染を合併したACTH依存性Cushing症候群の1例,
第253回徳島医学会学術集会(平成28年度夏期), 2016年7月. 渡邉佳一郎, 寺町順平, 天知良太, 小田明日香, 天眞寛文, 日浅雅博, 中村信元, 三木浩和, 遠藤逸朗, 川谷誠, 長田裕之, 田中栄二, 松本俊夫, 安倍正博 :
リベロマイシンAによる酸性環境での骨髄腫細胞の治療抵抗性の克服,
日本骨代謝学会学術集会プログラム抄録集 (1349-0761)34回 Page183(2016.07), 183, 2016年7月. 天眞寛文, 寺町順平, 小田明日香, 天知良太, 日浅雅博, 渡邉佳一郎, 中村信元, 三木浩和, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 :
破骨細胞はTAK1の発現誘導を介しアポトーシスを抑制しTRAILにより成熟活性化される,
日本骨代謝学会学術集会プログラム抄録集 (1349-0761)34回 Page183(2016.07), 183, 2016年7月. 倉橋清衛, 遠藤逸朗, Nakamura Mayuko, Ohnishi Yukiyo, 近藤剛史, Aizawa Shinichi, 福本誠二, 安倍正博 :
カルシウム感知受容体活性型変異による耐糖能異常,
第34回日本骨代謝学会学術総会, 2016年7月. 寺町順平, 日浅雅博, 小田明日香, 天眞寛文, 天知良太, 原田武志, 渡邉佳一郎, 中村信元, 三木浩和, 遠藤逸朗, 羽地達次, 松本俊夫, 安倍正博 :
骨髄腫腫瘍進展と骨破壊病変形成におけるTAK1-Pim-2経路の役割,
日本骨代謝学会学術集会プログラム抄録集, 2016年7月. 寺町順平, 日浅雅博, 小田明日香, 原田武志, 天眞寛文, 中村信元, 天知良太, 藤井志朗, 渡邉佳一郎, 賀川久美子, 三木浩和, 遠藤逸朗, 羽地達次, 松本俊夫, 安倍正博 :
Pim-2は骨髄腫における破骨細胞形成促進の必須媒介因子である,
第41回日本骨髄腫学会学術集会, 2016年5月. 天眞寛文, 寺町順平, 小田明日香, 天知良太, 日浅雅博, 渡邉佳一郎, 中村信元, 三木浩和, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 :
TRAILは破骨細胞に細胞死を誘導せず，破骨細胞分化・生存を促進する.,
第41回日本骨髄腫学会, 2016年5月. 布村俊幸, 吉田守美子, 森本佳奈, 倉橋清衛, 近藤剛史, 遠藤逸朗, 粟飯原賢一, 松久宗英, 松本俊夫, 安倍正博 :
副腎に接する神経線維腫を合併したレックリングハウゼン病の1例,
第114回日本内科学会四国地方会, 2016年5月. 倉橋清衛, 河野恵理, 宮本千伸, 津川和江, 親泊美帆, 木村千寿子, 久永哲, 森本雅俊, 山川哲生, 谷内秀輔, 張君, 三宅雅人, 安倍正博, 親泊政一 :
ラベルフリー測定によるハイスループットスクリーニングを用いた新規インスリン分泌促進薬の探索,
第59回日本糖尿病学会年次学術集会, 2016年5月. 橋本晶慶, 鶴尾美穂, 秋田賢子, 森岡隆子, 黒田暁生, 湯浅智之, 近藤剛史, 木内美瑞穂, 松本俊夫, 安倍正博, 松久宗英, 寺澤敏秀 :
糖尿病教室のスタッフ間の相互評価による改善効果,
第59回日本糖尿病学会年次学術集会, 2016年5月. 森本佳奈, 粟飯原賢一, 吉田守美子, 倉橋清衛, 近藤剛史, 田蒔基行, 黒田暁生, 遠藤逸朗, 船木真理, 福本誠二, 松久宗英, 安倍正博 :
減塩による2型糖尿病入院症例の降圧予測指標,
第59回日本糖尿病学会年次学術集会, 2016年5月. 森本佳奈, 粟飯原賢一, 吉田守美子, 倉橋清衛, 田蒔基行, 近藤剛史, 黒田暁生, 遠藤逸朗, 松久宗英, 安倍正博 :
血糖管理入院症例における減塩降圧効果と関連する因子および降圧薬に関する検討,
第5回臨床高血圧フォーラム, 2016年5月. 森本佳奈, 粟飯原賢一, 吉田守美子, 倉橋清衛, 近藤剛史, 田蒔基行, 黒田暁生, 遠藤逸朗, 松久宗英, 安倍正博 :
2型糖尿病患者の塩分制限による降圧効果を規定する因子の検討,
第89回日本内分泌学会学術総会, 2016年4月. 粟飯原賢一, 吉田守美子, 森本佳奈, 倉橋清衛, 近藤剛史, 田蒔基行, 黒田暁生, 遠藤逸朗, 松久宗英, 安倍正博 :
心筋リモデリングおよび頸動脈硬化症におけるアンジオテンシンII受容体拮抗薬の効果検証,
第89回日本内分泌学会学術総会, 2016年4月. 山上紘規, 倉橋清衛, 森本佳奈, 近藤剛史, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 黒田暁生, 明比祐子, 船木真理, 松久宗英, 福本誠二, 安倍正博 :
インターフェロンβ治療中に糖尿病ケトアシドーシスを契機とし，急性発症1A型糖尿病と診断された一例,
第252回徳島医学会学術集会長井記念ホール, 2016年2月. 森本佳奈, 粟飯原賢一, 吉田守美子, 倉橋清衛, 田蒔基行, 近藤剛史, 黒田暁生, 遠藤逸朗, 松久宗英, 安倍正博 :
2型糖尿病患者における血糖指標と減塩がもたらす血圧低下との連関,
第252回徳島医学会学術集会長井記念ホール, 2016年2月. 林亜紀, 近藤剛史, 遠藤逸朗, 倉橋清衛, 吉田守美子, 福本誠二, 粟飯原賢一, 安倍正博 :
オクトレオチドLARで画像上，下垂体腺腫が消失した先端巨大症の一例,
第113回日本内科学会四国地方会, 2015年12月. 森本佳奈, 近藤剛史, 遠藤逸朗, 倉橋清衛, 田蒔基行, 吉田守美子, 黒田暁生, 松久宗英, 福本誠二, 粟飯原賢一, 安倍正博 :
著明な低カルシウム血症を来した胃癌の骨転移の一例,
第25回臨床内分泌Update, 2015年11月. 小山広士, 近藤剛史, 森本佳奈, 遠藤逸朗, 倉橋清衛, 田蒔基行, 吉田守美子, 黒田暁生, 松久宗英, 福本誠二, 粟飯原賢一, 安倍正博 :
ACTH，コルチゾール基礎値正常のACTH単独欠損症の一例,
第25回臨床内分泌Update, 2015年11月. 近藤剛史, 遠藤逸朗, 森本佳奈, 倉橋清衛, 田蒔基行, 吉田守美子, 黒田暁生, 松久宗英, 福本誠二, 粟飯原賢一, 安倍正博 :
テタニーで来院し，Gitelman症候群を疑った一例,
第25回臨床内分泌Update, 2015年11月. 伊勢孝之, 西條良仁, 三木浩和, 賀川久美子, 瀬野弘光, 上野理絵, 原知也, 齋藤友子, 坂東美佳, 坂東左知子, 伊藤浩敬, 松浦朋美, 山口浩司, 飛梅威, 八木秀介, 山田博胤, 添木武, 若槻哲三, 安倍正博, 佐田政隆 :
auto-PBSCT とBortezomibの併用が著効した高度心機能障害を伴う原発性心アミロイドーシスの1例,
第107回日本循環器学会四国地方会, 2015年11月. 花房剛志, 岡田直人, 生田賢治, 小中健, 川添和義, 中村敏己, 寺岡和彦, 安倍正博, 石澤啓介 :
自家末梢血幹細胞移植併用大量化学療法施行時の味覚障害に対するクライオセラピーの有用性,
第54回中国四国支部学術大会(高知), 2015年11月. 花房剛志, 岡田直人, 生田賢治, 小中健, 川添和義, 中村敏己, 寺岡和彦, 安倍正博, 石澤啓介 :
自家末梢血幹細胞移植併用大量化学療法施行時の味覚障害に対するクライオセラピーの有用性,
第54回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会,, 2015年11月. 粟飯原賢一, 吉田守美子, 森本佳奈, 倉橋清衛, 近藤剛史, 田蒔基行, 黒田暁生, 明比祐子, 遠藤逸朗, 船木真理, 福本誠二, 松久宗英, 安倍正博 :
2型糖尿病患者の左室形態および機能における強化インスリン療法の効果,
日本糖尿病学会第53回中国四国地方会, 2015年10月. 鶴尾美穂, 黒田暁生, 近藤剛史, 湯浅智之, 木内美瑞穂, 安倍正博, 松本俊夫, 松久宗英, 寺澤敏秀 :
Sensor Angmented Pump(SAP)療法が有効であった高齢1型糖尿病の1例,
第53回日本糖尿病学会中国四国地方会, 2015年10月. 岡田祐輝, 近藤剛史, 森本佳奈, 倉橋清衛, 田蒔基行, 吉田守美子, 黒田暁生, 遠藤逸朗, 松久宗英, 福本誠二, 粟飯原賢一, 安倍正博 :
高CPR血症からグリメピリド誤内服を診断し得た遷延性低血糖の一例,
第53回日本糖尿病学会中国四国地方会米子コンベンションセンター, 2015年10月. 粟飯原賢一, 吉田守美子, 森本佳奈, 倉橋清衛, 近藤剛史, 田蒔基行, 黒田暁生, 明比祐子, 遠藤逸朗, 船木真理, 福本誠二, 松久宗英, 安倍正博 :
2型糖尿病患者の左室形態および機能における強化インスリン療法の効果,
第53回日本糖尿病学会中国・四国地方会米子コンベンションセンター, 2015年10月. 林亜紀, 吉田守美子, 黒田暁生, 七篠あつ子, 苛原稔, 鶴尾美穂, 森本佳奈, 倉橋清衛, 近藤剛史, 田蒔基行, 明比祐子, 遠藤逸朗, 船木真理, 松久宗英, 福本誠二, 粟飯原賢一, 安倍正博 :
分娩前に10g/日以上の蛋白尿を合併し，出産に至った糖尿病腎症の1例,
日本糖尿病学会中国四国地方会第53回総会, 2015年10月. 谷口諭, 黒田暁生, 田蒔基行, 銀花, 森本佳奈, 倉橋清衛, 近藤剛史, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 松久宗英 :
CGM iPRO2と人工膵臓STG-55との測定グルコース濃度の比較,
第53回日本糖尿病学会中国・四国地方会米子コンベンションセンター, 2015年10月. Ryota Amachi, Masahiro Hiasa, Jumpei Teramachi, A Oda, Hirofumi Tenshin, Keiichiro Watanabe, Shingen Nakamura, H Miki, Kumiko Kagawa, Shiroh Fujii, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
Mechanism of the TRPV1 up-regulatation in myeloma cells and adaptation to an acidic microenvironment,
第77回日本血液学会学術集会, Oct. 2015. Keiichiro Watanabe, Jumpei Teramachi, H Mori, Y Ochi, Ryota Amachi, A Oda, Masahiro Hiasa, T Harada, Shiroh Fujii, Shingen Nakamura, H Miki, Kumiko Kagawa, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
Potent induction of bone formation by anti-resorptive cathepsin K inhibitor in myeloma,
第77回日本血液学会学術集会, Oct. 2015. 森本佳奈, 粟飯原賢一, 吉田守美子, 倉橋清衛, 田蒔基行, 近藤剛史, 黒田暁生, 遠藤逸朗, 松久宗英, 安倍正博 :
2型糖尿病入院患者における減塩血圧低下効果に影響を及ぼす血糖指標の検討,
第38日本高血圧学会総会, 2015年10月. 粟飯原賢一, 吉田守美子, 森本佳奈, 倉橋清衛, 田蒔基行, 近藤剛史, 黒田暁生, 遠藤逸朗, 松久宗英, 安倍正博 :
長期のアンジオテンシンII受容体拮抗薬基盤高血圧治療による心筋リモデリングおよび頸動脈硬化症への効果検証,
第38日本高血圧学会総会, 2015年10月. 寺町順平, 日浅雅博, Asuka Oda, 天眞寛文, 天知良太, Takeshi Harada, 渡邉佳一郎, 藤井志朗, 賀川久美子, 中村信元, 三木浩和, 遠藤逸朗, 羽地達次, 松本俊夫, 安倍正博 :
Potent suppression of osteoclastogenesis in myeloma by Pim inhibition,
第77回日本血液学会学術集会, 2015年10月. Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Keiichiro Watanabe, Shiroh Fujii, Kumiko Kagawa, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe :
Tumor reduction and bone restoration in myeloma by TAK-1 inhibition,
第77回日本血液学会学術集会, Oct. 2015. 寺町順平, 日浅雅博, 岡村裕彦, 安倍正博, 羽地達次 :
Pim-2を標的とした骨髄腫細胞による骨破壊の抑制,
日本解剖学会第70回中国・四国支部学術集会, 2015年10月. 森本佳奈, 近藤剛史, 遠藤逸朗, 倉橋清衛, 田蒔基行, 吉田守美子, 黒田暁生, 松久宗英, 福本誠二, 粟飯原賢一, 安倍正博 :
診断まで長時間を要したACTH分泌低下症の一例,
第15回日本内分泌学会四国支部学術集会高知大学, 2015年9月. 加藤正樹, 森本佳奈, 粟飯原賢一, 吉田守美子, 倉橋清衛, 田蒔基行, 近藤剛史, 黒田暁生, 遠藤逸朗, 松久宗英, 福本誠二, 安倍正博 :
2型糖尿病患者の減塩療法による血圧低下に関連する因子の解析,
第15回日本内分泌学会四国支部学術集会, 2015年9月. 森本佳奈, 粟飯原賢一, 吉田守美子, 倉橋清衛, 田蒔基行, 近藤剛史, 黒田暁生, 遠藤逸朗, 松久宗英, 安倍正博 :
2型糖尿病における血糖指標と減塩がもたらす血圧低下との連関,
第251回徳島医学会学術集会ポスター, 2015年8月. 寺町順平, 日浅雅博, 小田明日香, 天眞寛文, 天知良太, 中村信元, 三木浩和, 遠藤逸朗, 羽地達次, 松本俊夫, 安倍正博 :
Pim阻害による骨髄種骨病変の治療:破骨細胞形成の抑制,
日本骨代謝学会学術集会プログラム抄録集, 2015年7月. 寺町順平, 日浅雅博, 小田明日香, 天眞寛文, 天知良太, 中村信元, 三木浩和, 遠藤逸朗, 羽地達次, 松本俊夫, 安倍正博 :
骨髄腫腫瘍進展と骨破壊病変形成における TAK-1の枢軸的役割,
日本骨代謝学会学術集会プログラム抄録集, 2015年7月. 天眞寛文, 寺町順平, 小田明日香, 天知良太, 渡邉佳一郎, 中村信元, 三木浩和, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 :
TRAILは破骨細胞分化・生存を促進する:TAK-1による生と死の運命制御,
第1回日本骨免疫学会, 137, 2015年7月. 天知良太, 日浅雅博, 寺町順平, 小田明日香, 天眞寛文, 渡邉佳一郎, 中村信元, 賀川久美子, 三木浩和, 藤井志朗, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 :
酸環境での骨髄腫細胞のDR4発現抑制:酸によるエピジェネティックな遺伝子発現制御,
第1回日本骨免疫学会, 108, 2015年7月. 天知良太, 日浅雅博, 寺町順平, 小田明日香, 渡邉佳一郎, 天眞寛文, 中村信元, 三木浩和, 遠藤逸朗, 近藤剛史, 田中栄二, 松本俊夫, 安倍正博 :
酸性環境での骨髄腫細胞のTRPV1の発現亢進と酸環境への適応,
日本骨代謝学会学術集会プログラム抄録集, 165, 2015年7月. 天眞寛文, 寺町順平, 小田明日香, 天知良太, 日浅雅博, 渡邉佳一郎, 中村信元, 三木浩和, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 :
アポトーシス誘導因子TRAILによる破骨細胞分化・生存の促進,
日本骨代謝学会学術集会プログラム抄録集, 164, 2015年7月. 寺町順平, 日浅雅博, 小田明日香, 原田武志, 天知良太, 天眞寛文, 三木浩和, 中村信元, 藤井志朗, 賀川久美子, 遠藤逸朗, 松本俊夫, 安倍正博 :
Pim阻害による骨髄腫骨吸収亢進の抑制,
第40回日本骨髄腫学会学術集会, 2015年5月. 寺町順平, 日浅雅博, 小田明日香, 原田武志, 天知良太, 天眞寛文, 三木浩和, 中村信元, 藤井志朗, 賀川久美子, 遠藤逸朗, 松本俊夫, 安倍正博 :
TAK-1は骨髄腫腫瘍進展と骨破壊病変形成の枢軸的な媒介因子である,
第40回日本骨髄腫学会学術集会, 2015年5月. 中村信元, 三木浩和, 安倍正博 :
Pim阻害薬と抗骨髄腫治療薬の併用効果の検討,
第40回日本骨髄腫学会, 2015年5月. Bingzi Dong, 遠藤逸朗, 近藤剛史, 大西幸代, 阪上浩, 相澤慎一, 安倍正博, 松本俊夫 :
Interleukin-11は脂肪細胞分化を抑制する,
第88回日本内分泌学会, 2015年4月. 中村信元, 東桃代, 三木浩和, 賀川久美子, 安倍正博 :
当院で経験した重症熱性血小板減少症候群の3例,
第89回日本感染症学会, 2015年4月. 岡田直人, 伏谷秀治, 東桃代, 中村敏己, 寺岡和彦, 川添和義, 渡邊浩良, 安倍正博, 石澤啓介 :
病棟薬剤によるプロトコルに基づく薬物治療管理の実践∼抗MRSA薬の適正使用に対する効果∼,
日本薬学会第135年会, 2015年3月. 岡田直人, 伏谷秀治, 東桃代, 中村敏己, 寺岡和彦, 川添和義, 渡邊浩良, 安倍正博, 石澤啓介 :
病棟薬剤によるプロトコルに基づく薬物治療管理の実践∼抗MRSA薬の適正使用に対する効果,
日本薬学会第135年会(神戸), 2015年3月. 丸橋朋子, 中村信元, 曽我部公子, 八木ひかる, 高橋真美子, 宇高憲吾, 藤井志朗, 三木浩和, 賀川久美子, 安倍正博, 西條敦郎, 中野万有里, 東桃代, 西岡安彦, 近藤憲保, 井内新, 藤田博己, 馬原文彦 :
当院で経験した重症熱性血小板減少症候群の3例,
第250回徳島医学会学術集会, 2015年2月. 寺町順平, 日浅雅博, 原田武志, 天知良太, 賀川久美子, 三木浩和, 中村信元, 藤井志朗, 遠藤逸朗, 松本俊夫, 安倍正博 :
Therapeutic impact of Pim inhibition on myeloma bone disease: blockade of NF-B-mediated suppression of osteoblastogenesis and stimulation of osteoclastogenesis,
日本血液学会, 2014年10月. 天知良太, 日浅雅博, 渡邉佳一郎, 寺町順平, 小田明日香, 渡邉佳一郎, 中村信元, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 :
酸が惹起する骨髄腫細胞の酸感受と生存シグナルの悪循環,
日本骨代謝学会学術集会プログラム抄録集, 225, 2014年7月. Dong Bingzi, 遠藤逸朗, 近藤剛史, 大西幸代, 安倍正博, 福本誠二, 網塚憲生, 長谷川智香, 相澤慎一, 松本俊夫 :
常染色体優性低Ca血症モデルマウスに対するcalcilyticsの効果,
第32回日本骨代謝学会学術集会, 2014年7月. 寺町順平, 日浅雅博, 小田明日香, 天知良太, 中村信元, 遠藤逸朗, 松本俊夫, 安倍正博 :
Pim-2キナーゼはTNF-αによる骨芽細胞分化抑制および破骨細胞形成促進の必須媒介因子である:Pim阻害薬の骨髄腫骨病変改善効果,
第32回日本骨代謝学会学術集会, 2014年7月. 遠藤逸朗, 安倍正博, 松本俊夫 :
骨転移に対するdenosumab療法:低Ca血症発現の実態と対策,
第32回日本骨代謝学会, 2014年7月. 遠藤逸朗, 安倍正博, 松本俊夫 :
骨転移に対するdenosumab療法, --- 低Ca血症発現の実態と対策 ---,
第32回日本骨代謝学会学術集会, 2014年7月. Keiichiro Watanabe, Masahiro Abe, H Mori, K Udaka, M Iwasa, D Hanson, Ryota Amachi, Masahiro Hiasa, T Harada, Shiroh Fujii, Shingen Nakamura, H Miki, Kumiko Kagawa, Itsuro Endo, Eiji Tanaka and Toshio Matsumoto :
Bone restoration and tumor suppression in myeloma by cathepsin K inhibition with Bortezomib,
第75回日本血液学会学術集会, Oct. 2013. 天知良太, 渡邉佳一郎, 日浅雅博, 安倍正博, 松本俊夫, 田中栄二 :
酸性環境が骨髄腫細胞の破骨細胞活性に及ぼす影響,
第72回日本矯正歯科学会大会プログラム・抄録集, 2013年10月. 安倍正博 :
骨髄腫骨病変と腫瘍免疫．シンポジウム5骨免疫と炎症性疾患,
第34回日本炎症・再生医学会, 2013年7月. 近藤直樹, 藤田拓朗, 河上和代, 野上浩子, 守時政宏, 西岡聡, 西島陽子, 祖父江理, 森脇久美子, 原大雅, 河野雅和, 久保治信, 田中勉, 渡瀬謙仁, 美馬晶, 高橋利和, 土井俊夫, 三木浩和, 安倍正博 :
免疫抑制療法実施中に赤芽球癆再発した血液透析患者の1例,
第58回日本透析医学会総会, 2013年6月. 中村教泰, 林幸壱朗, 三木浩和, 尾崎修治, 安倍正博, 松本俊夫, 石村和敬 :
有機シリカ・マルチ蛍光ナノプローブによるSeamless蛍光イメーシング,
第8回日本分子イメージング学会学術集会, 2013年5月. Ryota Amachi, Keiichiro Watanabe, Shiroh Fujii, T Harada, H Miki, S Nakamura, A Oda, Masahiro Hiasa, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
An acdic milieu confers the resistance to TRAIL in myeloma cells through the PI3K-Akt-mediated epigenetic down-regulation of the TRAIL receptor DR4,
International Bone and Mineral Society 2013, May 2013. Keiichiro Watanabe, Masahiro Abe, H Mori, Ryota Amachi, Masahiro Hiasa, T Harada, Shiroh Fujii, S Nakamura, H Miki, K Kagawa, I Endo, Eiji Tanaka and Toshio Matsumoto :
Induction of cathepsin K induce bone formation in myeloma osteolytic lesions,
International Bone and Mineral Society 2013, May 2013. Ryota Amachi, Keiichiro Watanabe, Shiroh Fujii, T Harada, H Miki, S Nakamura, A Oda, Masahiro Hiasa, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe :
An acdic milieu suppresses histone acetylation in myeloma cells to down-regulate the TRAIL receptor DR4 expression,
14th International Myeloma Workshop, Apr. 2013. Keiichiro Watanabe, Masahiro Abe, Ryota Amachi, Masahiro Hiasa, T Harada, Shiroh Fujii, S Nakamura, H Miki, K Kagawa, I Endo, Eiji Tanaka and Toshio Matsumoto :
Induction of bone formation in myeloma osteolytic lesions by cathepsin K inhibition,
14th International Myeloma Workshop, Apr. 2013. 三木浩和, 中村信元, 竹内恭子, 原田武志, 岩佐昌美, 藤井志朗, 賀川久美子, 安倍正博, 松本俊夫 :
赤芽球癆を合併した多中心性Castleman病の1例,
日本内科学会第107回四国地方会, 2012年12月. 遠藤逸朗, 大薗卓也, 斉藤光恵, 松本俊夫, 安倍正博 :
骨転移に対するdenosumab 120mg皮下注後の重症低Ca血症発現の実態,
癌と骨代謝研究会, 2012年11月. 松浦元一, 山田諭, 柴田恵理子, 渡瀬謙仁, 岸史, 岸誠司, 美馬晶, 長井幸二郎, 安部秀斉, 中村信元, 安倍正博, 土井俊夫 :
腎生検にてγ重鎖沈着症が疑われた糸球体沈着症の一例,
第42回日本腎臓学会西部学術大会, 2012年10月. Masahiro Abe :
Multiple myeloma: Topics in basic science applicable to the development of novel therapies,
第74回日本血液学会総会, Oct. 2012. 藤井志朗, 安倍正博, 天知良太, 渡邉佳一郎, 日浅雅博, 竹内恭子, 岩佐昌美, 原田武志, 中村信元, 三木浩和, 賀川久美子, 松本俊夫 :
Pim inhibition preferentially induces anti-myeloma activity in an acidic milien,
第74回日本血液学会学術集会, 2012年10月. Masahiro Hiasa, Masahiro Abe, Kumiko Kagawa, Hirokazu Miki, Shingen Nakamura, Harada Takeshi, Fujii Shirou, Keiichiro Watanabe, Ryota Amachi, Kenzo Asaoka and Toshio Matsumoto :
Pim-2 acts as a common downstream mediator to suppress bone formation in myeloma.,
第74回に本血液学会, Oct. 2012. Ryota Amachi, Masahiro Abe, Keiichiro Watanabe, Masahiro Hiasa, Eiji Tanaka and Toshio Matsumoto :
An acidic milieu suppresses DR4 editing and induces p22 c-FLIP to cause myeloma resistance to TRAIL,
第74回日本血液学会学術集会, Oct. 2012. 原田武志, 尾崎修治, 岩佐昌美, 藤井志朗, 中村信元, 三木浩和, 賀川久美子, 柴田泰伸, 重清俊雄, 岡田直人, 長尾多美子, 鈴木麗子, 先山正二, 安倍正博, 松本俊夫 :
徳島県のエイズ拠点病院におけるHIV感染症及び後天性免疫不全症候群の現状,
第245回徳島県医学会学術総会, 2012年7月. 渡邉佳一郎, 安倍正博, 天知良太, 日浅雅博, 中村信元, 遠藤逸郎, 森裕史, 田中栄二, 松本俊夫 :
カテプシンK 阻害剤KK1-300-01 は骨髄腫骨病変部の骨破壊を抑制し骨形成を惹起する,
第30回日本骨代謝学会学術大会, 217, 2012年7月. 日浅雅博, 安倍正博, 新垣理恵子, 山田安希子, 淺岡憲三, 松本俊夫, 林良夫, 石丸直澄 :
RelBは古典的NF-κB経路の活性化を阻害し骨芽細胞分化を正に制御する,
第30回日本骨代謝学会, 2012年7月. 天知良太, 安倍正博, 渡邉佳一郎, 中村信元, 日浅雅博, 田中栄二, 松本俊夫 :
酸性環境は骨髄腫細胞にDR4 の発現抑制とcFLIP の活性化を惹起しTRAIL に対する抵抗性を獲得させる,
第30回日本骨代謝学会学術集会, 259, 2012年7月. 大黒由加里, 中村信元, 岩佐昌美, 原田武志, 藤井志朗, 賀川久美子, 安倍正博, 松本俊夫, 三木浩和 :
腰痛と副腎不全症状で発症した両側副腎原発DLBCLの1例,
日本内科学会第106回四国地方会, 2012年6月. 中村教泰, 林幸壱朗, Aziz Awaad, 三木浩和, 尾崎修治, 安倍正博, 松本俊夫, 石村和敬 :
有機シリカ粒子技術を用いた近赤外蛍光ナノプローブの作製とユニバーサル蛍光イメージング,
第7回日本分子イメージング学会学術集会, 2012年5月. 原田武志, 藤井志朗, 中村信元, 三木浩和, 中野綾子, 賀川久美子, 竹内恭子, 安倍正博, 松本俊夫 :
徳島県における多発性骨髄腫の治療成績の検討,
第109回日本内科学会総会・講演会, 2012年4月. 原田武志, 尾崎修治, 小田明日香, 天羽宏枝, 藤井志朗, 中村信元, 三木浩和, 中野綾子, 賀川久美子, 竹内恭子, 安倍正博, 柴田泰伸, 松本俊夫 :
Lenalidomide 治療中の多発性骨髄腫患者におけるCRP上昇の検討,
第51回日本血液学会中国四国地方会, 2012年3月. 賀川久美子, 原田武志, 藤井志朗, 中村信元, 三木浩和, 竹内恭子, 安倍正博, 松本俊夫 :
遺伝子組み替えヒトトロンボモジュリン投与中に硬膜下血腫を来した同腫骨髄移植2症例,
第34回日本造血細胞移植学会, 2012年2月. 賀川久美子, 原田武志, 藤井志朗, 中村信元, 三木浩和, 竹内恭子, 安倍正博, 松本俊夫 :
遺伝子組み換えヒトトロンボモジュリン投与中に硬膜下血腫を来した同腫骨髄移植2症例,
第34回日本造血細胞移植学会, 2012年2月. 日浅雅博, 新垣理恵子, 山田安希子, 大浦徳永律子律子, 安倍正博, 松本俊夫, 林良夫, 石丸直澄, 淺岡憲三 :
A novel role of NF-B relB in bone remodeling.,
第40回日本免疫学会学術集会, 2011年11月. Keiichiro Watanabe, Masahiro Abe, Q Cui, Masahiro Hiasa, M Kawatani, T Harada, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, A Nakano, K Kagawa, K Takeuchi, H Osada, Eiji Tanaka and Toshio Matsumoto :
Targeting an acidic microenvironment by reveromycin A to overcome drug resistance to myeloma cells and ameliorate bone disease.,
第36回日本骨髄腫研究会総会, Nov. 2011. 日浅雅博, 安倍正博, 中野綾子, 竹内恭子, 賀川久美子, 中村信元, 三木浩和, 田中栄二, 淺岡憲三, 矢田健一郎, 松本俊夫 :
Pimキナーゼ阻害による腫瘍進展と骨破壊の抑制,
第73回日本血液学会, 2011年10月. Takayuki Ise, Takashi Iwase, Kumiko Kagawa, Toshiyuki Niki, Kenya Kusunose, 冨田紀子, Yuka Ueda, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masahiro Abe, Masashi Akaike and Masataka Sata :
Successful Autologous Peripheral Blood Stem Cell Transplantation for Primary Cardiac Amyloidosis Patients with Heart Failure : three cases report.,
第15回日本心不全学会学術集会, Oct. 2011. Masahiro Hiasa, A Nakano, Keiichiro Watanabe, C Qu, T Harada, S Fujii, H Miki, S Nakamura, K Kagawa, K Takeuchi, Eiji Tanaka, Kenzo Asaoka, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe :
Prevention of tumor growth and bone destruction in myeloma by Pim kinase inhibition,
Bone Biology Forum, 19-21st Aug, 2011, Shizuoka., Aug. 2011. 藤岡啓介, 西條敦郎, 豊田優子, 柿内聡司, 埴淵昌毅, 吾妻雅彦, 西岡安彦, 竹内恭子, 藤井志朗, 中村信元, 賀川久美子, 安倍正博, 水谷友哉 :
不明熱で発症し皮膚生検が診断に有効であった血管内リンパ腫の1例,
第243回徳島医学会学術集会, 2011年7月. 日浅雅博, 安倍正博, 中野綾子, 渡邉佳一郎, 中村信元, 田中栄二, 淺岡憲三, 松本俊夫 :
Pimキナーゼの阻害は骨芽細胞分化を促進し，骨髄腫骨病変の形成と腫瘍進展を抑制する,
日本骨代謝学会学術集会プログラム抄録集, 178, 2011年7月. 渡邉佳一郎, 安倍正博, 川谷誠, 日浅雅博, 中村信元, 田中栄二, 長田裕之, 松本俊夫 :
リベロマイシンAによる酸性環境がもたらす骨髄腫薬剤耐性の克服と骨病変形成の抑制,
日本骨代謝学会学術集会プログラム抄録集, 208, 2011年7月. 日浅雅博, 安倍正博, 中野綾子, 渡邉佳一郎, 中村信元, 田中栄二, 淺岡憲三, 松本俊夫 :
Pimキナーゼの阻害は骨芽細胞分化を促進し，骨髄腫骨病変の形成と腫瘍進展を抑制する,
日本骨代謝学会学術集会プログラム抄録集, 178, 2011年.

(キーワード): *癌原遺伝子蛋白質(拮抗物質・阻害物質); *骨芽細胞; *骨疾患(病因,実験的); *骨髄腫(合併症,実験的); 細胞分化; *Protein-Serine-Threonine Kinases(拮抗物質・阻害物質) / *Mouse Pim2 Protein(拮抗物質・阻害物質) / マウス; 動物

渡邉佳一郎, 安倍正博, 川谷誠, 日浅雅博, 中村信元, 田中栄二, 長田裕之, 松本俊夫 :
リベロマイシンAによる酸性環境がもたらす骨髄腫薬剤耐性の克服と骨病変形成の抑制,
日本骨代謝学会学術集会プログラム抄録集, 208, 2011年.

(キーワード): *Pyrans; *Spiro Compounds; *骨疾患; *骨髄腫; *抗腫瘍剤耐性 / *Reveromycin A

渡邉佳一郎, 安倍正博, Cui Qu, Kawatani Makoto, 日浅雅博, Nakano Ayako, Jinno Tadashi, Harada Takeshi, 藤井志朗, 中村信元, Miki Hirokazu, 賀川久美子, 竹内恭子, 尾崎修治, 田中栄二, Osada Hiroyuki, 松本俊夫 :
Reveromycin A prevents bone destruction and suppresses tumor growth in myeloma,
第72回日本血液学会, 2010年12月. 宇高憲吾, 松井尚子, 宮本亮介, 寺澤由佳, 佐藤健太, 浅沼光太郎, 和泉唯信, 梶龍兒, 藤井志朗, 竹内恭子, 安倍正博, 原田雅史 :
多発性骨髄腫の経過中に進行性多巣性白質脳症をきたした一例,
四国医学雑誌, Vol.66, No.5-6, 198, 2010年12月.

(キーワード): Cytarabine(治療的利用); Prednisolone(治療的利用); 自家移植; *骨髄腫-多発性(合併症,治療); *白質脳症-進行性多巣性(合併症,画像診断,薬物療法); Mirtazapine(治療的利用); FLAIR法; 末梢血幹細胞移植 / ヒト; 中年(45∼64); 男

賀川久美子, 神野雅, 原田武志, Cui Qu, 渡邉佳一郎, 日浅雅博, 小田明日香, 天羽宏枝, 池亀彰茂, 三木浩和, 藤井志朗, 中野綾子, 竹内恭子, 尾崎修治, 安倍正博, 松本俊夫 :
Sensitization of hematopietic malignant cells to TRAIL with bortezomib and a TACE inhibitor,
第72回日本血液学会, 2010年9月. 中村信元, 安倍正博, Cui Qu, 渡邉佳一郎, 池亀彰茂, 日浅雅博, 三木浩和, 中野綾子, 小田明日香, 天羽宏枝, 神野雅, 原田武志, 藤井志朗, 賀川久美子, 竹内恭子, 尾崎修治, 松本俊夫 :
Bortezomib-induced osteoblast differentiation is hampered by excessive ER stress,
第72回日本血液学会, 2010年9月. 日浅雅博, 安倍正博, 中野綾子, 小田明日香, 天羽宏枝, 竹内恭子, 賀川久美子, 中村信元, 三木浩和, 矢田健一郎, 渡邉佳一郎, 尾崎修治, 淺岡憲三, 田中栄二, 松本俊夫 :
Bone marrow stromal cells supress TACE activity in monocytes to induce osteoclastogenesis,
第72回日本血液学会, 2010年9月. Cui Qu, Masahiro Abe, Miki Hirokazu, Shingen Nakamura, Keiichiro Watanabe, Akishige Ikegame, Masahiro Hiasa, Nakano Ayako, Jinnno Tadashi, Harada Takeshi, Shiroh Fujii, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki and Toshio Matsumoto :
Bone marrow stromal cells attenuate gama delta T,
第72回日本血液学会, Sep. 2010. 日浅雅博, 安倍正博, 松本俊夫, 淺岡憲三 :
骨髄間質細胞は単球のTACE活性を抑制し樹状細胞分化を抑制し破骨細胞分化を誘導する,
第3回ナノ・バイオメディカル学会大会, 2010年9月. 日浅雅博, 安倍正博, 中野綾子, 小田明日香, 天羽宏枝, 竹内恭子, 賀川久美子, 中村信元, 三木浩和, 矢田健一郎, 渡邉佳一郎, 尾崎修治, 淺岡憲三, 田中栄二, 松本俊夫 :
骨髄間質細胞は，単球のTACE活性を抑制し樹状細胞分化を抑制し破骨細胞文化を誘導する,
第28回日本骨代謝学会, 2010年7月. 渡邉佳一郎, 安倍正博, Kawatani Makoto, 日浅雅博, 中村信元, 田中栄二, 長田裕之, 松本俊夫 :
リベロマイシンAは骨髄腫骨破壊病変の形成と腫瘍進展を抑制する,
第28回日本骨代謝学会, 2010年7月. 中村信元, 安倍正博, Cui Qu, 渡邉佳一郎, 池亀彰茂, 日浅雅博, 三木浩和, 中野綾子, 小田明日香, 天羽宏枝, 神野雅, 原田武志, 藤井志朗, 賀川久美子, 竹内恭子, 尾崎修治, 松本俊夫 :
ボルテゾミブによる骨芽細胞分化の促進は過剰な小胞体ストレスによって抑制される,
第28回日本骨代謝学会, 2010年7月. 辻大輔, 尾崎修治, 池亀彰茂, 伊藤良和, 徳田美幸, 岡野和真, 安倍正博, 松本俊夫, 伊藤孝司 :
ヒト多発性骨髄腫由来ガン幹細胞の単離及び性質決定,
第82回日本生化学会大会, 2009年10月. 遠藤逸朗, 大西幸代, 木戸里佳, 倉橋清衛, 吉田守美子, 藤中雄一, 粟飯原賢一, 安倍正博, 福本誠二, 松本俊夫 :
新規calcilytics，JTT305は常染色体優性低Ca血症におけるCa感知受容体活性型変異シグナルを抑制する,
第27回日本骨代謝学会学術集会, 195, 2009年7月.

(キーワード): シグナルトランスダクション *染色体異常 *低カルシウム血症(薬物療法) 変異 *Calcium-Sensing Receptors(拮抗物質・阻害物質)

賀川久美子, 矢田健一郎, 田中修, 中村信元, 三木浩和, 竹内恭子, 安倍正博, 尾崎修治, 吉田守美子, 遠藤逸朗 :
心筋への広範な直接浸潤を来したNK/T cell lymphoma 鼻型の一例,
第48回に本血液学会中国四国地方会, 2009年3月. 日浅雅博, 安倍正博, 竹内恭子, 矢田健一郎, 賀川久美子, 三木浩和, 尾崎修治, 淺岡憲三, 松本俊夫 :
骨髄間質細胞は単球のM-CSFR発現を増強し単球由来樹状細胞分化を抑制し骨髄腫細胞による破骨細胞分化を促進する,
日本骨代謝学会・学術総会, 2008年10月. 竹内恭子, 安倍正博, 日浅雅博, 田中修, 中村信元, 三木浩和, 賀川久美子, 矢田健一郎, 尾崎修治, 松本俊夫 :
骨髄腫骨病変部由来TGF-βは，脂肪細胞分化を抑制し骨髄内に間質細胞を誘導する,
日本骨代謝学会・学術総会, 2008年10月. 竹内恭子, 安倍正博, 日浅雅博, 田中修, 中村信元, 三木浩和, 賀川久美子, 矢田健一郎, 尾崎修治, 松本俊夫 :
TGF-βによる間質細胞からの脂肪細胞分化の抑制,
日本血液学会, 2008年10月. 矢田健一郎, 安倍正博, 日浅雅博, 竹内恭子, 田中修, 中村信元, 三木浩和, 賀川久美子, 尾崎修治, 松本俊夫 :
骨髄腫細胞と間質細胞の共存は単球M-CSFR発現増強を介し単球分化を破骨細胞側に偏らせる,
日本血液学会, 2008年10月. 日浅雅博, 安倍正博, 淺岡憲三, 松本俊夫 :
M-CSFRのectodomain sheddingによる破骨細胞分化の抑制,
17, 2008年8月. 岩瀬俊, 住友由佳, 八木秀介, 池田康将, 粟飯原賢一, 尾崎修治, 赤池雅史, 安倍正博, 松本俊夫, 北川哲也 :
エリスロポイエチンを用いた新たな血管新生療法の試み,
第104回日本内科学会総会・講演会, Vol.96, No.Suppl., 133, 2007年4月.

(キーワード): *Erythropoietin(治療的利用) 血液成分除去法 *動脈閉塞性疾患(治療) *末梢血幹細胞移植ヒト

日浅雅博, 安倍正博, 橋本年弘, 尾崎修治, 井上大輔, 木戸慎介, 森山啓司, 松本俊夫 :
GM-CSFとIL-4は単球のM-CSF破骨細胞分化を抑制し樹状細胞分化を誘導する,
日本骨形態計測学会雑誌, Vol.16, No.3, 66, 2006年12月.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1573668925326077696

(CiNii: 1573668925326077696) 宮本貴子, 木戸慎介, 安倍正博, 松本俊夫, 谷口寿章 :
Differential Proteomicsによる骨芽細胞分化の解析,
第24回日本骨代謝学会, 2006年7月. 塩屋園敦, 大庭康雄, 日浅雅博, 安倍正博, 松本俊夫, 森山啓司 :
歯の移動時の歯周組織におけるケモカインの発現,
第64回日本矯正歯科学会大会, 2005年10月. 田中洋一, 安倍正博, 日浅雅博, 橋本年弘, 木戸慎介, 井上大輔, 尾崎修治, 森山啓司, 松本俊夫 :
骨髄腫細胞，破骨細胞と血管内皮細胞の細胞間相互作用:腫瘍進展，骨破壊と血管新生の促進,
第23回日本骨代謝学会学術集会, 2005年7月.

研究会・報告書: 李悦子, 瀧本朋美, 小田直輝, 伊藤正一, 荻山佳子, 加地剛, 吉田あつ子, 須賀健一, 中川竜二, 佃恵里加, 三木浩和, 安倍正博 :
抗Jra保有妊婦に重症胎児貧血を認め，胎児輸血が奏功した一症例,
第69回日本輸血・細胞治療学会学術総会, 2021年6月. 遠藤ふうり, 吉田守美子, 辻本賀美, 工藤千晶, 安井沙耶, 桝田志保, 三井由香里, 倉橋清衛, 明比祐子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 福本誠二 :
ソマトスタチンアナログ治療中に胆嚢癌を認めた先端巨大症の1例,
第29回臨床内分泌代謝Update in Kochi, 2019年11月. 工藤千晶, 倉橋清衛, 辻本賀美, 安井沙耶, 遠藤ふうり, 三井由香里, 桝田志保, 吉田守美子, 明比祐子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 福本誠二 :
ニボルマブ投与により3系統の内分泌障害を発症した2例,
第29回臨床内分泌代謝Update in Kochi, 2019年11月. 辻本賀美, 三井由香里, 工藤千晶, 安井沙耶, 遠藤ふうり, 桝田志保, 倉橋清衛, 吉田守美子, 明比祐子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 福本誠二 :
免疫関連有害事象の末ロイド治療中ACTH分泌低下症を認めた1例,
第29回臨床内分泌代謝Update in Kochi, 2019年11月. 三井由香里, 辻本賀美, 工藤千晶, 安井沙耶, 遠藤ふうり, 桝田志保, 倉橋清衛, 吉田守美子, 明比祐子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 福本誠二 :
治療拒否により甲状腺クリーゼを繰り返したバセドウ病の1例,
第29回臨床内分泌代謝Update in Kochi, 2019年11月. 倉橋清衛, 青山万里子, 滝沢宏光, 遠藤ふうり, 三井由香里, 桝田志保, 吉田守美子, 明比祐子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 福本誠二 :
薬物治療に抵抗性で，日和見感染も合併したバセドウ病の一例,
第29回臨床内分泌代謝Update in Kochi, 2019年11月. 寺町順平, 天眞寛文, 遠藤逸朗, 松本俊夫, 安倍正博 :
骨髄腫特異的抗腫瘍活性と骨再生をもたらす新規分子標的薬の開発,
2018 先端医学交流セミナー, 2018年8月. Jumpei Teramachi, Masahiro Hiasa and Masahiro Abe :
Development of novel anti-myeloma agents with potent bone anabolic actions,
14th Bone Biology Forum, Aug. 2017. Masahiro Hiasa, T Okui, Masahiro Abe and T Yoneda :
Targeting the myeloma-induced acidic microenvironment decreases bone pain,
第78回日本血液学会学術集会, Oct. 2016. 遠藤逸朗, 賀川久美子, 三木浩和, 高橋真美子, 安倍正博 :
B細胞リンパ腫を合併した先端巨大症の一例,
第3回四国GH/IGF1フォーラム, 2014年2月. 天知良太, 安倍正博, 渡邉佳一郎, 賀川久美子, 藤井志朗, 原田武志, 三木浩和, 渡邉佳一郎, 小野明日香, 日浅雅博, 田中栄二, 松本俊夫 :
骨髄腫の酸性環境はTRAIL受容体発現をエピジェネティックに抑制し，TRAIL抵抗性をもたらす,
第20回徳島骨代謝研究会, 2013年11月. Dong Bingzi, Itsuro Endo, Takeshi Kondo, Yukiyo Ohnishi, Masahiro Abe, Shin-ichi Yoshizawa, Seiji Fukumoto and Toshio Matsumoto :
The Effect of calcilytics on activating mutation of calcium-sensing repceptor knock-in mice model of autosomal dominant hypocalcemia,
骨とCaクラスターミニリトリート, Feb. 2013. 遠藤逸朗, 大薗卓也, 齋藤光恵, 久保田由紀子, 安倍正博, 松本俊夫 :
骨転移に対するdenosumab 120mg 皮下注後の重傷低Ca血症発現の実態,
第15回癌と骨病変研究会, 2012年11月. 渡邉佳一郎, 安倍正博, 松本俊夫 :
リベロマイシンAによる酸性環境がもたらす骨髄腫薬剤耐性の克服と骨病変形成の制御,
第15回癌と骨病変研究会, 2012年11月. 天知良太, 安倍正博, 渡邉佳一郎, 賀川久美子, 藤井志郎, 原田武志, 三木浩和, 中村信元, 小田明日香, 日浅雅博, 田中栄二, 松本俊夫 :
酸環境は骨髄腫細胞のTRAILに対する抵抗性を増強する,
第3回骨バイオサイエンス研究会, 2012年7月. 日浅雅博, 安倍正博, 中野綾子, 渡邉佳一郎, 竹内恭子, 賀川久美子, 三木浩和, 中村信元, 藤井志朗, 原田武志, 尾崎修治, 田中栄二, 淺岡憲三, 松本俊夫 :
Pimキナーゼの阻害による骨髄腫の進展抑制,
癌と骨病変研究会, 2011年11月. 渡邉佳一郎, 安倍正博, 崔衢, 川谷誠, 日浅雅博, 長田裕之, 田中栄二, 松本俊夫 :
A novel anti-resorptive agent, reveromycin A, ameliorates bone destruction and tumor growth in myeloma,
第2回骨バイオサイエンス研究会, 2011年7月. 日浅雅博, 安倍正博, 中野綾子, 小田明日香, 天羽宏枝, 竹内恭子, 賀川久美子, 中村信元, 三木浩和, 矢田健一郎, 渡邉佳一郎, 尾崎修治, 淺岡憲三, 田中栄二, 松本俊夫 :
骨髄間質細胞は，単球のTACE活性を抑制し樹状細胞分化を抑制し破骨細胞文化を誘導する,
第17回徳島骨代謝研究会, 2010年11月. 渡邉佳一郎, 安倍正博, 崔衢, 川谷誠, 長田裕之, 田中栄二, 松本俊夫 :
リベロマイシンAの骨髄腫骨病変と腫瘍進展抑制作用,
第1回骨バイオサイエンス研究会, 2010年6月. 遠藤逸朗, 大西幸代, 木戸里佳, 倉橋清衛, 藤中雄一, 粟飯原賢一, 吉田守美子, 安倍正博, 福本誠二, 松本俊夫 :
Ca感知受容体機能に及ぼすcalcilyticsの作用,
第3回瀬戸内フォーラム, 2009年8月. 矢田健一郎, 安倍正博, 竹内恭子, 日浅雅博, 中野綾子, 三木浩和, 田中修, 中村信元, 賀川久美子, 尾崎修治, 松本俊夫 :
骨髄間質細胞はγδT細胞による抗骨髄腫効果を減弱させる,
日本骨髄腫研究会総会, 2008年11月.

特許: 寺町順平, 中尾允泰, 佐野茂樹, 安倍正博, 原田武志 : PIM2阻害剤, 特願2021- 14411 (2021年2月), 特許第110000796号 (2021年2月). 中山淳, 寺町順平, 安倍正博, 難波康祐, 伊藤孝司, 辻大輔 : 新規イノン化合物及びその用途, (2019年10月), 特許第PCT/JP2019/042086号 (2019年10月). 中山淳, 寺町順平, 安倍正博, 難波康祐, 伊藤孝司, 辻大輔 : 新規イノン化合物及びその用途, (2018年10月), 特許第2018-203219号 (2018年10月).
作品: 研究者総覧に該当データはありませんでした。
補助金・競争的資金: 加齢性サルコペニアへの炎症性サイトカインの関与とTAK1阻害による治療法の開発 (研究課題/領域番号: 21K07339 )
TAK1-Pim-2経路がもたらす骨髄腫の難治性と骨破壊の役割とその克服法の開発 (研究課題/領域番号: 18K08329 )
多元計算解剖モデルを利用した腫瘍診断支援システム (研究課題/領域番号: 26108007 )
骨髄腫骨髄微小環境がもたらす骨髄腫増殖制御機構の解明と新規治療法の開発 (研究課題/領域番号: 26461422 )
骨格系の分子制御機構の解明とその異常による病態の治療法の開発 (研究課題/領域番号: 25293215 )
骨髄腫骨髄微小環境がもたらす腫瘍進展と骨病変形成機序の解明と新規治療法の開発 (研究課題/領域番号: 23591390 )
計算解剖モデルに基づく診断支援 (研究課題/領域番号: 21103005 )
骨格系の制御システムと脂肪・血管制御系との連関およびその異常に基づく病態の解明 (研究課題/領域番号: 20249050 )
骨格系のホメオスターシス維持と病態発症に関わる分子制御機構の解明と治療法の開発 (研究課題/領域番号: 17209035 )
破骨細胞由来新規骨髄腫増殖促進因子の同定と同因子を標的とした治療法の開発 (研究課題/領域番号: 15591010 )
HM1.24坑原を介するシグナル伝達の解明と造血器腫瘍の治療への応用 (研究課題/領域番号: 14570984 )
多発性骨髄腫の骨病変形成におけるケモカインMIP-1の役割の解明と治療法の開発 (研究課題/領域番号: 13671067 )
腫瘍化リンパ球特異抗原(2D7)を標的とした造血器腫瘍の免疫療法の開発 (研究課題/領域番号: 13557082 )
骨格系の制御に関わる転写因子と骨粗鬆症におけるその異常 (研究課題/領域番号: 12137207 )
破骨細胞分化誘導シグナルと骨吸収性病変におけるその異常の解明(細胞接着から分化制御遺伝子の発現に至る情報伝達機構) (研究課題/領域番号: 11470227 )
研究者番号（80263812）による検索

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2024年11月15日更新

専門分野・研究分野: 医学 (Medicine)
血液学 (Hematology)
腫瘍学 (Oncology)
所属学会・所属協会: 日本血液学会
社団法人日本内科学会
日本骨髄腫学会
日本骨代謝学会
International Myeloma Workshop
委員歴・役員歴: 日本血液学会 (代議員 [2005年〜2019年3月])
日本血液学会 (プログラム企画委員 [2011年4月])
日本血液学会 (専門医認定委員会委員 [2009年4月])
日本血液学会 (中国四国地方会評議員 [2005年4月〜2018年3月])
日本血液学会 (Internal Journal of Hematology編集委員 [2008年4月〜2010年3月])
社団法人日本内科学会 (四国地方会評議員 [2010年4月〜2017年3月])
日本骨髄腫学会 (理事 [2012年〜2017年3月])
日本骨代謝学会 (評議員 [2010年7月〜2018年3月])
日本骨代謝学会 (あり方委員会委員 [2008年4月])
日本骨代謝学会 (プログラム選定委員 [2009年4月])
International Myeloma Workshop (組織委員 [2012年〜2014年7月])
日本骨髄腫学会 (臨床研究委員会委員 [2013年4月〜2017年3月])
日本血液学会 (造血器腫瘍診療ガイドライン作成委員会委員 [2012年〜2017年3月])
日本骨髄腫学会 (広報委員会委員長 [2016年6月〜2018年3月])
受賞: 2001年10月, The Award in Akis Memory (International Myeloma Foundation)
2004年12月, 徳島大学医学部研究奨励賞 (徳島大学)
2005年12月, 第4回徳島新聞医学研究助成金 (社団法人徳島新聞社)
2008年10月, 第26回日本骨代謝学会学術集会学術賞(内科臨床系) (日本骨代謝学会)
2010年, Young Investigator Award, 2010. (2010 ASBMR)
2010年9月, Travel Grant Award, 2010. (10th International Conference Cancer-Induced Bone Disease)
2010年11月, 平成21年度公益信託日本白血病研究基金一般研究賞 (公益信託日本白血病研究基金)
2010年12月, 52nd ASH Travel Award (52nd ASH)
2011年7月, 優秀演題賞 (第29回日本骨代謝学会)
2011年7月, 高得点演題賞 (日本骨代謝学会)
2012年9月, Young Investigator Award, 2012 (ANZBMS)
2013年10月, Plenary poster & Young Investigator Travel Award (米国骨代謝学会)
2016年7月, 第34回日本骨代謝学会学術集会・第3回アジア太平洋骨代謝学会議,Young investigator award. (日本骨代謝学会)
2016年7月, 第34回日本骨代謝学会学術集会尾形賞 (日本骨代謝学会)
2017年6月, ANZBMS Plenary Poster Award. (Australian and New Zealand Bone and Mineral Society)
2019年7月, 第36回日本骨代謝学会学術集会研究奨励賞. (日本骨代謝学会)
2021年9月, 第83回日本血液学会学術集会優秀ポスター賞 (一般社団法人日本血液学会)
2022年5月, 第47回日本骨髄腫学会学術集会優秀ポスター賞 (日本骨髄腫学会)
活動: 日本骨髄バンク (連絡責任医師 [2006年4月〜2017年3月])
徳島県骨髄バンク推進協議会 (会長 [2010年4月〜2017年3月])
骨髄腫患者の会 (顧問医師)
徳島大学病院血液内科科長 (2003年4月〜2018年3月)
安全管理感染対策部門長 (2006年10月〜2008年3月)
HIV/エイズ治療小委員会委員長 (2011年4月〜2017年3月)
輸血・細胞治療部長 (2014年4月〜2017年3月)
卒後臨床研修センター長 (2016年6月〜2017年3月)

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2024年11月10日更新

2024年11月9日更新

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Jグローバル最終確認日: 2024/11/9 01:14
氏名（漢字）: 安倍正博
氏名（フリガナ）: アベマサヒロ
氏名（英字）: Abe Masahiro
所属機関: 徳島大学大学院医歯薬学研究部教授

リサーチマップ

researchmap最終確認日: 2024/11/10 01:15
氏名（漢字）: 安倍正博
氏名（フリガナ）: アベマサヒロ
氏名（英字）: Abe Masahiro
プロフィール: リサーチマップAPIで取得できませんでした。
登録日時: 2006/1/6 00:00
更新日時: 2024/1/31 08:59
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所属ID: 0344000000
所属: 徳島大学大学院医歯薬学研究部
部署: 血液・内分泌代謝内科学分野
職名: 教授
学位: 博士(医学)
学位授与機関: 徳島大学
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2024年11月9日更新

研究者番号: 80263812

所属（現在）: KAKEN APIで取得できませんでした。

所属（過去の研究課題 情報に基づく）*注記: 2018/4/1 – 2023/4/1 : 徳島大学, 大学院医歯薬学研究部(医学域), 教授
2016/4/1 – 2017/4/1 : 徳島大学, 大学院医歯薬学研究部(医学系), 教授
2015/4/1 : 徳島大学, 大学院医歯薬学研究部, 教授
2014/4/1 : 徳島大学, ヘルスバイオサイエンス研究部, 教授
2013/4/1 : 徳島大学, 大学院ヘルスバイオサイエンス研究部, 准教授
2011/4/1 – 2013/4/1 : 徳島大学, ヘルスバイオサイエンス研究部, 准教授
2007/4/1 – 2010/4/1 : 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 准教授
2006/4/1 : 徳島大学, バイオヘルスサイエンス研究部, 助教授
2003/4/1 – 2005/4/1 : 徳島大学, 医学部・歯学部附属病院, 講師
2003/4/1 : 徳島大学, 歯学部附属病院, 講師
2002/4/1 : 徳島大学, 医学部附属病院, 講師
2001/4/1 : 徳島大学, 医学部・附属病院, 講師
1999/4/1 – 2001/4/1 : 徳島大学, 医学部, 講師

審査区分/研究分野

研究代表者

生物系 / 医歯薬学 / 内科系臨床医学 / 血液内科学
医学 / 内科 / 血液内科学
小区分54010:血液および腫瘍内科学関連

研究代表者以外

生物系 / 医歯薬学 / 内科系臨床医学 / 内分泌学
医学 / 内科 / 内分泌学
医学 / 内科 / 血液内科学
生物系
理工系
小区分52010:内科学一般関連
小区分57020:病態系口腔科学関連

キーワード

研究代表者

血液腫瘍学 / 多発性骨髄腫 / 骨病変 / Pimキナーゼ / 骨髄腫 / 骨芽細胞 / 薬剤耐性 / アポトーシス / 骨破壊病変 / 酸環境 / 骨形成 / TRPV1 / Pim-2 / TAK-1 / 酸性環境 / 骨髄微小環境 / ケモカイン / MIP-1 / 破骨細胞 / RANKL / VLA-4 / multiple myeloma / chemokine / osteoclast / 骨髄腫細胞 / 血管新生 / オステオポンチン / IL-6 / myeloma / angiogenesis / osteopontin / 骨破壊 / TAK1 / PIM2 / 阻害薬 / TAK１ / 骨髄間質細胞 / バイオマーカー / 貧血 / 骨代謝

研究代表者以外

骨芽細胞 / 破骨細胞 / AP-1 / 細胞分化 / 転写因子 / インターロイキン-11 / 破骨細部 / 内科 / 老化 / 多発性骨髄腫 / 骨粗鬆症 / 糖尿病 / 動脈硬化 / interleukin-11 / Wntシグナル / アンドロゲン / 計算解剖学 / コンピュータ支援診断システム / がん（肺がん、肝がん、大腸がん） / 慢性閉塞疾患(COPD) / 心血管・リンパ節疾患 / がん（肺がん、肝がん、膵臓がん、大腸がん） / がん(肺がん、肝がん、膵臓がん、大腸がん) / 計算解剖モデル / マルチモダリティ画像データベース / インターロイキン-11 (IL-11) / 脂肪細胞 / 骨髄腫 / Pim-2 / 遺伝子 / シグナル伝達 / 脂質 / 多元計算解剖モデル / 腫瘍診断支援システム / マルチスケール・マルチモダリティ画像データベース / 肺を中心に大腸・腎臓に発生する悪性腫瘍の本態解明 / 3次元ミクロからマクロの病態 / 肺・大腸・肝臓に発生する悪性腫瘍の本態解明 / マルチスケール・マルチモダリティ画像 / 骨吸収 / RANK ligand / ケモカイン / MIP-1 / オステオポンチン / インテグリン / bone resorption / osteoclast / transcription factor / myeloma / chemokine / 造血器腫瘍 / モノクローナル抗体 / 免疫療法 / hematoloeical malienanc / monoclonal antibody / immunotherary / 造血器鍾瘍 / 分子標的治療 / hematological malignancy / immnnotherapy / molecular targeting therapy / 力学的負荷 / IL-11 / ΔFosB / Wnt / 血管新生 / グルココルチコイド / 血管内皮機能 / g / DeltaFosB / Mechanical stress / Interleukin-11 (IL-11) / AFosB / Multiple myeloma / Wnt signal / Angiogenesis / Gluencorticoid / Endothelial cells / 炎症性サイトカイン / 骨格筋萎縮 / サルコペニア / TAK1 / PP2A / CIP2A / 脱リン酸化

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2019年10月1日

がんの統合的診断・治療を目指した分子から組織のマルチスケール・バイブレーショナル光学顕微鏡の創成（南川丈夫）

南川丈夫古部昭広安井武史松本健志北研二獅々堀正幹南康夫越山顕一朗佐藤克也柳谷伸一郎安倍正博常山幸一冨田江一三木浩和日浅雅博尾矢剛志清水真祐子

2020年5月20日

リード薬の構造展開による新規阻害薬の創出とその物性・治療活性の最適化

安倍正博遠藤逸朗吉田守美子中村信元三木浩和原田武志日浅雅博天眞寛文寺町順平藤猪英樹村上圭史難波康祐中山淳佐野茂樹中尾允泰

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安倍正博