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埴淵昌毅

徳島大学

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2024年5月17日更新

職名: 特任教授
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学歴: 1993/3: 徳島大学医学部医学科卒業
1994/4: 徳島大学大学院医学研究科博士課程入学
1998/3: 徳島大学大学院医学研究科博士課程修了
学位: 博士(医学) (徳島大学) (1998年3月)
職歴・経歴: 1993/6: 徳島大学医学部附属病院医員
1999/4: 国立療養所刀根山病院呼吸器内科
2001/8: 徳島大学医学部助手
2003/7: 徳島大学医学部附属病院講師
2005/10: 徳島赤十字病院呼吸器科
2007/1: 徳島大学病院講師
2009/5: M.D. Anderson Cancer Center, Visiting Associate Professor
2011/3: 徳島大学病院講師
2012/2: 徳島大学大学院ヘルスバイオサイエンス研究部准教授
2015/4: 徳島大学大学院医歯薬学研究部准教授

専門分野・研究分野: 内科学 (Internal Medicine)
呼吸器病学 (Respiratory Disease)

研究者総覧で最新データを確認する

2024年5月17日更新

専門分野・研究分野: 内科学 (Internal Medicine)
呼吸器病学 (Respiratory Disease)
担当経験のある授業科目: 免疫・呼吸器 (学部)
内科学第三 (学部)
呼吸器コース(3年) (学部)
指導経験: 研究者総覧に該当データはありませんでした。

研究者総覧で最新データを確認する

2024年5月17日更新

専門分野・研究分野: 内科学 (Internal Medicine)
呼吸器病学 (Respiratory Disease)

研究テーマ: 肺癌の多剤耐性および遠隔転移因子を標的とした免疫遺伝子治療に関する研究 (肺癌, 多剤耐性, 遠隔転移, 免疫遺伝子治療)

著書

埴淵昌毅, 西岡安彦 :
分子生物学的にみた間質性肺炎および肺癌,
2017年10月. 埴淵昌毅, 西岡安彦 :
じん肺症(珪肺，アスベスト肺),
2017年7月. 後東久嗣, 埴淵昌毅, 西岡安彦 :
先端医療シリーズ46. 呼吸器疾患診療の最先端. 全国主要呼吸器診療施設一覧. 徳島大学病院呼吸器・膠原病内科,
東京, 2015年8月. 埴淵昌毅 :
歯界展望別冊・歯科医師のための医学ハンドブック Chapter 12 感染症結核,
2014年5月. 埴淵昌毅 :
歯界展望別冊・歯科医師のための医学ハンドブック Chapter 1 症候咳嗽・痰,
東京, 2014年5月. 埴淵昌毅 :
歯界展望別冊・歯科医師のための医学ハンドブック Chapter 1 症候発熱,
東京, 2014年5月. 矢野聖二, 佐野峻子, 竹内伸司, 埴淵昌毅 :
癌と骨. Chapter 3 骨転移の成立・進展のメカニズム 3. 骨転移の増殖・進展メカニズム ―2. 肺癌―,
東京, 2013年10月.

論文

Hiroyuki Kozai, Hirokazu Ogino, Atsushi Mitsuhashi, Thi Na Nguyen, Yuki Tsukazaki, Yohei Yabuki, Ryohiko Ozaki, Hiroto Yoneda, Seidai Satou, Masaki Hanibuchi, Tsutomu Shinohara, Hiroshi Nokihara and Yasuhiko Nishioka :
Potential of fluoropyrimidine to be an immunologically optimal partner of immune checkpoint inhibitors through inducing immunogenic cell death for thoracic malignancies.,
Journal of Thoracic Oncology, Vol.15, No.5, 369-378, 2023.

(要約): 5-FU induced cell surface expression of CRT and ATP secretion most efficiently among the several chemotherapeutic agents. This effect was enhanced when it was combined with platinum. In the antitumor vaccination assay in vivo, we found that vaccination with dying-AB1-HA (a murine malignant mesothelioma cell line) cells treated with 5-FU, but neither PEM nor PTX, reduced the tumor growth of living-AB1-HA cells inoculated 1 week after vaccination by recruiting CD3
(キーワード): Humans / Animals / Mice / Carcinoma, Non-Small-Cell Lung / Immune Checkpoint Inhibitors / CD8-Positive T-Lymphocytes / Platinum / Immunogenic Cell Death / Lung Neoplasms / Pemetrexed / Antimetabolites / Cell Line, Tumor / Taxoids / Fluorouracil / Adenosine Triphosphate / Tumor Microenvironment
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/1759-7714.15200
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38146645; ● Search Scopus @ Elsevier (PMID): 38146645; ● Search Scopus @ Elsevier (DOI): 10.1111/1759-7714.15200

(DOI: 10.1111/1759-7714.15200, PubMed: 38146645) Hiroto Yoneda, Atsushi Mitsuhashi, Aito Yoshida, Hirokazu Ogino, Satoshi Itakura, Thi Na Nguyen, Hiroshi Nokihara, Seidai Satou, Tsutomu Shinohara, Masaki Hanibuchi, Shinji Abe, K Mika Kaneko, Yukinari Kato and Yasuhiko Nishioka :
Antipodoplanin antibody enhances the antitumor effects of CTLA-4 blockade against malignant mesothelioma by natural killer cells.,
Cancer Science, Vol.115, No.2, 357-368, 2023.

(要約): -f and CTLA-4 blockade in vivo. These findings indicated the essential role of NK cells in novel combination immunotherapy targeting PDPN and shed light on the therapeutic strategy in advanced MPM.
(キーワード): Rats / Mice / Animals / Cricetinae / Mesothelioma, Malignant / Antibodies, Monoclonal / CTLA-4 Antigen / Membrane Glycoproteins / Mesothelioma / Killer Cells, Natural / Cricetulus / CHO Cells
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/cas.16046
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38148492; ● Search Scopus @ Elsevier (PMID): 38148492; ● Search Scopus @ Elsevier (DOI): 10.1111/cas.16046

(DOI: 10.1111/cas.16046, PubMed: 38148492) Yohei Yabuki, Masaki Hanibuchi, Eiji Takeuchi, Takashi Haku, Takanori Kanematsu, Naoki Nishimura, Yuko Toyoda, Atsushi Mitsuhashi, Kenji Otsuka, Seidai Satou, Hisatsugu Goto, Hiroto Yoneda, Hirokazu Ogino, Hiroshi Nokihara, Tsutomu Shinohara and Yasuhiko Nishioka :
A multicenter, open-label, phase II trial of pemetrexed plus bevacizumab in elderly patients with previously untreated advanced or recurrent nonsquamous non-small cell lung cancer.,
Thoracic Cancer, Vol.14, No.32, 3232-3239, 2023.

(要約): The median age at initiating chemotherapy was 80 years old. Almost all patients (92.6%) had adenocarcinoma histology. The median number of cycles administered was 6, and the objective response rate was 40.7%. The median progression-free survival, overall survival and 1-year survival were 8.8 months, 27.2 months and 79%, respectively. The treatment was well-tolerated, and no treatment-related death was observed.
(キーワード): Humans / Aged / Aged, 80 and over / Carcinoma, Non-Small-Cell Lung / Pemetrexed / Bevacizumab / Lung Neoplasms / Treatment Outcome / Antineoplastic Combined Chemotherapy Protocols
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/1759-7714.15115
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37718463; ● Search Scopus @ Elsevier (PMID): 37718463; ● Search Scopus @ Elsevier (DOI): 10.1111/1759-7714.15115

(DOI: 10.1111/1759-7714.15115, PubMed: 37718463) Hiroki Takahashi, Hirokazu Ogino, Hiroki Bando, Atsushi Mitsuhashi, Yuki Tsukazaki, Yohei Yabuki, Ryohiko Ozaki, Hiroto Yoneda, Seidai Satou, Masaki Hanibuchi and Yasuhiko Nishioka :
FoundationOne CDx detected an uncovered variant of epidermal growth factor receptor exon 19 deletion by Oncomine Dx target test in a patient with lung adenocarcinoma.,
Respiratory Medicine Case Reports, Vol.45, 101893, 2023.

(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.rmcr.2023.101893
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37485237; ● Search Scopus @ Elsevier (PMID): 37485237; ● Search Scopus @ Elsevier (DOI): 10.1016/j.rmcr.2023.101893

(DOI: 10.1016/j.rmcr.2023.101893, PubMed: 37485237) Atsushi Mitsuhashi, Kazuya Koyama, Hirokazu Ogino, Tania Afroj, Thi Na Nguyen, Hiroto Yoneda, Kenji Otsuka, Masamichi Sugimoto, Osamu Kondoh, Hiroshi Nokihara, Masaki Hanibuchi, Hiromitsu Takizawa, Tsutomu Shinohara and Yasuhiko Nishioka :
Identification of fibrocyte cluster in tumors reveals the role in antitumor immunity by PD-L1 blockade.,
Cell Reports, Vol.42, No.3, 112162, 2023.

(要約): fibrocytes is enhanced by anti-PD-L1 antibody. Peritumoral implantation of fibrocytes enhances the antitumor effect of PD-L1 blockade in vivo; CD86
(キーワード): Humans / 血管内皮増殖因子 (vascular endothelial growth factor) / Neoplasms / B7-H1 Antigen / 免疫療法 (immunotherapy) / Tumor Microenvironment
(徳島大学機関リポジトリ): ● Metadata: 118888
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.celrep.2023.112162
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36870329; ● Search Scopus @ Elsevier (PMID): 36870329; ● Search Scopus @ Elsevier (DOI): 10.1016/j.celrep.2023.112162

(徳島大学機関リポジトリ: 118888, DOI: 10.1016/j.celrep.2023.112162, PubMed: 36870329) Masaki Hanibuchi, Atsushi Mitsuhashi, Atsuro Saijo, Tatsuya Kajimoto, Seidai Satou, Tetsuya Kitagawa and Yasuhiko Nishioka :
A case of atopic cough with aphonia showed a prominent response to a histamine H1 receptor antagonist.,
The Journal of Medical Investigation : JMI, Vol.70, No.1.2, 281-284, 2023.

(要約): -RA, a diagnosis of AC was made. To the best of our knowledge, this is the first report of an AC patient who presented severe cough with aphonia. J. Med. Invest. 70 : 281-284, February, 2023.
(キーワード): 成人 (adult) / 女性 (female) / Humans / Aphonia / Cough / Histamine H1 Antagonists
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.70.281
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37164735; ● Search Scopus @ Elsevier (PMID): 37164735; ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.70.281

(DOI: 10.2152/jmi.70.281, PubMed: 37164735) Momoyo Azuma, Kazunori Oishi, Yukihiro Akeda, Saeko Morino, Yumi Motoki, Masaki Hanibuchi and Yasuhiko Nishioka :
Safety and immunogenicity of sequential administration of PCV13 followed by PPSV23 in pneumococcal vaccine-naïve adults aged ≥ 65 years: Comparison of booster effects based on intervals of 0.5 and 1.0 year.,
Vaccine, Vol.41, No.5, 1042-1049, 2022.

(要約): The 1.0-y interval provided better booster effects induced by PPSV23 than those of the 0.5-y interval in a sequential administration in pneumococcal vaccine-naïve adults aged ≥ 65 years. No difference was found in the safety profile between both intervals.
(キーワード): Humans / Antibodies, Bacterial / Double-Blind Method / Immunogenicity, Vaccine / Immunoglobulin G / Pneumococcal Infections / Pneumococcal Vaccines / Streptococcus pneumoniae / Vaccines, Conjugate
(徳島大学機関リポジトリ): ● Metadata: 118625
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.vaccine.2022.12.060
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36593171; ● Search Scopus @ Elsevier (PMID): 36593171; ● Search Scopus @ Elsevier (DOI): 10.1016/j.vaccine.2022.12.060

(徳島大学機関リポジトリ: 118625, DOI: 10.1016/j.vaccine.2022.12.060, PubMed: 36593171) Masaki Hanibuchi, Atsushi Mitsuhashi, Tatsuya Kajimoto, Atsuro Saijo, Seidai Satou, Tetsuya Kitagawa and Yasuhiko Nishioka :
Clinical significance of fractional exhaled nitric oxide and periostin as potential markers to assess therapeutic efficacy in patients with cough variant asthma.,
Respiratory Investigation, Vol.61, No.1, 16-22, 2022.

(要約): Our observations indicate the usefulness of FeNO and periostin as potential "therapeutic" markers for CVA. To the best of our knowledge, this is the first report demonstrating the clinical significance of these factors as potential biomarkers to assess therapeutic efficacy in patients with CVA.
(キーワード): Humans / Cough / Fractional Exhaled Nitric Oxide Testing / Prospective Studies / Clinical Relevance / ROC Curve / 一酸化窒素 (nitric oxide) / Exhalation / Asthma / Biomarkers / Breath Tests
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.resinv.2022.10.006
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36463016; ● Search Scopus @ Elsevier (PMID): 36463016; ● Search Scopus @ Elsevier (DOI): 10.1016/j.resinv.2022.10.006

(DOI: 10.1016/j.resinv.2022.10.006, PubMed: 36463016) Masaki Hanibuchi, Atsuro Saijo, Atsushi Mitsuhashi, Tatsuya Kajimoto, Tetsuya Kitagawa and Yasuhiko Nishioka :
The efficacy of mass screening for chronic obstructive pulmonary disease using screening questionnaires in a medical health check-up population.,
Respiratory Investigation, Vol.60, No.6, 815-821, 2022.

(要約): Mass screening for COPD using screening questionnaires, particularly the COPD-PS questionnaire, might be useful to identify the early stages of COPD in a medical health check-up population.
(キーワード): Humans / Forced Expiratory Volume / Cross-Sectional Studies / Reproducibility of Results / Pulmonary Disease, Chronic Obstructive / Spirometry / Mass Screening / Surveys and Questionnaires
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.resinv.2022.07.005
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36057534; ● Search Scopus @ Elsevier (PMID): 36057534; ● Search Scopus @ Elsevier (DOI): 10.1016/j.resinv.2022.07.005

(DOI: 10.1016/j.resinv.2022.07.005, PubMed: 36057534) Toshifumi Tezuka, Masahiko Azuma, Hirohisa Ogawa, Mayo Kondou, Hisanori Uehara, Yoshinori Aono, Masaki Hanibuchi and Yasuhiko Nishioka :
A RAS inhibitor reduces allergic airway remodeling via regulating IL-33-derived type 2 innate lymphoid cells.,
Experimental Lung Research, Vol.47, No.9, 451-463, 2021.

(要約): The RAS signal pathway plays a crucial role in allergen-induced airway remodeling associated with ILC2s. XRP44X may have therapeutic potential for refractory asthma.
(キーワード): Airway Remodeling / Animals / Hypersensitivity / 自然免疫 (innate immunity) / Interleukin-33 / Lymphocytes / Mice
(出版サイトへのリンク): ● Publication site (DOI): 10.1080/01902148.2021.1999536
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34739349; ● Search Scopus @ Elsevier (PMID): 34739349; ● Search Scopus @ Elsevier (DOI): 10.1080/01902148.2021.1999536

(DOI: 10.1080/01902148.2021.1999536, PubMed: 34739349) Kenji Otsuka, Atsushi Mitsuhashi, Hisatsugu Goto, Masaki Hanibuchi, Kazuya Koyama, Hirohisa Ogawa, Hirokazu Ogino, Atsuro Saijo, Hiroyuki Kozai, Hiroto Yoneda, Makoto Tobiume, Masatoshi Kishuku, Keisuke Ishizawa and Yasuhiko Nishioka :
Anti-PD-1 antibody combined with chemotherapy suppresses the growth of mesothelioma by reducing myeloid-derived suppressor cells.,
Lung Cancer, Vol.146, 86-96, 2020.

(要約): The combination of anti-PD-1 antibody with CDDP + PEM may be a promising therapy for MPM via inhibiting the accumulation of MDSCs and vessels in tumors.
(キーワード): Animals / Cell Line, Tumor / Lung Neoplasms / Mesothelioma / Mice / Myeloid-Derived Suppressor Cells / Pemetrexed
(徳島大学機関リポジトリ): ● Metadata: 115324
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.lungcan.2020.05.023
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32526602; ● Search Scopus @ Elsevier (PMID): 32526602; ● Search Scopus @ Elsevier (DOI): 10.1016/j.lungcan.2020.05.023

(徳島大学機関リポジトリ: 115324, DOI: 10.1016/j.lungcan.2020.05.023, PubMed: 32526602) 福家麻美, 荻野広和, 坪井未希, 近藤真代, 香川耕造, 埴淵昌毅, 山﨑博輝, 宮本亮介, 豊田優子, 西岡安彦 :
エタンブトールによる脱髄性末梢神経障害により急速進行性の歩行障害を呈した結核性胸膜炎の1例,
日本結核・非結核性抗酸菌症学会, Vol.95, No.2, 73-77, 2020年. Takashi Ogura, Nagio Takigawa, Keisuke Tomii, Kazuma Kishi, Yoshikazu Inoue, Eiki Ichihara, Sakae Homma, Kazuhisa Takahashi, Hiroaki Akamatsu, Satoshi Ikeda, Naohiko Inase, Tae Iwasawa, Yuichiro Ohe, Hiromitsu Ohta, Hiroshi Onishi, Isamu Okamoto, Kazumasa Ogawa, Kazuo Kasahara, Hiroki Karata, Takumi Kishimoto, Yuka Kitamura, Akihiko Gemma, Hirotsugu Kenmotsu, Hiroyuki Sakashita, Susumu Sakamoto, Katsutoshi Sekine, Yuichi Takiguchi, Yuji Tada, Shinichi Toyooka, Yuko Nakayama, Yasuhiko Nishioka, Koichi Hagiwara, Masaki Hanibuchi, Junya Fukuoka, Yuji Minegishi, Toyoshi Yanagihara, Nobuyuki Yamamoto, Hiromasa Yamamoto, Mina Gaga, M Kwun Fong, A Charles Powell and Katsuyuki Kiura :
Summary of the Japanese Respiratory Society statement for the treatment of lung cancer with comorbid interstitial pneumonia.,
Respiratory Investigation, Vol.57, No.6, 512-533, 2019.

(要約): Dramatic progress in targeted therapy and immunotherapy has been changing clinical practices in lung cancer. With the accumulation of clinical practice, it has become clear that pre-existing interstitial pneumonia (IP) could be a risk factor for drug-induced lung injury, which has enhanced awareness regarding the difficulty in treating lung cancer with comorbid IP. Unfortunately, there is only low-grade evidence in the field of lung cancer with comorbid IP, because almost all clinical trials exclude such patients. There have been very few specialized clinical trials for patients with lung cancer and underlying IPs thus far. Therefore, it is necessary to treat such cases empirically or to give up on the treatment itself. Considering these circumstances, establishing how to treat lung cancer with comorbid IP is an urgent issue. This paper is a summary of the official statement reported by the Diffuse Lung Disease/Thoracic Oncology Assembly and the Japanese Respiratory Society (JRS) in 2017, which attempts to approach lung cancer with comorbid IP systematically.
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.resinv.2019.06.001
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31377122; ● Search Scopus @ Elsevier (PMID): 31377122; ● Search Scopus @ Elsevier (DOI): 10.1016/j.resinv.2019.06.001

(DOI: 10.1016/j.resinv.2019.06.001, PubMed: 31377122) Masaki Hanibuchi, Akira Kanoh, Takuya Kuramoto, Tatsuro Saito, Makoto Tobiume, Atsuro Saijo, Hiroyuki Kozai, Mayo Kondou, Shun Morizumi, Hiroto Yoneda, Kozo Kagawa, Hirokazu Ogino, Seidai Satou, Hiroshi Kawano, Kenji Otsuka, Yuko Toyoda, Hiroshi Nokihara, Hisatsugu Goto and Yasuhiko Nishioka :
Development, validation, and comparison of gene analysis methods for detecting mutation from non-small cell lung cancer patients-derived circulating free DNA.,
Oncotarget, Vol.10, No.38, 3654-3666, 2019.

(徳島大学機関リポジトリ): ● Metadata: 115668
(出版サイトへのリンク): ● Publication site (DOI): 10.18632/oncotarget.26951
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31217900; ● Search Scopus @ Elsevier (PMID): 31217900; ● Search Scopus @ Elsevier (DOI): 10.18632/oncotarget.26951

(徳島大学機関リポジトリ: 115668, DOI: 10.18632/oncotarget.26951, PubMed: 31217900) Atsuro Saijo, Masaki Hanibuchi, Hirokazu Ogino, Kenji Otsuka, Hisatsugu Goto, Hiroshi Nokihara and Yasuhiko Nishioka :
Paclitaxel for relapsed small-cell lung cancer patients with idiopathic interstitial pneumonias.,
Molecular and Clinical Oncology, Vol.10, No.5, 541-546, 2019.

(要約): Although first-line chemotherapy is highly sensitive against small-cell lung cancer (SCLC), most patients subsequently experience disease progression. Topotecan is the standard therapy for sensitive-relapsed SCLC patients, and subgroup analysis of a randomized phase III trial suggests that amrubicin is effective for refractory-relapsed SCLC. However, because of the lack of the evidence based on clinical trials, the effectiveness of systemic chemotherapy for relapsed SCLC patients with idiopathic interstitial pneumonias (IIPs) is unclear. In the presentstudy, 17 relapsed SCLC patients with IIPs who received a paclitaxel (PTX)-containing regimen as a second-line chemotherapy were retrospectively reviewed. The overall response rate and the disease control rate of the PTX-containing regimens were 29.4 and 47.1%, respectively. The median progression-free survival and the overall survival of the regimens were 2.7 months [95% confidence interval (CI), 1.6-3.6 months] and 3.6 months (95% CI, 2.3-14.0 months), respectively. Grade 3-4 neutropenia and febrile neutropenia occurred in 12 (70.6%) and 2 (11.8%) patients, respectively. During the treatment period, acute exacerbation (AE) of IIPs was observed in five patients (29.4%). Treatment-associated fatality was observed in 1 patient with febrile neutropenia and in 1 patient with AE of IIPs. PTX had promising anti-tumor activity against refractory-relapsed SCLC with IIPs. However, the survival benefit of the treatment was limited because of the high incidence of AE of IIPs and treatment-related death.
(出版サイトへのリンク): ● Publication site (DOI): 10.3892/mco.2019.1828
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30967948; ● Search Scopus @ Elsevier (PMID): 30967948; ● Search Scopus @ Elsevier (DOI): 10.3892/mco.2019.1828

(DOI: 10.3892/mco.2019.1828, PubMed: 30967948) Hirokazu Ogino, Masaki Hanibuchi, Satoshi Sakaguchi, Yuko Toyoda, Toshifumi Tezuka, Hiroshi Kawano, Soji Kakiuchi, Kenji Otsuka, Atsuro Saijo, Masahiko Azuma, Hiroshi Nokihara, Hisatsugu Goto and Yasuhiko Nishioka :
The clinical features of older patients with lung cancer in comparison with their younger counterparts.,
Respiratory Investigation, Vol.57, No.1, 40-48, 2019.

(要約): We should positively consider standard treatments for older patients. However, not only their shorter life expectancy but also their poor PS and multiple comorbidities that sometimes render patients unable to receive standard treatments and several chemotherapy regimens, make their prognosis poor. The standard treatments for older patients, especially in locally advanced stages, require modification.
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.resinv.2018.10.003
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30448243; ● Search Scopus @ Elsevier (PMID): 30448243; ● Search Scopus @ Elsevier (DOI): 10.1016/j.resinv.2018.10.003

(DOI: 10.1016/j.resinv.2018.10.003, PubMed: 30448243) Masaki Hanibuchi, Soji Kakiuchi, Shinji Atagi, Fumitaka Ogushi, Eiji Shimizu, Takashi Haku, Yuko Toyoda, Masahiko Azuma, Mayo Kondo, Hiroshi Kawano, Kenji Otsuka, Satoshi Sakaguchi, Hiroshi Nokihara, Hisatsugu Goto and Yasuhiko Nishioka :
A multicenter, open-label, phase II trial of S-1 plus carboplatin in advanced non-small cell lung cancer patients with interstitial lung disease.,
Lung Cancer, Vol.125, 93-99, 2018.

(要約): A total of 33 advanced or recurrent NSCLC patients with ILD were prospectively enrolled in this multicenter, open-label, phase II study. Every 4 weeks, CBDCA at a dose of AUC 5 on day 1 and S-1 at a dose of 80 mg/m
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.lungcan.2018.09.007
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30429044; ● Search Scopus @ Elsevier (PMID): 30429044; ● Search Scopus @ Elsevier (DOI): 10.1016/j.lungcan.2018.09.007

(DOI: 10.1016/j.lungcan.2018.09.007, PubMed: 30429044) Atsuro Saijo, Hisatsugu Goto, Nakano Mayuri, Mitsuhashi Atsushi, Yoshinori Aono, Masaki Hanibuchi, Hirohisa Ogawa, Hisanori Uehara, Kazuya Kondo and Yasuhiko Nishioka :
Bone marrow-derived fibrocytes promote stem cell-like properties of lung cancer cells.,
Cancer Letters, Vol.421, 17-27, 2018.

(要約): Cancer stem cells (CSCs) represent a minor population that have clonal tumor initiation and self-renewal capacity and are responsible for tumor initiation, metastasis, and therapeutic resistance. CSCs reside in niches, which are composed of diverse types of stromal cells and extracellular matrix components. These stromal cells regulate CSC-like properties by providing secreted factors or by physical contact. Fibrocytes are differentiated from bone marrow-derived CD14 monocytes and have features of both macrophages and fibroblasts. Accumulating evidence has suggested that stromal fibrocytes might promote cancer progression. However, the role of fibrocytes in the CSC niches has not been revealed. We herein report that human fibrocytes enhanced the CSC-like properties of lung cancer cells through secreted factors, including osteopontin, CC-chemokine ligand 18, and plasminogen activator inhibitor-1. The PIK3K/AKT pathway was critical for fibrocytes to mediate the CSC-like functions of lung cancer cells. In human lung cancer specimens, the number of tumor-infiltrated fibrocytes was correlated with high expression of CSC-associated protein in cancer cells. These results suggest that fibrocytes may be a novel cell population that regulates the CSC-like properties of lung cancer cells in the CSC niches.
(徳島大学機関リポジトリ): ● Metadata: 111437
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.canlet.2018.02.016
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29448000; ● Summary page in Scopus @ Elsevier: 2-s2.0-85042214220

(徳島大学機関リポジトリ: 111437, DOI: 10.1016/j.canlet.2018.02.016, PubMed: 29448000, Elsevier: Scopus) Sho Tabata, Masatatsu Yamamoto, Hisatsugu Goto, Akiyoshi Hirayama, Maki Ohishi, Takuya Kuramoto, Ryuji Ikeda, Misako Haraguchi, Kohichi Kawahara, Yoshinari Shinsato, Kentaro Minami, Atsuro Saijo, Yuko Toyoda, Masaki Hanibuchi, Yasuhiko Nishioka, Saburo Sone, Hiroyasu Esumi, Masaru Tomita, Tomoyoshi Soga, Tatsuhiko Furukawa and Shin-ichi Akiyama :
Thymidine catabolism promotes NADPH oxidase-derived reactive oxygen species (ROS) signalling in KB and yumoto cells.,
Scientific Reports, Vol.8, No.1, 6760, 2018.

(要約): Thymidine phosphorylase (TP) is a rate-limiting enzyme in the thymidine catabolic pathway. TP is identical to platelet-derived endothelial cell growth factor and contributes to tumour angiogenesis. TP induces the generation of reactive oxygen species (ROS) and enhances the expression of oxidative stress-responsive genes, such as interleukin (IL)-8. However, the mechanism underlying ROS induction by TP remains unclear. In the present study, we demonstrated that TP promotes NADPH oxidase-derived ROS signalling in cancer cells. NADPH oxidase inhibition using apocynin or small interfering RNAs (siRNAs) abrogated the induction of IL-8 and ROS in TP-expressing cancer cells. Meanwhile, thymidine catabolism induced by TP increased the levels of NADPH and intermediates of the pentose phosphate pathway (PPP). Both siRNA knockdown of glucose 6-phosphate dehydrogenase (G6PD), a rate-limiting enzyme in PPP, and a G6PD inhibitor, dihydroepiandrosterone, reduced TP-induced ROS production. siRNA downregulation of 2-deoxy-D-ribose 5-phosphate (DR5P) aldolase, which is needed for DR5P to enter glycolysis, also suppressed the induction of NADPH and IL-8 in TP-expressing cells. These results suggested that TP-mediated thymidine catabolism increases the intracellular NADPH level via the PPP, which enhances the production of ROS by NADPH oxidase and activates its downstream signalling.
(徳島大学機関リポジトリ): ● Metadata: 114957
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/s41598-018-25189-y
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29713062; ● Search Scopus @ Elsevier (PMID): 29713062; ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-018-25189-y

(徳島大学機関リポジトリ: 114957, DOI: 10.1038/s41598-018-25189-y, PubMed: 29713062) Hisatsugu Goto, Okano Yoshio, Machida Hisanori, Hatakeyama Nobuo, Ogushi Fumitaka, Haku Takashi, Takanori Kanematsu, Tomoyuki Urata, Souji Kakiuchi, Masaki Hanibuchi, Saburo Sone and Yasuhiko Nishioka :
Phase II study of tailored S-1 monotherapy with a 1-week interval after a 2-week dosing period in elderly patients with advanced non-small cell lung cancer.,
Respiratory Investigation, Vol.56, No.1, 80-86, 2018.

(要約): S-1 is an oral fluoropyrimidine that is active in the treatment of non-small cell lung cancer (NSCLC); however, an optimal treatment schedule and appropriate dose adjustments of S-1 in elderly patients have not yet been established. We conducted a phase II trial to evaluate the efficacy and safety of a 2-week S-1 monotherapy treatment followed by a 1-week interval as a first-line treatment of elderly NSCLC patients, by adjusting the dose based on the individual creatinine clearance (Ccr) and body surface area (BSA). The primary endpoint was the disease control rate. Forty patients were enrolled. The disease control and response rates were 89.5% (95% confidence interval [CI] = 79.8-99.2) and 7.9% (95% CI = 0.0-16.4), respectively. The median progression-free survival and overall survival times were 4.4 months (95% CI = 4.2-8.5) and 17.0 months (95% CI = 11.2-18.7), respectively. Neutropenia, anorexia, hyponatremia, hypokalemia, and pneumonia of grade ≥ 3 occurred in 5.0%, 7.5%, 5.0%, 2.5%, and 2.5% of patients, respectively. Among the patient-reported outcomes, most of the individual factors in the patients' quality of life, including upper intestine-related symptoms improved with the treatment, except for dyspnea, which slightly albeit continuously worsened throughout the study. In elderly patients with previously untreated advanced NSCLC, a 2-week S-1 monotherapy treatment, tailored to both the Ccr and BSA, with a 1-week interval was well tolerated and demonstrated promising efficacy. This study was registered at the University Hospital Medical Information Network (UMIN) Center (ID: UMIN000002035), Japan.
(キーワード): Administration, Oral / Aged / Aged, 80 and over / Antimetabolites, Antineoplastic / Body Surface Area / Carcinoma, Non-Small-Cell Lung / Creatinine / Drug Administration Schedule / Drug Combinations / Female / Humans / Lung Neoplasms / Male / Metabolic Clearance Rate / Oxonic Acid / Precision Medicine / Survival Rate / Tegafur / Treatment Outcome
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.resinv.2017.09.003
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29325686; ● Summary page in Scopus @ Elsevier: 2-s2.0-85031768203

(DOI: 10.1016/j.resinv.2017.09.003, PubMed: 29325686, Elsevier: Scopus) 瀧倉輝実, 埴淵昌毅, 豊田優子, 近藤真代, 香西博之, 福家麻美, 西岡安彦 :
胸水中に多数のLanghans型巨細胞を認めた胸水IL-6濃度が高値であったMycobacterium avium症に伴う胸膜炎の一例,
結核, Vol.92, No.9, 559-566, 2017年. Sho Tabata, Masatatsu Yamamoto, Hisatsugu Goto, Akiyoshi Hirayama, Maki Ohishi, Takuya Kuramoto, Atsushi Mitsuhashi, Ryuji Ikeda, Misako Haraguchi, Kohichi Kawahara, Yoshinari Shinsato, Kentaro Minami, Atsuro Saijo, Masaki Hanibuchi, Yasuhiko Nishioka, Saburo Sone, Hiroyasu Esumi, Masaru Tomita, Tomoyoshi Soga, Tatsuhiko Furukawa and Shin-ichi Akiyama :
Thymidine Catabolism as a Metabolic Strategy for Cancer Survival.,
Cell Reports, Vol.19, No.7, 1313-1321, 2017.

(要約): Thymidine phosphorylase (TP), a rate-limiting enzyme in thymidine catabolism, plays a pivotal role in tumor progression; however, the mechanisms underlying this role are not fully understood. Here, we found that TP-mediated thymidine catabolism could supply the carbon source in the glycolytic pathway and thus contribute to cell survival under conditions of nutrient deprivation. In TP-expressing cells, thymidine was converted to metabolites, including glucose 6-phosphate, lactate, 5-phospho-α-D-ribose 1-diphosphate, and serine, via the glycolytic pathway both in vitro and in vivo. These thymidine-derived metabolites were required for the survival of cells under low-glucose conditions. Furthermore, activation of thymidine catabolism was observed in human gastric cancer. These findings demonstrate that thymidine can serve as a glycolytic pathway substrate in human cancer cells.
(徳島大学機関リポジトリ): ● Metadata: 115054
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.celrep.2017.04.061
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28514652; ● Search Scopus @ Elsevier (PMID): 28514652; ● Search Scopus @ Elsevier (DOI): 10.1016/j.celrep.2017.04.061

(徳島大学機関リポジトリ: 115054, DOI: 10.1016/j.celrep.2017.04.061, PubMed: 28514652) Atsuro Saijo, Masaki Hanibuchi, Hisatsugu Goto, Yuko Toyoda, Toshifumi Tezuka and Yasuhiko Nishioka :
An analysis of the clinical features of lung cancer in patients with connective tissue diseases.,
Respiratory Investigation, Vol.55, No.2, 153-160, 2017.

(要約): LC patients with CTD had a high prevalence of ILD, and the presence of CTD-ILD was significantly associated with poor prognosis.
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.resinv.2016.11.003
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28274531; ● Search Scopus @ Elsevier (PMID): 28274531; ● Search Scopus @ Elsevier (DOI): 10.1016/j.resinv.2016.11.003

(DOI: 10.1016/j.resinv.2016.11.003, PubMed: 28274531) Soji Kakiuchi, Masaki Hanibuchi, Toshifumi Tezuka, Atsuro Saijo, Kenji Otsuka, Satoshi Sakaguchi, Yuko Toyoda, Hisatsugu Goto, Hiroshi Kawano, Masahiko Azuma, Fumitaka Ogushi and Yasuhiko Nishioka :
Analysis of acute exacerbation of interstitial lung disease associated with chemotherapy in patients with lung cancer: A feasibility of S-1.,
Respiratory Investigation, Vol.55, No.2, 145-152, 2016.

(要約): Although this was a small retrospective study, its findings showed that S-1 and etoposide may be relatively safe options for the treatment of patients with lung cancer and concomitant ILD.
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.resinv.2016.10.008
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28274530; ● Search Scopus @ Elsevier (PMID): 28274530; ● Search Scopus @ Elsevier (DOI): 10.1016/j.resinv.2016.10.008

(DOI: 10.1016/j.resinv.2016.10.008, PubMed: 28274530) Yuko Toyoda, Ryohiko Ozaki, Jun Kishi, Masaki Hanibuchi, Katsuhiro Kinoshita, Toshifumi Tezuka, Hisatsugu Goto, Hiroyuki Ono, Kojiro Nagai, Yoshimi Bando, Toshio Doi and Yasuhiko Nishioka :
An Autopsy Case of Aortic Intimal Sarcoma Initially Diagnosed as Polyarteritis Nodosa.,
Internal Medicine, Vol.55, No.21, 3191-3195, 2016.

(要約): A 61-year-old man had hypertension with stenosis in the left renal artery. When his fever, abdominal pain, and renal dysfunction progressed, he was admitted to our hospital. He was diagnosed with polyarthritis nodosa. His renal function rapidly deteriorated despite immunosuppressive therapy. His digestive tract perforated twice, and he subsequently died. An autopsy revealed that aortic intimal sarcoma caused stenosis in multiple arteries. Both polyarteritis nodosa and aortic intimal sarcoma are very rare diseases and the diagnoses are very difficult. It is very important to consider these entities when making a differential diagnosis of vasculitis.
(キーワード): Abdominal Pain / Aorta / Autopsy / Diagnosis, Differential / Fatal Outcome / Fever / Humans / Male / Middle Aged / Polyarteritis Nodosa / Renal Artery Obstruction / Sarcoma / Vascular Neoplasms
(徳島大学機関リポジトリ): ● Metadata: 114395
(出版サイトへのリンク): ● Publication site (DOI): 10.2169/internalmedicine.55.7152
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27803418; ● Search Scopus @ Elsevier (PMID): 27803418; ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.55.7152

(徳島大学機関リポジトリ: 114395, DOI: 10.2169/internalmedicine.55.7152, PubMed: 27803418) Hirokazu Ogino, Masaki Hanibuchi, Souji Kakiuchi, Atsuro Saijo, Toshifumi Tezuka, Yuko Toyoda, Makoto Tobiume, Kenji Otsuka, Satoshi Sakaguchi, Hisatsugu Goto, Kokichi Arisawa and Yasuhiko Nishioka :
Analysis of the prognostic factors of extensive disease small-cell lung cancer patients in Tokushima University Hospital,
The Journal of Medical Investigation : JMI, Vol.63, No.3 4, 286-293, 2016.

(要約): Small-cell lung cancer (SCLC) presents aggressive clinical behavior, and its prognosis is still poor. Previously, performance status (PS), or the existence of brain, bone, or liver metastasis were reported to be unfavorable prognostic factors. Given the recent progress of treatment modalities such as radiotherapy techniques and bone modifying agents, the prognostic factors might be different from previous findings. Therefore, we analyzed the prognostic factors of extensive disease SCLC (ED-SCLC) in recent years. ED-SCLC patients treated in Tokushima University Hospital between 2010 and 2016 were analyzed. Log-rank test and the Cox proportional hazards regression model was used in univariate and multivariate analysis, respectively. Totally, 79 patients were analyzed. In the univariate analysis, age, PS, interstitial pneumonia (IP), liver metastasis, pleural dissemination, neutrophil counts, hypoalbuminemia, hypercalcemia and several liver and biliary enzymes were identified as poor prognostic factors. In the multivariate analysis, age, PS, IP, and liver and biliary enzymes were identified. Moreover, the PS in patients with liver metastasis was significantly worsened. In this study, we newly demonstrated that IP was a significant poor prognostic factor of ED-SCLC. Although liver metastasis was not extracted in multivariate analysis, it may have an impact on the prognosis of ED-SCLC. J. Med. Invest. 63: 286-293, August, 2016.
(徳島大学機関リポジトリ): ● Metadata: 111196
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.63.286
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27644574; ● Summary page in Scopus @ Elsevier: 2-s2.0-84987918312

(徳島大学機関リポジトリ: 111196, DOI: 10.2152/jmi.63.286, PubMed: 27644574, Elsevier: Scopus) Yuko Toyoda, Masaki Hanibuchi, Jun Kishi, Hiroshi Kawano, Shun Morizumi, Seidai Satou, M Kondo, Terumi Takikura, Toshifumi Tezuka, Hisatsugu Goto and Yasuhiko Nishioka :
Clinical features and outcome of acute exacerbation of interstitial pneumonia associated with connective tissue disease.,
The Journal of Medical Investigation : JMI, Vol.63, No.3,4, 294-299, 2016.

(要約): Acute exacerbation (AE) of interstitial lung disease is reported to be developed in not only idiopathic pulmonary fibrosis but also connective tissue disease-associated interstitial pneumonia (CTD-IP). As the significance of AE of CTD-IP has not been so widely recognized, its clinical feature is not fully elucidated. In the present study, we investigated the incidence, clinical features and outcome of AE of CTD-IP. We retrospectively reviewed admitted cases in our department with medical record from 2011 to 2015. Among 155 patients with CTD-IP, 10 (6.5%) cases developed AE (6 rheumatoid arthritis, 2 polymyositis/dermatomyositis, 1 systemic lupus erythematosus, 1 Sjögren syndrome), and one died of AE within 30 days. Median survival time after the onset of AE was 169 days in all 10 patients. The treatment with immunosuppressant just before AE onset might improve the prognosis of AE. The median survival time after the onset of AE was significantly longer in patients showing good response to corticosteroid compared with those with poor response to corticosteroid (805 days and 45 days, respectively) (p <0.05), suggesting that there are some cases in CTD-IP, showing the good response to corticosteroid even when AE was complicated. J. Med. Invest. 63: 294-299, August, 2016.
(徳島大学機関リポジトリ): ● Metadata: 111197
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.63.294
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27644575; ● Summary page in Scopus @ Elsevier: 2-s2.0-84987881651

(徳島大学機関リポジトリ: 111197, DOI: 10.2152/jmi.63.294, PubMed: 27644575, Elsevier: Scopus) 山子泰斗, 埴淵昌毅, 荻野広和, 村上永尚, 梶龍兒, 西岡安彦 :
多彩な神経症状を呈した小細胞肺癌に伴う傍腫瘍性神経症候群の1例,
肺癌, Vol.56, No.3, 199-204, 2016年.

(要約): 背景．傍腫瘍性神経症候群は担癌患者に生じる神経障害であり，腫瘍の転移や浸潤・圧排，代謝異常や栄養障害によるものではなく，自己免疫学的機序による神経系の障害により生じる．傍腫瘍性神経症候群を合併する腫瘍は小細胞肺癌が最も多いとされている．症例．77歳男性．従来自立した生活を送っていたがX年10月頃より倦怠感が出現した．その後歩行障害が進行し排尿障害も出現したため，X+1年5月中旬に当院紹介となった．構音・嚥下障害や両下肢の運動・感覚障害，自律神経失調など多彩な神経症状を認め，精査によりLambert-Eaton症候群と診断された．自己抗体検査では，抗amphiphysin抗体，抗ガングリオシド(GM1，GT1b)抗体が陽性であった．精査にて小細胞肺癌cTXN2M1b(Stage IV)と診断した．PS 4のため化学療法の適応はないと判断した．免疫グロブリン大量療法を施行するも神経所見は改善しなかった．緩和医療目的に近医に転院し，X+1年10月下旬に死亡した．結論．複数の自己抗体が検出され多彩な神経症状を呈した小細胞肺癌に伴う傍腫瘍性神経症候群の1例を経験した．
(キーワード): 傍腫瘍性神経症候群 / 小細胞肺癌 / Lambert-Eaton症候群 / 抗amphiphysin抗体 / 抗ガングリオシド抗体
(徳島大学機関リポジトリ): ● Metadata: 117547
(出版サイトへのリンク): ● Publication site (DOI): 10.2482/haigan.56.199
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390001204681086464; ● Search Scopus @ Elsevier (DOI): 10.2482/haigan.56.199

(徳島大学機関リポジトリ: 117547, DOI: 10.2482/haigan.56.199, CiNii: 1390001204681086464) Lee Jeong Ho, Masaki Hanibuchi, Kim Sun-Jin, Hyunkyung Yu, Kim Seungwook Mark, He Junqin, Langley R. Robert, Lehembre Francois, Regenass Urs and Fidler J. Isaiah :
Treatment of experimental human breast cancer and lung cancer brain metastases in mice by macitentan, a dual antagonist of endothelin receptors, combined with paclitaxel,
Neuro-Oncology, Vol.18, No.4, 486-496, 2016.

(要約): We recently demonstrated that brain endothelial cells and astrocytes protect cancer cells from chemotherapy through an endothelin-dependent signaling mechanism. Here, we evaluated the efficacy of macitentan, a dual endothelin receptor (ETAR and ETBR) antagonist, in the treatment of experimental breast and lung cancer brain metastases. The effect of macitentan on astrocyte- and brain endothelial cell-mediated chemoprotective properties was measured in cytotoxic assays. We compared survival of mice bearing established MDA-MB-231 breast cancer or PC-14 non-small cell lung cancer (NSCLC) brain metastases that were treated with vehicle, macitentan, paclitaxel, or macitentan plus paclitaxel. Cell division, apoptosis, tumor vasculature, and expression of survival-related proteins were assessed by immunofluorescent microscopy. Cancer cells and tumor-associated endothelial cells expressed activated forms of AKT and MAPK in vehicle- and paclitaxel-treated groups in both metastasis models, but these proteins were downregulated in metastases of mice that received macitentan. The survival-related proteins Bcl2L1, Gsta5, and Twist1 that localized to cancer cells and tumor-associated endothelial cells in vehicle- and paclitaxel-treated tumors were suppressed by macitentan. Macitentan or paclitaxel alone had no effect on survival. However, when macitentan was combined with paclitaxel, we noted a significant reduction in cancer cell division and marked apoptosis of both cancer cells and tumor-associated endothelial cells. Moreover, macitentan plus paclitaxel therapy significantly increased overall survival by producing complete responses in 35 of 35 mice harboring brain metastases. Dual antagonism of ETAR and ETBR signaling sensitizes experimental brain metastases to paclitaxel and may represent a new therapeutic option for patients with brain metastases.
(出版サイトへのリンク): ● Publication site (DOI): 10.1093/neuonc/now037
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26995790; ● Summary page in Scopus @ Elsevier: 2-s2.0-84966533797

(DOI: 10.1093/neuonc/now037, PubMed: 26995790, Elsevier: Scopus) Seidai Satou, Masaki Hanibuchi, Takahashi Mikiko, Fukuda Yuh, Morizumi Shun, Yuko Toyoda, Hisatsugu Goto and Yasuhiko Nishioka :
A patient with idiopathic pleuroparenchymal fibroelastosis showing a sustained pulmonary function due to treatment with pirfenidone,
Internal Medicine, Vol.55, No.5, 497-501, 2016.

(要約): The patient was a 68-year-old man presenting with body weight loss and exertional dyspnea. High-resolution computed tomography of the chest showed dense subpleural consolidation with traction bronchiectasis and volume loss predominantly in bilateral apical lesions and upper lobes. A histopathological analysis of a specimen of the right upper lobe showed histological patterns which were consistent with idiopathic pleuroparenchymal fibroelastotis (IPPFE). Treatment with pirfenidone was introduced with the expectation of its potential benefit. The effect of pirfenidone was satisfactory, and a decline in forced vital capacity was inhibited during treatment. This is the first case report suggesting the efficacy of pirfenidone for patients with IPPFE.
(徳島大学機関リポジトリ): ● Metadata: 114388
(出版サイトへのリンク): ● Publication site (DOI): 10.2169/internalmedicine.55.5047
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26935370; ● Summary page in Scopus @ Elsevier: 2-s2.0-84959267460

(徳島大学機関リポジトリ: 114388, DOI: 10.2169/internalmedicine.55.5047, PubMed: 26935370, Elsevier: Scopus) Hirokazu Ogino, Masaki Hanibuchi, Hiromitsu Takizawa, Shoji Sakiyama, Sumitomo Hiroyuki, Seiji Iwamoto, Hitoshi Ikushima, Nakajima Kohei, Shinji Nagahiro, Yamago Taito, Yuko Toyoda, Yoshimi Bando and Yasuhiko Nishioka :
Primary Pulmonary Synovial Sarcoma Showing a Prolonged Survival with Multimodality Therapy,
Internal Medicine, Vol.55, No.4, 381-387, 2016.

(要約): A 54-year-old man was referred to our hospital due to a mass shadow noted on a chest X-ray. Thoracoscopic lobectomy yielded a diagnosis of primary pulmonary synovial sarcoma according to the histology and SYT-SSX1 gene analyses. Five months after the thoracic surgery, he developed brain metastasis; therefore, we performed resection of the brain metastatic focus followed by radiotherapy. As a local recurrence in the thoracic cavity concurrently emerged, systemic chemotherapy was also administered. These observations indicated that a multidisciplinary approach may be useful against primary pulmonary synovial sarcoma, although there is presently no established therapeutic strategy due to its rarity and highly aggressive nature.
(徳島大学機関リポジトリ): ● Metadata: 114387
(出版サイトへのリンク): ● Publication site (DOI): 10.2169/internalmedicine.55.5169
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26875964; ● Search Scopus @ Elsevier (PMID): 26875964; ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.55.5169

(徳島大学機関リポジトリ: 114387, DOI: 10.2169/internalmedicine.55.5169, PubMed: 26875964) 梶田敬介, 佐藤正大, 豊田優子, 坂口暁, 手塚敏史, 後東久嗣, 埴淵昌毅, 西岡安彦 :
クリゾチニブが奏効したperformance status不良anaplastic lymphoma kinase遺伝子転座陽性肺腺癌の1例,
四国医学雑誌, Vol.71, No.5,6, 141-148, 2015年.

(要約): A 27-year-old female was referred to our hospital for further examination of hoarseness, cough, and hemoptysis. Positron emission tomography-computed tomography revealed FDG accumulation in a huge mass in the left lower lobe, lymph nodes in the hilum, mediastinum and right cervical lesion left scapula and vertebral body. Further examination yielded the diagnosis of primary lung adenocarcinoma (cT2aN3M1b : Stage IV) harboring the anaplastic lymphoma kinase (ALK) fusion oncogene. Although her general condition was getting worse due to rapid increase of the pleural effusion, crizotinib promptly diminish the pleural effusion and ameliorated the patient's condition. The adverse events of crizotinib, such as nausea, vomiting and visual disturbance, were generally mild and well tolerable during treatment. These findings suggest that crizotinib is a promising candidate for ALK-positive non-small cell lung cancer patients even with poor performances.
(キーワード): crizotinib / anaplastic lymphoma kinase / non-small cell lung cancer / performance status
(徳島大学機関リポジトリ): ● Metadata: 109939
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1050564287418456448

(徳島大学機関リポジトリ: 109939, CiNii: 1050564287418456448) Mitsuhashi Atsushi, Hisatsugu Goto, Atsuro Saijo, Trung The Van, Yoshinori Aono, Hirokazu Ogino, Kuramoto Takuya, Tabata Sho, Hisanori Uehara, Keisuke Izumi, Mitsuteru Yoshida, Kobayashi Hiroaki, Takahashi Hidefusa, Gotoh Masashi, Kakiuchi Soji, Masaki Hanibuchi, Seiji Yano, Yokomise Hiroyasu, Shoji Sakiyama and Yasuhiko Nishioka :
Fibrocyte-like cells mediate acquired resistance to anti-angiogenic therapy with bevacizumab,
Nature Communications, Vol.6, 8792, 2015.

(要約): Bevacizumab exerts anti-angiogenic effects in cancer patients by inhibiting vascular endothelial growth factor (VEGF). However, its use is still limited due to the development of resistance to the treatment. Such resistance can be regulated by various factors, although the underlying mechanisms remain incompletely understood. Here we show that bone marrow-derived fibrocyte-like cells, defined as alpha-1 type I collagen-positive and CXCR4-positive cells, contribute to the acquired resistance to bevacizumab. In mouse models of malignant pleural mesothelioma and lung cancer, fibrocyte-like cells mediate the resistance to bevacizumab as the main producer of fibroblast growth factor 2. In clinical specimens of lung cancer, the number of fibrocyte-like cells is significantly increased in bevacizumab-treated tumours, and correlates with the number of treatment cycles, as well as CD31-positive vessels. Our results identify fibrocyte-like cells as a promising cell biomarker and a potential therapeutic target to overcome resistance to anti-VEGF therapy.
(徳島大学機関リポジトリ): ● Metadata: 115640
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/ncomms9792
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26635184; ● Summary page in Scopus @ Elsevier: 2-s2.0-84949310071

(徳島大学機関リポジトリ: 115640, DOI: 10.1038/ncomms9792, PubMed: 26635184, Elsevier: Scopus) 埴淵昌毅, 西岡安彦 :
Current topics from major journals-英文抄読会から ALK陽性非小細胞肺癌に対する1次治療でのクリゾチニブと化学療法の比較試験,
日本胸部臨床, Vol.74, No.6, 717, 2015年. Hiroshi Kawano, Masaki Hanibuchi, Yoshijima Terumi, Yuko Toyoda, Jun Kishi, Toshifumi Tezuka and Yasuhiko Nishioka :
A case of atypical Takayasu arteritis initially presenting with peripheral artery disease,
Case Reports in Clinical Pathology, Vol.2, No.2, 34-40, 2015.

(出版サイトへのリンク): ● Publication site (DOI): 10.5430/crcp.v2n2p34
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.5430/crcp.v2n2p34

(DOI: 10.5430/crcp.v2n2p34) 中野万有里, 吉田成二, 中山正, 大串文隆, 埴淵昌毅, 西岡安彦 :
インフルエンザ (H1N1) 2009に伴うARDSにPMX-DHP療法が奏効した1例,
感染症学雑誌, Vol.89, No.3, 416-421, 2015年.

(要約): A 51-year-old man was admitted to our hospital because of fever and diarrhea. Chest X-ray revealed consolidation in the left lower lung field. Ceftriaxone and minocycline were given empirically, under the suspicion of bacterial or atypical pneumonia. In spite of treatment with antibiotics, the disease rapidly progressed to systemic inflammatory response syndrome. The diagnosis of acute respiratory distress syndrome (ARDS) accompanied with influenza (H1N1) 2009 was made because of positive findings of real-time polymerase chain reaction. While multidisciplinary treatment was performed, his condition was further deteriorated suggesting the excessive pro-inflammatory mediators. To remove them, we conducted polymyxin-B immobilized column-direct hemoperfusion (PMX-DHP), and his general condition recovered successfully. PMX-DHP may be a useful treatment choice for ARDS accompanied with influenza.
(キーワード): influenza (H1N1) 2009 / ARDS / PMX-DHP
(出版サイトへのリンク): ● Publication site (DOI): 10.11150/kansenshogakuzasshi.89.416
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390282680028294784; ● Summary page in Scopus @ Elsevier: 2-s2.0-84953344678

(DOI: 10.11150/kansenshogakuzasshi.89.416, CiNii: 1390282680028294784, Elsevier: Scopus) 埴淵昌毅, 大塚憲司, 塚﨑佑貴, 坂下直実, 功刀しのぶ, 福田悠, 西岡安彦 :
Acute fibrinous and organizing pneumoniaパターンの特発性間質性肺炎が示唆された1例,
THE LUNG perspectives, Vol.23, No.2, 2-5, 2015年. Toshifumi Tezuka, Hirohisa Ogawa, Masahiko Azuma, Hisatsugu Goto, Hisanori Uehara, Yoshinori Aono, Masaki Hanibuchi, Yamaguchi Yoichi, Fujikawa Tomoyuki, Itai Akiko and Yasuhiko Nishioka :
IMD-4690, a novel specific inhibitor for plasminogen activator inhibitor-1, reduces allergic airway remodeling in a mouse model of chronic asthma via regulating angiogenesis and remodeling-related mediators,
PLoS ONE, Vol.10, No.3, e0121615, 2015.

(要約): Plasminogen activator inhibitor (PAI)-1 is the principal inhibitor of plasminogen activators, and is responsible for the degradation of fibrin and extracellular matrix. IMD-4690 is a newly synthesized inhibitor for PAI-1, whereas the effect on allergic airway inflammation and remodeling is still unclear. We examined the in vivo effects by using a chronic allergen exposure model of bronchial asthma in mice. The model was generated by an immune challenge for 8 weeks with house dust mite antigen, Dermatophagoides pteronyssinus (Dp). IMD-4690 was intraperitoneally administered during the challenge. Lung histopathology, hyperresponsiveness and the concentrations of mediators in lung homogenates were analyzed. The amount of active PAI-1 in the lungs was increased in mice treated with Dp. Administration with IMD-4690 reduced an active/total PAI-1 ratio. IMD-4690 also reduced the number of bronchial eosinophils in accordance with the decreased expressions of Th2 cytokines in the lung homogenates. Airway remodeling was inhibited by reducing subepithelial collagen deposition, smooth muscle hypertrophy, and angiogenesis. The effects of IMD-4690 were partly mediated by the regulation of TGF-, HGF and matrix metalloproteinase. These results suggest that PAI-1 plays crucial roles in airway inflammation and remodeling, and IMD-4690, a specific PAI-1 inhibitor, may have therapeutic potential for patients with refractory asthma due to airway remodeling.
(キーワード): Acetates / Airway Remodeling / Animals / Antigens, Dermatophagoides / Asthma / Biphenyl Compounds / Bronchi / Bronchoalveolar Lavage Fluid / Chronic Disease / Cytokines / Dermatophagoides pteronyssinus / Disease Models, Animal / Eosinophils / Female / Immunoglobulin E / Mice / Neovascularization, Pathologic / Plasminogen Activator Inhibitor 1 / Tissue Plasminogen Activator
(徳島大学機関リポジトリ): ● Metadata: 109460
(出版サイトへのリンク): ● Publication site (DOI): 10.1371/journal.pone.0121615
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25785861; ● Summary page in Scopus @ Elsevier: 2-s2.0-84925425817

(徳島大学機関リポジトリ: 109460, DOI: 10.1371/journal.pone.0121615, PubMed: 25785861, Elsevier: Scopus) Seidai Satou, Masaki Hanibuchi, Makoto Tobiume, Jun Kishi, Yuko Toyoda, Hiroshi Kawano, Mikiko Takahashi, Yuh Fukuda and Yasuhiko Nishioka :
A case of IgG4-related interstitial lung disease showing usual interstitial pneumonia pattern: Unusual case for histological features with pathological proof,
Case Reports in Clinical Pathology, Vol.2, No.1, 6-11, 2015.

(出版サイトへのリンク): ● Publication site (DOI): 10.5430/crcp.v2n1p6
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.5430/crcp.v2n1p6

(DOI: 10.5430/crcp.v2n1p6) Seidai Satou, Masaki Hanibuchi, Asami Fukuya, Youhei Yabuki, Hiroki Bando, Terumi Yoshijima, Hisatsugu Goto, Hirohisa Ogawa and Yasuhiko Nishioka :
Idiopathic pleuroparenchymal fibroelastosis is characterized by an elevated serum level of surfactant protein-D, but not krebs von den lungen-6,
Lung, Vol.192, No.5, 711-717, 2014.

(要約): Idiopathic pleuroparenchymal fibroelastosis (IPPFE) is a recently reported rare disease entity characterized by fibrotic thickening of the pleural and subpleural parenchyma predominantly in the upper lobes in idiopathic interstitial pneumonias (IIPs). Because the clinical features of this rare disease are not fully elucidated, we examined the clinical characteristics of IPPFE, especially for serum interstitial biomarkers, surfactant protein-D (SP-D), and Krebs von den Lungen-6 (KL-6). Four consecutive cases of IPPFE who fulfilled the diagnostic criteria were studied. All cases were more than 60 years of age, and were classified as underweight by body mass index. A severe restrictive ventilatory defect was found in all cases on admission. High-resolution computed tomography showed intense pleural thickening associated with fibrosis predominant in upper lobes. Histopathological findings were also confirmed in three out of four cases. Interestingly, the serum level of SP-D was markedly elevated in all cases, while KL-6 was within normal range in three out of four cases. As compared with major IIPs such as idiopathic pulmonary fibrosis and fibrotic nonspecific interstitial pneumonia, IPPFE significantly showed higher frequency of cases with a unique pattern of serum biomarkers, which is characterized by an elevated level of SP-D with a normal range of KL-6. In IPPFE, SP-D might tend to be elevated, while KL-6 was within a normal range. Further study is required to determine the pathogenesis and clinical significance of the elevated SP-D in IPPFE.
(キーワード): Aged / Autopsy / Biological Markers / Biopsy / Fatal Outcome / Humans / Idiopathic Interstitial Pneumonias / Lung / Male / Middle Aged / Mucin-1 / Pleural Diseases / Pulmonary Surfactant-Associated Protein D / Pulmonary Ventilation / Retrospective Studies / Spirometry / Time Factors / Tomography, X-Ray Computed / Treatment Outcome / Up-Regulation
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s00408-014-9599-0
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24880792; ● Summary page in Scopus @ Elsevier: 2-s2.0-84931443666

(DOI: 10.1007/s00408-014-9599-0, PubMed: 24880792, Elsevier: Scopus) Masaki Hanibuchi, SJ Kim, IJ Fidler and Yasuhiko Nishioka :
The molecular biology of lung cancer brain metastasis: an overview of current comprehensions and future perspectives,
The Journal of Medical Investigation : JMI, Vol.61, No.3,4, 241-253, 2014.

(要約): Brain metastases occur in 20-40% of patients with advanced malignancies and lung cancer is one of the most common causes of brain metastases. The occurrence of brain metastases is associated with poor prognosis and high morbidity in patients with advanced lung cancer, even after intensive multimodal therapy. Progress in treating brain metastases has been hampered by a lack of model systems, a lack of human tissue samples, and the exclusion of brain metastatic patients from many clinical trials. While the biology of brain metastasis is still poorly understood, it is encouraging to see more efforts are beginning to be directed toward the study of brain metastasis. During the multi-step process of metastasis, functional significance of gene expressions, changes in brain vasculature, abnormal secretion of soluble factors and activation of autocrine/paracrine signaling are considered to contribute to the brain metastasis development. A better understanding of the mechanism of this disease will help us to identify the appropriate therapeutic strategies, which leads to circumvent brain metastases. Recent findings on the biology of lung cancer brain metastases and translational leads identified by molecular studies are discussed in this review.
(徳島大学機関リポジトリ): ● Metadata: 109563
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.61.241
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25264041; ● Search Scopus @ Elsevier (PMID): 25264041; ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.61.241

(徳島大学機関リポジトリ: 109563, DOI: 10.2152/jmi.61.241, PubMed: 25264041) Kenji Yokoi, Tomonori Tanei, Biana Godin, Anne de van L. Ven, Masaki Hanibuchi, Aika Matsunoki, Jenolyn Alexander and Mauro Ferrari :
Serum biomarkers for personalization of nanotherapeutics-based therapy in different tumor and organ microenvironments,
Cancer Letters, Vol.345, No.1, 48-55, 2014.

(要約): Enhanced permeation and retention (EPR) effect, the mechanism by which nanotherapeutics accumulate in tumors, varies in patients based on differences in the tumor and organ microenvironment. Surrogate biomarkers for the EPR effect will aid in selecting patients who will accumulate higher amounts of nanotherapeutics and show better therapeutic efficacy. Our data suggest that the differences in the vascular permeability and pegylated liposomal doxorubicin (PLD) accumulation are tumor type as well as organ-specific and significantly correlated with the relative ratio of MMP-9 to TIMP-1 in the circulation, supporting development of these molecules as biomarkers for the personalization of nanoparticle-based therapy.
(キーワード): Animals / Antibiotics, Antineoplastic / Biomarkers, Tumor / Brain Neoplasms / Capillary Permeability / Doxorubicin / Drug Delivery Systems / Female / Liver Neoplasms, Experimental / Matrix Metalloproteinase 9 / Mice / Mice, Inbred BALB C / Mice, Inbred C57BL / Mice, Nude / ナノ粒子 (nanoparticles) / Neoplasms, Experimental / Polyethylene Glycols / Tissue Inhibitor of Metalloproteinase-1 / Tumor Microenvironment / Xenograft Model Antitumor Assays
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.canlet.2013.11.015
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24370567; ● Summary page in Scopus @ Elsevier: 2-s2.0-84893793833

(DOI: 10.1016/j.canlet.2013.11.015, PubMed: 24370567, Elsevier: Scopus) Yuko Toyoda, Sho Tabata, Jun Kishi, Takuya Kuramoto, Atsushi Mitsuhashi, Atsuro Saijo, Hiroshi Kawano, Hisatsugu Goto, Yoshinori Aono, Masaki Hanibuchi, Hideaki Horikawa, Toshihiro Nakajima, Tatsuhiko Furukawa, Saburo Sone, Shin-ichi Akiyama and Yasuhiko Nishioka :
Thymidine Phosphorylase Regulates the Expression of CXCL10 in Rheumatoid Arthritis Fibroblast-like Synoviocytes,
Arthritis & Rheumatology, Vol.66, No.3, 560-568, 2014.

(要約): Thymidine phosphorylase (TP) in rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLS) is induced by tumor necrosis factor α (TNFα) and other cytokines that have been reported to be major inflammation mediators in RA. We previously demonstrated that TP plays an important role in angiogenesis and tumor growth, invasion, and metastasis. The aim of this study was to investigate whether the role of TP in the pathogenesis of RA is similar to its role in tumors. In FLS obtained from 2 patients with RA, the expression of TP, interferon-γ (IFNγ)-inducible protein 10 (CXCL10), and other cytokines was measured by quantitative real-time polymerase chain reaction, immunoblotting, and enzyme-linked immunosorbent assays. Microarray analysis was performed using FLS transfected with TYMP complementary DNA and treated with a TP inhibitor. The expression of TP in FLS was up-regulated by TNFα, interleukin-1β (IL-1β), IL-17, IFNγ, and lipopolysaccharide. Microarray analysis of FLS overexpressing TP identified CXCL10 as a thymidine phosphorylase-related gene. The expression of CXCL10 was induced by TNFα, and this induction was suppressed by TYMP small interfering RNA and TP inhibitor. Furthermore, the combination of TNFα and IFNγ synergistically augmented the expression of TP and CXCL10. TP-induced CXCL10 expression was suppressed by the antioxidant EUK-8. In the synovial tissue of patients with RA, TP levels were significantly correlated with CXCL10 expression. The combination of TNFα and IFNγ strongly induced the expression of thymidine phosphorylase in RA FLS. The induction of thymidine phosphorylase enhanced the expression of CXCL10, which may contribute to the Th1 phenotype and bone destruction observed in RA.
(キーワード): Arthritis, Rheumatoid / Cells, Cultured / Chemokine CXCL10 / Cytokines / Humans / Interferon-gamma / Synovial Membrane / Thymidine Phosphorylase / Tumor Necrosis Factor-alpha
(徳島大学機関リポジトリ): ● Metadata: 106062
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/art.38263
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24574215; ● Summary page in Scopus @ Elsevier: 2-s2.0-84896289470

(徳島大学機関リポジトリ: 106062, DOI: 10.1002/art.38263, PubMed: 24574215, Elsevier: Scopus) 中瀬勝則, 鶴尾美穂, 島田久夫, 木下成三, 豊纒, 杉野聡, 浦聡明, 山下恵実, 古味勝美, 小田芳栄, 服部順子, 西岡安彦, 埴淵昌毅, 吾妻雅彦 :
徳島市医師会のCOPD対策,
四国医学雑誌, Vol.69, No.5-6, 233-242, 2013年.

(要約): In the national project Health Japan 21 (2nd edition) put forward in April 2013, the Ministry of Health, Labour, and Welfare specified chronic obstructive pulmonary disease (COPD) as a targeted lifestyle-related disease, in addition to cancer, heart diseases, and diabetes, and concluded that the establishment of COPD management systems is an important issue to maintain Japanese people's healthy lives, as the number of deaths from this disease is likely to rapidly increase in the future. In Tokushima Prefecture, the mortality rate associated with COPD has been stably high over the past years ; the nation' s highest in 2010 and third highest in 2011. In some regions of the western area, particularly mountainous regions, and southern area of the prefecture, the standardized mortality rate among males is double the national mean, highlighting the necessity of rapidly taking countermeasures. Under such circumstances, the Tokushima City Medical Association regarded COPD management as a priority item when developing annual projects this year, and organized the COPD Management and Smoking Cessation Promotion Committee in May. The medical association also presented a tentative plan to conduct association-led individualized COPD assessment at its own expense to the local government of Tokushima, with a view to materializing COPD assessment projects to clarify, evaluate, and analyze the actual situation, including surveys on citizens' recognition of COPD and those conducted by family doctors to examine the statuses of their patients, involving the local government in the future. During deliberations to examine the feasibility of this plan, the local government proposed a new COPD assessment plan based on the conventional mass pulmonary cancer examination system, in order to deal with those at a high risk of COPD ; following some revisions, the new plan was adopted. The plan consisted of the following steps : > Targeting those meeting the 3 diagnostic criteria specified in the pulmonary cancer interview sheet for COPD assessment : 1) age of 60 or over ; 2) previous smoking habit ; 3) presence of at least one of the subjective COPD symptoms (chronic coughing, sputum, and shortness of breath during activity). > Providing these patients with a free-consultation coupon to undergo assessment in a registered primary medical examination institution. > Conducting airway obstruction evaluation in primary medical examination institutions using the mass COPD screening interview sheet (COPD-PSTM) and spirometry. > Conducting insurance-covered medical examinations, such as the respiratory function test, chest XP, and CT scans, in secondary medical examination institutions (chest physicians) to establish a definite diagnosis. > Reporting the results of these examinations to family doctors. > If treatment is necessary, developing initial pharmacotherapy plans as part of the standardized treatment of COPD for approximately 3 months, which are implemented by family doctors. In consideration of the rapidly aging Japanese population, the number of potential COPD patients aged 40 and over is expected to reach nearly 7 million soon. In order to deal with such a large number of COPD patients, it is primary care physicians' duty to provide early diagnosis and treatment, and local medical associations are charged with promoting spirometry through their activities as part of COPD assessment projects, aiming to establish cooperative systems to manage the disease between primary care physicians providing treatment during the stable period and chest physicians providing it during the exacerbation period. As future perspectives, spirometry-promoting seminars to be held in clinical environments are being considered ; participation in these seminars will be a requirement for registered primary COPD examination institutions, and those who have completed such programs will be Tokushima City Medical Association-certified COPD specialists (tentative name). It is expected that these approaches to carry out the nation's first COPD assessment projects will improve clinical environments in communities, such as support for smoking cessation, medical professionals' knowledge of COPD, and the standardization of diagnosis and treatment.
(キーワード): COPD / COPD management / COPD examination / COPD screening / COPD assessment
(徳島大学機関リポジトリ): ● Metadata: 109731
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1050845762395118848

(徳島大学機関リポジトリ: 109731, CiNii: 1050845762395118848) Jun Huang, Sho Tabata, Souji Kakiuchi, Trung Van The, Hisatsugu Goto, Masaki Hanibuchi and Yasuhiko Nishioka :
Identification of pregnancy-associated plasma protein A as a migration-promoting gene in malignant pleural mesothelioma cells: a potential therapeutic target.,
Oncotarget, Vol.4, No.8, 1172-1184, 2013.

(要約): Despite recent advances in treatment, malignant pleural mesothelioma (MPM) remains a deadly disease. Targeted therapy generated broad interests and is highly expected for the treatment of MPM, yet promising preclinical results have not been translated into substantial clinical benefits for the patients. In this study, we tried to identify the genes which play functional roles in cell migration as well as to test whether they can be used as novel targets for molecular targeted therapy for MPM in preclinical model. In our study, pregnancy-associated plasma protein A (PAPPA) was identified as a gene whose expression level is correlated with MPM cell migration by correlation analysis combining MPM cell migration ability and their gene expression profiles. Highly migratory cells were selected from MPM cell lines, MSTO-211H, NCI-H290 and EHMES-1 in vitro and up-regulation of PAPPA in these cells were confirmed. In vitro, PAPPA was demonstrated to stimulate the MPM cell migration via cleavage of insulin-like growth factor-binding protein-4 and subsequent release of IGF-1. Gene silencing of PAPPA in MPM cells led to reduced migration, invasion and proliferation. Furthermore, PAPPA shRNA transfected NCI-H290 when orthotopically inoculated into pleural cavity of severe combined immunodeficiency recipient mice, failed to develop tumors and produce bloody pleural effusion as control shRNA transfected cells did. Our study suggests that PAPPA plays a functional role in promoting MPM cell migration and it might serve as a potential therapeutic target for the treatment of MPM.
(キーワード): Animals / Cell Growth Processes / Cell Line, Tumor / Cell Movement / Female / Gene Silencing / Genetic Therapy / Heterografts / Humans / Insulin-Like Growth Factor Binding Protein 4 / Insulin-Like Growth Factor I / Lung Neoplasms / Male / Mesothelioma / Mice / Mice, SCID / Neoplasm Transplantation / Pregnancy / Pregnancy-Associated Plasma Protein-A / RNA, Small Interfering / Transfection
(徳島大学機関リポジトリ): ● Metadata: 105907
(出版サイトへのリンク): ● Publication site (DOI): 10.18632/oncotarget.1126
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23896451; ● Summary page in Scopus @ Elsevier: 2-s2.0-84884321230

(徳島大学機関リポジトリ: 105907, DOI: 10.18632/oncotarget.1126, PubMed: 23896451, Elsevier: Scopus) Shinji Abe, Yuki Morita, Mika Kato Kaneko, Masaki Hanibuchi, Yuta Tsujimoto, Hisatsugu Goto, Souji Kakiuchi, Yoshinori Aono, Jun Huang, Seidai Sato, Masatoshi Kishuku, Yuki Taniguchi, Mami Azuma, Kazuyoshi Kawazoe, Yoshitaka Sekido, Seiji Yano, Shin-ichi Akiyama, Saburo Sone, Kazuo Minakuchi, Yukinari Kato and Yasuhiko Nishioka :
A novel targeting therapy of malignant mesothelioma using anti-podoplanin antibody,
The Journal of Immunology, Vol.190, No.12, 6239-6249, 2013.

(要約): Podoplanin (Aggrus), which is a type I transmembrane sialomucin-like glycoprotein, is highly expressed in malignant pleural mesothelioma (MPM). We previously reported the generation of a rat anti-human podoplanin Ab, NZ-1, which inhibited podoplanin-induced platelet aggregation and hematogenous metastasis. In this study, we examined the antitumor effector functions of NZ-1 and NZ-8, a novel rat-human chimeric Ab generated from NZ-1 including Ab-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity against MPM in vitro and in vivo. Immunostaining with NZ-1 showed the expression of podoplanin in 73% (11 out of 15) of MPM cell lines and 92% (33 out of 36) of malignant mesothelioma tissues. NZ-1 could induce potent ADCC against podoplanin-positive MPM cells mediated by rat NK (CD161a(+)) cells, but not murine splenocytes or human mononuclear cells. Treatment with NZ-1 significantly reduced the growth of s.c. established tumors of MPM cells (ACC-MESO-4 or podoplanin-transfected MSTO-211H) in SCID mice, only when NZ-1 was administered with rat NK cells. In in vivo imaging, NZ-1 efficiently accumulated to xenograft of MPM, and its accumulation continued for 3 wk after systemic administration. Furthermore, NZ-8 preferentially recognized podoplanin expressing in MPM, but not in normal tissues. NZ-8 could induce higher ADCC mediated by human NK cells and complement-dependent cytotoxicity as compared with NZ-1. Treatment with NZ-8 and human NK cells significantly inhibited the growth of MPM cells in vivo. These results strongly suggest that targeting therapy to podoplanin with therapeutic Abs (i.e., NZ-8) derived from NZ-1 might be useful as a novel immunotherapy against MPM.
(キーワード): Animals / Antibodies, Monoclonal / Flow Cytometry / Humans / Immunohistochemistry / Immunotherapy / Male / Membrane Glycoproteins / Mesothelioma / Mice / Mice, SCID / Pleural Neoplasms / Rats / Rats, Wistar / Recombinant Fusion Proteins / Xenograft Model Antitumor Assays
(出版サイトへのリンク): ● Publication site (DOI): 10.4049/jimmunol.1300448
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23690472; ● Search Scopus @ Elsevier (PMID): 23690472; ● Search Scopus @ Elsevier (DOI): 10.4049/jimmunol.1300448

(DOI: 10.4049/jimmunol.1300448, PubMed: 23690472) Atsushi Mitsuhashi, Hisatsugu Goto, Takuya Kuramoto, Sho Tabata, Sawaka Yukishige, Shinji Abe, Masaki Hanibuchi, Souji Kakiuchi, Atsuro Saijo, Yoshinori Aono, Hisanori Uehara, Seiji Yano, G Julie Ledford, Saburo Sone and Yasuhiko Nishioka :
Surfactant protein A suppresses lung cancer progression by regulating the polarization of tumor-associated macrophages.,
The American Journal of Pathology, Vol.182, No.5, 1843-1853, 2013.

(要約): Surfactant protein A (SP-A) is a large multimeric protein found in the lungs. In addition to its immunoregulatory function in infectious respiratory diseases, SP-A is also used as a marker of lung adenocarcinoma. Despite the finding that SP-A expression levels in cancer cells has a relationship with patient prognosis, the function of SP-A in lung cancer progression is unknown. We investigated the role of SP-A in lung cancer progression by introducing the SP-A gene into human lung adenocarcinoma cell lines. SP-A gene transduction suppressed the progression of tumor in subcutaneous xenograft or lung metastasis mouse models. Immunohistochemical analysis showed that the number of M1 antitumor tumor-associated macrophages (TAMs) was increased and the number of M2 tumor-promoting TAMs was not changed in the tumor tissue produced by SP-A-expressing cells. In addition, natural killer (NK) cells were also increased and activated in the SP-A-expressing tumor. Moreover, SP-A did not inhibit tumor progression in mice depleted of NK cells. Taking into account that SP-A did not directly activate NK cells, these results suggest that SP-A inhibited lung cancer progression by recruiting and activating NK cells via controlling the polarization of TAMs.
(徳島大学機関リポジトリ): ● Metadata: 106071
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.ajpath.2013.01.030
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23499372; ● Search Scopus @ Elsevier (PMID): 23499372; ● Search Scopus @ Elsevier (DOI): 10.1016/j.ajpath.2013.01.030

(徳島大学機関リポジトリ: 106071, DOI: 10.1016/j.ajpath.2013.01.030, PubMed: 23499372) Seidai Satou, Masaki Hanibuchi, Takuya Kuramoto, Nodoka Yamamori, Hisatsugu Goto, Hirohisa Ogawa, Atsushi Mitsuhashi, The Trung Van, Souji Kakiuchi, Shin-ichi Akiyama, Yasuhiko Nishioka and Saburo Sone :
Macrophage stimulating protein promotes liver metastases of small cell lung cancer cells by affecting the organ microenvironment.,
Clinical & Experimental Metastasis, Vol.30, No.3, 333-344, 2012.

(要約): The organ microenvironment significantly affects the processes of cancer metastasis. Elucidating the molecular mechanisms of interaction between tumor cells and the organ microenvironment is crucial for the development of effective therapeutic strategies to eradicate cancer metastases. Macrophage stimulating protein (MSP), an activator of macrophages, regulates a pleiotropic array of effects, including proliferation, cellular motility, invasiveness, angiogenesis, and resistance to anoikis. However, the role of MSP in cancer metastasis is still largely unknown. In this study, the action of MSP on the production of metastases was determined in a multiple-organ metastasis model. The murine MSP gene was transfected into two human SCLC cell lines, SBC-5 and H1048, to establish transfectants secreting biologically active MSP. MSP gene transduction did not affect cell proliferation and motility in vitro. Intravenously inoculated MSP transfectants produced significantly larger numbers of liver metastases than parental cells or vector control clones, while there were no significant differences in bone or lung metastases among them. Immunohistochemical analyses of liver metastases revealed that tumor-associated microvessel density and tumor-infiltrating macrophages were significantly increased in lesions produced by MSP transfectants. MSP could stimulate the migration of murine macrophages and endothelial cells in vitro. Consequently, MSP may be one of the major determinants that affects the properties of tumor stroma and that produces a permissive microenvironment to promote cancer metastasis.
(キーワード): Animals / Base Sequence / Blotting, Western / Cell Line, Tumor / Cell Proliferation / DNA Primers / Hepatocyte Growth Factor / Humans / Liver Neoplasms / Lung Neoplasms / Mice / Mice, SCID / Proto-Oncogene Proteins / Real-Time Polymerase Chain Reaction / Reverse Transcriptase Polymerase Chain Reaction / Transduction, Genetic / Tumor Microenvironment
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10585-012-9540-y
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23011677; ● Summary page in Scopus @ Elsevier: 2-s2.0-84875792986

(DOI: 10.1007/s10585-012-9540-y, PubMed: 23011677, Elsevier: Scopus) Takuya Kuramoto, Hisatsugu Goto, Atsushi Mitsuhashi, Sho Tabata, Hirohisa Ogawa, Hisanori Uehara, Atsuro Saijo, Souji Kakiuchi, Yoichi Maekawa, Koji Yasutomo, Masaki Hanibuchi, Shin-ichi Akiyama, Saburo Sone and Yasuhiko Nishioka :
Dll4-Fc, an inhibitor of Dll4-Notch signaling, suppresses liver metastasis of small cell lung cancer cells through down-regulation of NF-kappa-B activity,
Molecular Cancer Therapeutics, Vol.11, No.12, 2578-2587, 2012.

(要約): Notch signaling regulates cell-fate decisions during development and postnatal life. Little is known, however, about the role of Delta-like-4 (Dll4)-Notch signaling between cancer cells, or how this signaling affects cancer metastasis. We, therefore, assessed the role of Dll4-Notch signaling in cancer metastasis. We generated a soluble Dll4 fused to the IgG1 constant region (Dll4-Fc) that acts as a blocker of Dll4-Notch signaling and introduced it into human small cell lung cancer (SCLC) cell lines expressing either high levels (SBC-3 and H1048) or low levels (SBC-5) of Dll4. The effects of Dll4-Fc on metastasis of SCLC were evaluated using a mouse model. Although Dll4-Fc had no effect on the liver metastasis of SBC-5, the number of liver metastasis inoculated with SBC-3 and H1048 cells expressing Dll4-Fc was significantly lower than that injected with control cells. To study the molecular mechanisms of the effects of Dll4-Fc on liver metastasis, a PCR array analysis was conducted. Because the expression of NF-κB target genes was affected by Dll4-Fc, we conducted an electrophoretic mobility shift assay and observed that NF-κB activities, both with and without stimulation by TNF-α, were downregulated in Dll4-Fc-overexpressing SBC-3 and H1048 cells compared with control cells. Moreover, Dll4-Fc attenuates, at least in part, the classical and alternative NF-κB activation pathway by reducing Notch1 signaling. These results suggest that Dll4-Notch signaling in cancer cells plays a critical role in liver metastasis of SCLC by regulating NF-κB signaling.
(キーワード): Animals / アポトーシス (apoptosis) / Cell Growth Processes / Cell Movement / Down-Regulation / Humans / Liver Neoplasms, Experimental / Lung Neoplasms / Male / Mice / Mice, SCID / NF-kappa B / Receptors, Notch / Recombinant Fusion Proteins / シグナル伝達 (signal transduction) / Small Cell Lung Carcinoma / Transfection / Xenograft Model Antitumor Assays
(出版サイトへのリンク): ● Publication site (DOI): 10.1158/1535-7163.MCT-12-0640
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22989420; ● Search Scopus @ Elsevier (PMID): 22989420; ● Search Scopus @ Elsevier (DOI): 10.1158/1535-7163.MCT-12-0640

(DOI: 10.1158/1535-7163.MCT-12-0640, PubMed: 22989420) 矢野祖, 西條敦郎, 近藤真代, 河野弘, 豊田優子, 柿内聡司, 岸潤, 埴淵昌毅, 古川貴大, 藤田浩司, 西岡安彦 :
神経根障害で発症した神経サルコイドーシスの一例,
四国医学雑誌, Vol.68, No.3,4, 153-158, 2012年.

(要約): A52-year-old woman was referred to our hospital for further examination of thoracolumbarpain. As dysesthesia at Th4level was seen in neurological examination, thoracic radiculopathy ormyelopathy was suspected. Blood examination showed elevated level of serum ACE and lysozyme.Lymphadenopathy was evident in bilateral hila and mediastina with marked FDG and Galliumaccumulation in FDG-PET-CT and Gallium scintigraphy, respectively. The number of lymphocytesand the CD4/CD8ratio were increased in the BALF. Histological findings of specimens obtainedfrom the lung and the skin lesion revealed noncaseating epithelioid granuloma, which yielded thediagnosis of sarcoidosis. The cerebrospinal fluid examinations showed elevated level of cell counts,proteins and β2-microglobulin. Taken together, she was diagnosed as neurosarcoidosis with thoracicradiculopathy. Her symptoms were improved with oral administration of prednisolone, butthey were exacerbated when prednisolone dose was tapered to20mg/day. Combined therapy ofmethotrexate and prednisolone was initiated, thereafter her symptoms disappeared completely.
(キーワード): neurosarcoidosis / radiculopathy / prednisolone / methotrexate
(徳島大学機関リポジトリ): ● Metadata: 102837
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1050845763842119680

(徳島大学機関リポジトリ: 102837, CiNii: 1050845763842119680) Trung The Van, Masaki Hanibuchi, Hisatsugu Goto, Takuya Kuramoto, Sawaka Yukishige, Souji Kakiuchi, Seidai Sato, Satoshi Sakaguchi, Le Tan Dat, Yasuhiko Nishioka, Shin-ichi Akiyama and Saburo Sone :
SU6668, a multiple tyrosine kinase inhibitor, inhibits the progression of human malignant pleural mesothelioma in an orthotopic model,
Respirology, Vol.17, No.6, 984-990, 2012.

(要約): Malignant pleural mesothelioma (MPM) is an aggressive neoplasm of the mesothelium with high chemotherapeutic resistance. In this study, the preclinical therapeutic activity of the multiple tyrosine kinase inhibitor, SU6668, against MPM was examined. Two human MPM cell lines with different pro-angiogenic cytokine expression, Y-MESO-14 cells that express high levels of vascular endothelial growth factor (VEGF) and MSTO-211H cells that express high levels of basic fibroblast growth factor (bFGF), were orthotopically inoculated into the thoracic cavities of mice with severe combined immunodeficiency. The mice with MPM were treated or not treated with SU6668 (200 mg/kg/day). SU6668 abrogated the proliferation of endothelial cells stimulated by VEGF or bFGF, but did not directly affect the growth of human MPM cells in vitro. In this orthotopic implantation model, treatment with SU6668 effectively reduced tumour weight and pleural effusion volumes, in association with inhibition of the growth of tumour vasculature. More importantly, treatment with SU6668 significantly prolonged survival time in mice with MPM. These findings suggest that SU6668 has a promising therapeutic effect on the progression of MPM in vivo through its anti-angiogenic effects.
(キーワード): Animals / Antineoplastic Agents / Cell Line, Tumor / Cell Proliferation / Fibroblast Growth Factor 2 / Humans / Indoles / Male / Mesothelioma / Mice / Mice, SCID / Neovascularization, Pathologic / Pleural Effusion, Malignant / Pleural Neoplasms / Protein Kinase Inhibitors / Pyrroles / Vascular Endothelial Growth Factor A / Xenograft Model Antitumor Assays
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/j.1440-1843.2012.02193.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22574723; ● Search Scopus @ Elsevier (PMID): 22574723; ● Search Scopus @ Elsevier (DOI): 10.1111/j.1440-1843.2012.02193.x

(DOI: 10.1111/j.1440-1843.2012.02193.x, PubMed: 22574723) Adel Gomaa Mohammed Gabr, Hisatsugu Goto, Masaki Hanibuchi, Hirohisa Ogawa, Takuya Kuramoto, Minako Suzuki, Atsuro Saijo, Souji Kakiuchi, Van The Trung, Satoshi Sakaguchi, Yoichiro Moriya, Saburo Sone and Yasuhiko Nishioka :
Erlotinib prevents experimental metastases of human small cell lung cancer cells with no epidermal growth factor receptor expression,
Clinical & Experimental Metastasis, Vol.29, No.3, 207-216, 2012.

(要約): Epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) show dramatic antitumor activity in a subset of patients with non-small cell lung cancer who have an active mutation in the epidermal growth factor receptor (EGFR) gene. On the other hand, some lung cancer patients with wild type EGFR also respond to EGFR-TKIs, suggesting that EGFR-TKIs have an effect on host cells as well as tumor cells. However, the effect of EGFR-TKIs on host microenvironments is largely unknown. A multiple organ metastasis model was previously established in natural killer cell-depleted severe combined immunodeficient mice using human lung cancer cells. This model was used to investigate the therapeutic efficacy of erlotinib, an EGFR-TKI, on multiple organ metastases induced by human small cell lung cancer cells (SBC-5 cells) that did not express EGFR. Although erlotinib did not have any effect on the proliferation of SBC-5 cells in vitro, it significantly suppressed bone and lung metastases in vivo, but not liver metastases. An immunohistochemical analysis revealed that, erlotinib significantly suppressed the number of osteoclasts in bone metastases, whereas no difference was seen in microvessel density. Moreover, erlotinib inhibited EGF-induced receptor activator of nuclear factor kappa-B expression in an osteoblastic cell line (MC3T3-E1 cells). These results strongly suggested that erlotinib prevented bone metastases by affecting host microenvironments irrespective of its direct effect on tumor cells.
(キーワード): Animals / Bone Neoplasms / Carcinoma, Small Cell / Cell Line, Tumor / Cell Movement / Cell Proliferation / Epidermal Growth Factor / Humans / Lung Neoplasms / Male / Mice / Neoplasm Metastasis / Neovascularization, Pathologic / Osteoblasts / Osteoclasts / Protein Kinase Inhibitors / Quinazolines / RANK Ligand / Receptor, Epidermal Growth Factor
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10585-011-9443-3
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22170031; ● Search Scopus @ Elsevier (PMID): 22170031; ● Search Scopus @ Elsevier (DOI): 10.1007/s10585-011-9443-3

(DOI: 10.1007/s10585-011-9443-3, PubMed: 22170031) Keiko Miyake, Kenji Tani, Souji Kakiuchi, Chiyuki Suzuka, Yuko Toyoda, Jun Kishi, Toshifumi Tezuka, Shino Yuasa, Masaki Hanibuchi, Yoshinori Aono, Yasuhiko Nishioka and Saburo Sone :
Epidermal growth factor receptor-tyrosine kinase inhibitor (gefitinib) augments pneumonitis, but attenuates lung fibrosis in response to radiation injury in rats,
The Journal of Medical Investigation : JMI, Vol.59, No.1-2, 174-185, 2012.

(要約): Gefitinib, an inhibitor of epidermal growth factor receptor (EGFR) tyrosine kinase, has been reported to be associated with interstitial lung disorders, and their high incidence and mortality have become a matter of great concern, especially in Japan. In this study, we investigated the effect of gefitinib on different phases of radiation-induced lung disorders in an experimental model. The thoraxes of Wistar rats were irradiated on day 1 with a single X-ray dose of 20 Gy, and gefitinib (50 mg/kg/day) was orally administered from day 1 to 14. The rat lungs were harvested on days 15 and 57 and the bronchoalveolar lavage (BAL) was performed. Gefitinib treatment increased the infiltration of inflammatory cells, which produced more pro-inflammatory cytokines (IL-6, IL-1), in the lungs of the irradiated rats on days 15 and 57, while gefitinib treatment reduced collagen content of the lungs in irradiated rats and decreased proliferation and EGFR expression in the lung fibroblasts from irradiated rats on day 57. In irradiated rats, gefitinib treatment augmented lung inflammation, including inflammatory cell infiltration and pro-inflammatory cytokine expression, while gefitinib treatment attenuated fibrotic lung remodeling due to the inhibition of lung fibroblast proliferation.
(キーワード): Animals / Disease Models, Animal / Male / Protein Kinase Inhibitors / Pulmonary Fibrosis / Quinazolines / Radiation Pneumonitis / Rats / Rats, Wistar / Receptor, Epidermal Growth Factor
(徳島大学機関リポジトリ): ● Metadata: 106019
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.59.174
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22450006; ● Search Scopus @ Elsevier (PMID): 22450006; ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.59.174

(徳島大学機関リポジトリ: 106019, DOI: 10.2152/jmi.59.174, PubMed: 22450006) Le T Dat, Taisuke Matsuo, Tetsuro Yoshimaru, Souji Kakiuchi, Hisatsugu Goto, Masaki Hanibuchi, Takuya Kuramoto, Yasuhiko Nishioka, Saburo Sone and Toyomasa Katagiri :
Identification of genes potentially involved in bone metastasis by genome-wide gene expression profile analysis of non-small cell lung cancer in mice,
International Journal of Oncology, Vol.40, No.5, 1455-1469, 2012.

(要約): Lung cancer is commonly associated with multi-organ metastasis, and the bone is a frequent metastatic site for lung cancer. However, the molecular mechanism of organ-specific metastasis remains poorly understood. To elucidate this issue, we analyzed in this study genome-wide gene expression profiles of 15 metastatic lesions from three organs (bone, lung and liver) in a mouse model with multi-organ metastasis properties of human non-small cell lung cancer cells (ACC-LC319/bone2), using a combination of laser-microbeam microdissection and DNA microarrays. We identified 299 genes that could potentially be involved in the organ-selective nature of lung cancer metastasis. Among them, 77 were bone-specifically expressed elements, including genes involved in cell adhesion, cytoskeleton/cell motility, extracellular matrix remodeling and cell-cell signaling as well as genes already known to be involved in the bone metastasis of breast cancers. Quantitative RT-PCR confirmed the specific upregulation of eight genes in bone metastasis tumors, suggesting that these genes may be involved in bone metastasis. Our findings should be helpful for a better understanding of the molecular aspects of the metastatic process in different organs, and could lead to molecular target-based anticancer drugs and prevention of metastasis, especially bone metastasis.
(キーワード): Animals / Bone Neoplasms / Carcinoma, Non-Small-Cell Lung / Cell Line, Tumor / Cluster Analysis / Gene Expression Profiling / Gene Expression Regulation, Neoplastic / Genetic Predisposition to Disease / Genome-Wide Association Study / Humans / Laser Capture Microdissection / Lung Neoplasms / Male / Mice / Mice, SCID / Neoplasm Invasiveness / Neoplasm Transplantation / Oligonucleotide Array Sequence Analysis / Phenotype / Real-Time Polymerase Chain Reaction / Reverse Transcriptase Polymerase Chain Reaction
(出版サイトへのリンク): ● Publication site (DOI): 10.3892/ijo.2012.1348
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22294041; ● Search Scopus @ Elsevier (PMID): 22294041; ● Search Scopus @ Elsevier (DOI): 10.3892/ijo.2012.1348

(DOI: 10.3892/ijo.2012.1348, PubMed: 22294041) 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) Trung The Van, Masaki Hanibuchi, Souji Kakiuchi, Seidai Sato, Takuya Kuramoto, Hisatsugu Goto, Atsushi Mitsuhashi, Yasuhiko Nishioka, Shin-ichi Akiyama and Saburo Sone :
The therapeutic efficacy of S-1 against orthotopically implanted human pleural mesothelioma cells in severe combined immunodeficient mice.,
Cancer Chemotherapy and Pharmacology, Vol.68, No.2, 497-504, 2011.

(要約): Malignant pleural mesothelioma (MPM) is a highly lethal neoplasm. S-1 has been developed as a novel oral antineoplastic agent based on the modulation of 5-fluorouracil (5-FU) bioactivity. This study was conducted to investigate the preclinical therapeutic effect of S-1 on MPM. We used three human MPM cell lines, Y-MESO-14, NCI-H290 and MSTO-211H. In vitro proliferation of human MPM cells was determined by MTT assay. Human MPM cells were orthotopically implanted into thoracic cavity of SCID mice. Tumor-bearing mice were treated with S-1 or vehicle. The combination of 5-FU and 5-chloro-2,4-dihydroxypyridine (CDHP) was more effective than 5-FU alone in inhibiting MPM cell proliferation in vitro. This combination was most effective in Y-MESO-14 cells, which co-expressed high protein level of dihydropyrimidine dehydrogenase (DPD) and thymidine phosphorylase (TP). In vivo data showed that treatment with S-1 significantly reduced thoracic tumors and pleural effusion produced by Y-MESO-14 cells. Moreover, treatment with S-1 prolonged the survival of Y-MESO-14 cell-bearing SCID mice. We demonstrated that S-1 was effective for inhibiting the proliferation of MPM cells, particularly with both DPD and TP expressions, suggesting that S-1 might be therapeutically effective for control of MPM.
(キーワード): Animals / Antimetabolites, Antineoplastic / Antineoplastic Combined Chemotherapy Protocols / Cell Line, Tumor / Dihydrouracil Dehydrogenase (NADP) / Drug Combinations / Enzyme Inhibitors / Humans / Male / Mesothelioma / Mice / Mice, SCID / Neoplasm Proteins / Oxonic Acid / Pentosyltransferases / Pleural Neoplasms / Pyridines / Random Allocation / Survival Analysis / Tegafur / Thymidine Phosphorylase / Tumor Burden / Xenograft Model Antitumor Assays
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s00280-010-1503-x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21079960; ● Search Scopus @ Elsevier (PMID): 21079960; ● Search Scopus @ Elsevier (DOI): 10.1007/s00280-010-1503-x

(DOI: 10.1007/s00280-010-1503-x, PubMed: 21079960) Hisatsugu Goto, Masaki Hanibuchi, Satoshi Sakaguchi, Takanori Kanematsu, Souji Kakiuchi, Hideki Tomimoto, Masahiko Azuma, Toshifumi Tezuka, Hiroya Tada, Yukiyo Miki, Toshimi Nakamura, Saburo Sone and Yasuhiko Nishioka :
Investigation of the outpatient chemotherapy for lung cancer patients in Tokushima University Hospital.,
The Journal of Medical Investigation : JMI, Vol.58, No.3-4, 219-226, 2011.

(要約): Platinum-doublet regimens and docetaxel as first- and second-line chemotherapy, respectively, are shown to prolong the survival of lung cancer patients in various randomized phase III studies. However, the evidence for the efficacy of chemotherapy for lung cancer in the clinical practice is still insufficient. In the present study, we investigated the effectiveness and safety of outpatient chemotherapy for lung cancer in the clinical practice. Ninety-four lung cancer cases were retrospectively analyzed. Among these cases, 67 (71.3%) were non-small cell lung cancer (NSCLC) and 27 (28.7%) were small cell lung cancer (SCLC). The response rates in SCLC and NSCLC patients were 55.6% (15/27) and 16.9% (11/65), respectively. Objective tumor response rates for the patients were found to decrease substantially with each line of treatment as described previously. All adverse events were well tolerated and no treatment-related death was observed. Median time to treatment failures (TTFs) of first-line treatment were 10.1 months and 4.8 months in SCLC and NSCLC, respectively. These findings indicate that even in the setting of clinical practice, the efficacy and safety of chemotherapy is strictly insured by the appropriate therapeutic management.
(キーワード): Adult / Aged / Aged, 80 and over / Antineoplastic Agents / Carcinoma, Non-Small-Cell Lung / Carcinoma, Small Cell / Female / Hospitals, University / Humans / Lung Neoplasms / Male / Middle Aged / Outpatients / Retrospective Studies
(徳島大学機関リポジトリ): ● Metadata: 83836
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.58.219
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21921423; ● Search Scopus @ Elsevier (PMID): 21921423; ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.58.219

(徳島大学機関リポジトリ: 83836, DOI: 10.2152/jmi.58.219, PubMed: 21921423) Hirokazu Ogino, Masaki Hanibuchi, Souji Kakiuchi, Van The Trung, Hisatsugu Goto, Kenji Ikuta, Tadaaki Yamada, Hisanori Uehara, Akihiko Tsuruoka, Toshimitsu Uenaka, Wei Wang, Qi Li, Shinji Takeuchi, Seiji Yano, Yasuhiko Nishioka and Saburo Sone :
E7080 suppresses hematogenous multiple organ metastases of lung cancer cells with nonmutated epidermal growth factor receptor.,
Molecular Cancer Therapeutics, Vol.10, No.7, 1218-1228, 2011.

(要約): While epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors improve the prognosis of patients with EGFR mutant lung cancer, the prognosis of patients with nonmutant EGFR lung cancer, especially those with metastases, is still extremely poor. We have assessed the therapeutic efficacy of E7080, an orally available inhibitor of multiple tyrosine kinases including VEGF receptor 2 (VEGFR-2) and VEGFR-3, in experimental multiple organ metastasis of lung cancer cell lines without EGFR mutations. E7080 markedly inhibited the in vitro proliferation of VEGF-stimulated microvascular endothelial cells. Intravenous inoculation into natural killer cell-depleted severe combined immunodeficient mice of the small cell lung cancer cell lines H1048 (producing low amounts of VEGF) and SBC-5 (producing intermediate amounts of VEGF) resulted in hematogenous metastases into multiple organs, including the liver, lungs, kidneys, and bones, whereas intravenous inoculation of PC14PE6, a non-small cell lung cancer cell line producing high amounts of VEGF, resulted in lung metastases followed by massive pleural effusion. Daily treatment with E7080 started after the establishment of micrometastases significantly reduced the number of large (>2 mm) metastatic nodules and the amount of pleural effusion, and prolonged mouse survival. Histologically, E7080 treatment reduced the numbers of endothelial and lymph endothelial cells and proliferating tumor cells and increased the number of apoptotic cells in metastatic nodules. These results suggest that E7080 has antiangiogenic and antilymphangiogenic activity and may be of potential therapeutic value in patients with nonmutant EGFR lung cancer and multiple organ metastases. Mol Cancer Ther; 10(7); 1218-28. ©2011 AACR.
(出版サイトへのリンク): ● Publication site (DOI): 10.1158/1535-7163.MCT-10-0707
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21551260; ● Search Scopus @ Elsevier (PMID): 21551260; ● Search Scopus @ Elsevier (DOI): 10.1158/1535-7163.MCT-10-0707

(DOI: 10.1158/1535-7163.MCT-10-0707, PubMed: 21551260) Hideki Tomimoto, Masaki Hanibuchi, Fumitaka Ogushi, Yoshio Okano, Tsutomu Shinohara, Hiroyuki Doi, Akiyoshi Yamamoto, Eiji Takeuchi, Akihiko Yamamoto, Masahiko Azuma, Hiroya Tada, Takanori Kanematsu, Souji Kakiuchi, Hisatsugu Goto, Seiji Yano, Yasuhiko Nishioka and Saburo Sone :
A multi-institutional phase II study of combination chemotherapy with S-1 plus cisplatin in patients with advanced non-small cell lung cancer.,
Oncology Letters, Vol.2, No.3, 465-470, 2011.

(要約): S-1 is an oral anticancer fluoropyrimidine agent designed to elevate anticancer activity with a decrease in gastrointestinal toxicity. We conducted a phase II study to evaluate the efficacy and safety of combination chemotherapy with S-1 plus cisplatin in patients with advanced non-small cell lung cancer (NSCLC). Chemotherapy-naïve patients were treated with S-1 administered orally at 40 mg/m(2) twice a day for 21 consecutive days, and cisplatin (60 mg/m(2)) infused intravenously on day 8, repeated every 5 weeks. Of the 44 patients enrolled in the study, 40 were assessable for efficacy and safety. The median number of cycles administered was 3 (range 1-9 cycles). Among the 40 assessable patients, 7 partial responses were observed, with an overall response rate (RR) of 17.5% [95% confidence interval (CI), 5.2-29.8]. Patients with squamous cell carcinoma showed a significantly higher RR (55.5%) than those with adenocarcinoma (9.1%) or other types of NSCLC (0%). The median progression-free survival was 4.3 months (95% CI, 3.4-4.9), the median survival time was 17.9 months (95% CI, 15.0-20.8), and the 1- and 2-year survival rates were 63.3 and 27.3%, respectively. Major grade 3-4 hematologic toxicities were leukocytopenia (7.5%), neutropenia (5.0%), anemia (15.0%) and thrombocytopenia (2.5%). No grade 4 non-hematologic toxicity or treatment-related death occurred. These results suggest that combination chemotherapy with S-1 plus cisplatin is a promising therapeutic candidate for patients with advanced NSCLC, particularly squamous cell carcinoma.
(出版サイトへのリンク): ● Publication site (DOI): 10.3892/ol.2011.266
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22866104; ● Search Scopus @ Elsevier (PMID): 22866104; ● Search Scopus @ Elsevier (DOI): 10.3892/ol.2011.266

(DOI: 10.3892/ol.2011.266, PubMed: 22866104) 組橋由記, 埴淵昌毅, 富本英樹, 東桃代, 兼松貴則, 柿内聡司, 後東久嗣, 多田浩也, 西岡安彦, 曽根三郎 :
非小細胞肺癌患者のpatient-reported outcome(PRO)評価法の現状と問題点 ―第III 相臨床試験論文のreview―,
肺癌, Vol.50, No.6, 791-802, 2010年.

(要約): 背景．近年，癌患者のquality of life(QOL)評価は治療法選択に重要な要素として注目されている．欧米ではQOL を把握する目的からpatient-reported outcome( PRO)が評価項目の1 つとして評価されつつあるが，本邦においてはPRO の認知度は低い．目的．非小細胞肺癌のQOL 評価(PRO)の現状を検討する．対象と方法．今回，非小細胞肺癌に対する癌薬物療法の有用性を比較検討した第III 相臨床試験の中から，患者の自己申告によるQOL 評価であるPRO 評価を評価項目とした報告(24 試験)を抽出し，PRO の評価方法，評価時期， PRO 評価に対する患者のコンプライアンスなどについて検討した．結果．対象とした臨床試験の大多数では複数の評価方法によりPRO 評価が行われており，European Organization for Research and Treatment of Cancer-Quality of Life Questionnaire-Core 30(EORTC QLQ-C30)が最も頻用されていた(17 試験;70.8%)． PRO 評価の多くは治療開始前，各コース開始直前，治療終了時，その後1∼3 ヶ月ごとに行われていたが，患者のコンプライアンスは治療経過に伴って有意に低下し，全身状態の悪化などがその要因と考えられた．考察．PRO評価が，臨床試験における癌薬物療法の優劣を評価する方法の1 つとして十分な情報となるよう問題点の検討をさらに進めていく必要があると思われる．
(キーワード): 肺癌 (lung cancer) / 癌薬物療法 / Patient-reported outcome(PRO) / クオリティ・オブ・ライフ (QOL) / Chemotherapy
(出版サイトへのリンク): ● Publication site (DOI): 10.2482/haigan.50.791
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390001204681018368; ● Summary page in Scopus @ Elsevier: 2-s2.0-78650334692

(DOI: 10.2482/haigan.50.791, CiNii: 1390001204681018368, Elsevier: Scopus) Takanori Kanematsu, Masaki Hanibuchi, Hideki Tomimoto, Shoji Sakiyama, Koichiro Kenzaki, Kazuya Kondo, Bando Hiroyasu, Haku Takashi, Yoneda Kazuo, Hirose Toshiyuki, Toyoda Yuko, Hisatsugu Goto, Sakaguchi Satoshi, Katsuhiro Kinoshita, Momoyo Azuma, Kakiuchi Soji, Jun Kishi, Masahiko Azuma, Tada Hiroya, Sumitomo Masayuki, Yasuhiko Nishioka, Seiji Yano and Saburo Sone :
Epidemiological and clinical features of lung cancer patients from 1999 to 2009 in Tokushima Prefecture of Japan,
The Journal of Medical Investigation : JMI, Vol.57, No.3,4, 326-333, 2010.

(要約): Lung cancer is the leading cause of malignancy-related death worldwide. In the present study, we reviewed the epidemiologic and clinical features of lung cancer in Tokushima Prefecture, Japan. Between January 1999 and December 2009, 2,183 patients with lung cancer were enrolled in this study. One thousand five hundred ninety-one (73%) patients were male and 592 (27%) patients were female. Median age was 70 years, with a range of 15-93 years. Seventy-six percent of patients had smoking history. One thousand nine hundred five (87%) patients were non-small cell lung cancer and the predominant histological type was adenocarcinoma (51%). Among all 2,183 patients, 702 (32%) belonged to elderly population. Four hundred seventy-one (22%), 213 (10%), 24 (1%), 116 (5%), 238 (11%), 370 (17%) and 678 (31%) patients had stage IA, IB, IIA, IIB, IIIA, IIIB and IV lung cancer, respectively. In Tokushima University Hospital, 516 (29%), 191 (11%), 58 (3%), 755 (43%) and 216 (12%) patients were initially treated with chemotherapy, chemo-radiotherapy, thoracic radiotherapy, operation and best supportive care, respectively. The median time to progression (TTP) and the median survival time (MST) of patients treated with chemotherapy and chemo-radiotherapy were 3.5 months, 13.0 months and 7.0 months, 18.0 months, respectively. The median TTP and the MST of 33 elderly patients treated with chemotherapy were 3.3 months and 18.0 months, respectively, which were comparable with those of total population. These results indicated the benefit of chemotherapy in elderly patients with advanced lung cancer by proper selection.
(キーワード): Adolescent / Adult / Age Factors / Aged / Aged, 80 and over / Carcinoma, Non-Small-Cell Lung / Carcinoma, Small Cell / Female / Humans / Japan / Kaplan-Meier Estimate / Lung Neoplasms / Male / Middle Aged / Risk Factors / 喫煙 (smoking) / Young Adult
(徳島大学機関リポジトリ): ● Metadata: 79184
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.57.326
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20847534; ● Summary page in Scopus @ Elsevier: 2-s2.0-78649676894

(徳島大学機関リポジトリ: 79184, DOI: 10.2152/jmi.57.326, PubMed: 20847534, Elsevier: Scopus) Satoshi Sakaguchi, Hisatsugu Goto, Masaki Hanibuchi, Shinsaku Otsuka, Hirokazu Ogino, Souji Kakiuchi, Hisanori Uehara, Seiji Yano, Yasuhiko Nishioka and Saburo Sone :
Gender difference in bone metastasis of human small cell lung cancer, SBC-5 cells in natural killer-cell depleted severe combined immunodeficient mice.,
Clinical & Experimental Metastasis, Vol.27, No.5, 351-359, 2010.

(要約): Lung cancer frequently develops multiple organ metastases, which thus makes this disease a leading cause of malignancy-related death worldwide. A gender difference is reported to affect the incidence and mortality of lung cancer; however, whether and how the gender difference is involved in lung cancer metastasis is unclear. This study evaluated the gender difference in multiple organ metastases in human small cell lung cancer (SBC-5) cells by using natural killer cell-depleted severe combined immunodeficient mice. Among multiple organ metastases, only bone metastasis formation significantly increased in female mice in comparison to males, while no significant difference was observed in the metastases to the liver and lungs. The suppression of androgen by castration or androgen receptor antagonist treatment in male mice also induced a significant increase of bone metastases. The number of osteoclasts in the bone metastatic lesions was greater in female mice and in mice with androgen suppression than in control male. However, there was no significant difference in the serum concentration of parathyroid hormone-related protein (PTHrP) associated with gender or androgen suppression. An in vitro study also indicated that sex steroid treatment had no effect on the proliferation or PTHrP production in SBC-5 cells. These results indicate that the balance of sex steroids therefore plays an important role in the formation of bone metastasis in small cell lung cancer, and suggests diverse mechanisms of interaction between cancer cells and host cells in the bone microenvironment.
(キーワード): Androgens / Animals / Base Sequence / Bone Neoplasms / Carcinoma, Small Cell / Cell Line, Tumor / Cell Proliferation / DNA Primers / 女性 (female) / Humans / Killer Cells, Natural / Lung Neoplasms / Male / Mice / Mice, SCID / Orchiectomy / Parathyroid Hormone-Related Protein / Reverse Transcriptase Polymerase Chain Reaction / Sex Factors
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10585-010-9333-0
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20464627; ● Search Scopus @ Elsevier (PMID): 20464627; ● Search Scopus @ Elsevier (DOI): 10.1007/s10585-010-9333-0

(DOI: 10.1007/s10585-010-9333-0, PubMed: 20464627) Kenji Ikuta, Seiji Yano, Van The Trung, Masaki Hanibuchi, Hisatsugu Goto, Qi Li, Wei Wang, Tadaaki Yamada, Hirokazu Ogino, Soji Kakiuchi, Hisanori Uehara, Yoshitaka Sekido, Toshimitsu Uenaka, Yasuhiko Nishioka and Saburo Sone :
E7080, a multi-tyrosine kinase inhibitor, suppresses the progression of malignant pleural mesothelioma with different proangiogenic cytokine production profiles.,
Clinical Cancer Research, Vol.15, No.23, 7229-7237, 2009.

(要約): Malignant pleural mesothelioma (MPM) is a biologically heterogeneous malignant disease with a poor prognosis. We reported previously that the anti-vascular endothelial growth factor (VEGF) antibody, bevacizumab, effectively inhibited the progression of VEGF-high-producing (but not VEGF-low-producing) MPM cells in orthotopic implantation models, indicating the need for novel therapeutic strategies to improve the poor prognosis of this disease. Therefore, we focused on the multi-tyrosine kinase inhibitor E7080 and assessed its therapeutic efficacy against MPM cells with different proangiogenic cytokine production profiles.
(キーワード): Animals / Cell Line, Tumor / 細胞質分裂 (cytokinesis) / Fibroblast Growth Factor 2 / Humans / Male / Mesothelioma / Mice / Mice, SCID / Neoplasm Transplantation / Neovascularization, Pathologic / Phenylurea Compounds / リン酸化 (phosphorylation) / Platelet-Derived Growth Factor / Pleural Neoplasms / Quinolines / Vascular Endothelial Growth Factor A
(出版サイトへのリンク): ● Publication site (DOI): 10.1158/1078-0432.CCR-09-1980
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19934291; ● Search Scopus @ Elsevier (PMID): 19934291; ● Search Scopus @ Elsevier (DOI): 10.1158/1078-0432.CCR-09-1980

(DOI: 10.1158/1078-0432.CCR-09-1980, PubMed: 19934291) Shinsaku Otsuka, Masaki Hanibuchi, Kenji Ikuta, Seiji Yano, Hisatsugu Goto, Hirokazu Ogino, Tadaaki Yamada, Soji Kakiuchi, Yasuhiko Nishioka, Takashi Takahashi and Saburo Sone :
A bone metastasis model with osteolytic and osteoblastic properties of human lung cancer ACC-LC-319/bone2 in natural killer cell-depleted severe combined immunodeficient mice.,
Oncology Research, Vol.17, No.11-12, 581-591, 2009.

(要約): Lung cancer is commonly associated with multiple-organ metastasis, and bone is a frequent metastatic site for lung cancer. Lung cancer frequently develops osteolytic, and less frequently osteoblastic, metastasis to bone. Osteolytic metastasis models of lung cancer have been reported, but no osteoblastic metastasis model is available for lung cancer. In the present study, we established a reproducible model of human lung cancer with both osteolytic and osteoblastic changes in natural killer cell-depleted severe combined immunodeficient mice. Intravenous inoculation of ACC-LC-319/bone2 cells resulted in the development of metastatic colonies in the lung, liver, and bone of the mice. As assessed sequentially by X-ray photographs, osteolytic bone lesions were observed by day 28, and then osteoblastic lesions were detected by day 35. Histological examination revealed the presence of bony spurs, a hallmark of osteoblastic bone metastasis, where osteoclasts were hardly observed. Treatment with an anti-human vascular endothelial growth factor antibody, bevacizumab, as well as zoledronate, inhibited the number of experimental bone metastases, including osteoblastic changes produced by ACC-LC-319/bone2 cells. These results indicate that our bone metastasis model by ACC-LC319/bone2 might be useful to understand the molecular pathogenesis of osteolytic and osteoblastic metastasis, and to identify molecular targets to control bone metastasis of lung cancer.
(キーワード): Adenocarcinoma / Animals / Antibodies, Monoclonal / Bone Neoplasms / Cell Line, Tumor / Diphosphonates / Disease Models, Animal / Endothelin-1 / Humans / Imidazoles / Killer Cells, Natural / Lung Neoplasms / Male / Mice / Mice, Inbred ICR / Mice, SCID / Osteoblasts / Osteolysis / Vascular Endothelial Growth Factor A
(出版サイトへのリンク): ● Publication site (DOI): 10.3727/096504009789745511
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19806789; ● Search Scopus @ Elsevier (PMID): 19806789; ● Search Scopus @ Elsevier (DOI): 10.3727/096504009789745511

(DOI: 10.3727/096504009789745511, PubMed: 19806789) 埴淵昌毅, 古川千幸, 篠原勉 :
17歳で発症した低分化型肺扁平上皮癌の1例,
肺癌, Vol.47, No.4, 337-341, 2007年.

(キーワード): Lung cancer / Lung cancer in the young / Poorly differentiated squamous cell carcinoma / 肺癌 / 若年者肺癌 / 低分化型扁平上皮癌
(出版サイトへのリンク): ● Publication site (DOI): 10.2482/haigan.47.337
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390282679657836672; ● Search Scopus @ Elsevier (DOI): 10.2482/haigan.47.337

(DOI: 10.2482/haigan.47.337, CiNii: 1390282679657836672) 古川千幸, 埴淵昌毅, 篠原勉, 近藤治男, 佐藤幸一, 雫治彦 :
軟性気管支鏡と耳鼻科用鉗子を併用して摘出し得た気道異物(義歯)の1例,
徳島赤十字病医誌, Vol.11, 106-109, 2006年.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1572824500927894272

(CiNii: 1572824500927894272) 古川千幸, 埴淵昌毅, 篠原勉, 石倉久嗣, 木村秀 :
肺類上皮血管内皮腫の1例,
肺癌, Vol.46, No.7, 811-815, 2006年.

(キーワード): 肺類上皮血管内皮腫 / 胸腔鏡 / 第VIII因子関連抗原 / CD34
(出版サイトへのリンク): ● Publication site (DOI): 10.2482/haigan.46.811
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390282679659750784; ● Search Scopus @ Elsevier (DOI): 10.2482/haigan.46.811

(DOI: 10.2482/haigan.46.811, CiNii: 1390282679659750784) 山口普史, 池田康将, 藤村光則, 森岡将臣, 橋詰俊二, 加藤みどり, 粟飯原賢一, 赤池雅史, 東博之, 松本俊夫, 稲山真美, 埴淵昌毅 :
アミオダロン肺合併症との鑑別を要したマイコプラズマ肺炎合併拡張型心筋症の1例,
Progress in Medicine, Vol.25, No.Suppl.1, 1552-1556, 2005年.

(要約): 52歳男.47歳時に拡張型心筋症と診断され,持続性心室頻拍でアミオダロン150mg/日を開始した.その後,心室頻拍が頻回となり,心臓電気生理学的検査で心室細動が誘発されたため除細動器植込み術を受け,アミオダロンは増量して継続していた.今回,乾性咳が出現し,胸部X線で左右下肺野にスリガラス状陰影を指摘された.検査所見では高度の炎症所見を認めたが,KL-6は正常範囲で,C型肝炎ウイルスとヒトT細胞性白血病ウイルスI型のキャリアであった.胸部CTでは両側下肺野を中心として壁の肥厚を伴う気管支拡張や小葉中心性の粒状・樹枝状の陰影が多発しており,周囲の肺野に淡い濃度上昇を認めた.アミオダロンの副作用か感染症かは判断できなかったが,アミオダロンは中止し,アンピシリンナトリウム・スルバクタムナトリウム合剤を開始すると共にサイトメガロウイルス高力価免疫グロブリン投与を行った.入院10日目にマイコプラズマ抗体異常高値が判明し,マイコプラズマ肺炎と診断しミノサイクリン100mg/日を開始した.その結果,炎症所見,画像所見は徐々に軽快し,アミオダロンも再開して退院となった
(キーワード): *Amiodarone(治療的利用,毒性・副作用) Minocycline(治療的利用) 胸部X線診断 *心筋症-拡張型(合併症) 鑑別診断 X線CT 肺炎-マイコプラズマ性(合併症,X線診断) 頻拍-心室性(薬物療法) 肺炎-細菌性(合併症,X線診断,薬物療法) 肺炎-間質性(化学的誘発,X線診断) 胸部CT ヒト中年(45~64) 男

Masaki Hanibuchi, Seiji Yano, Nobutaka Edakuni, Mami Inayama and Saburo Sone :
A case of early-stage lung cancer detected by autofluorescence bronchoscopy,
The Journal of Medical Investigation : JMI, Vol.51, No.3-4, 234-237, 2004.

(要約): A 71-year-old man was referred to our hospital for further examination of abnormal sputum cytology. No abnormal nodular shadows were detected in chest X-ray and chest CT. The location of the tumor was clearly identified as a defect of autofluorescence by autofluorescence bronchoscopy at the bifurcation between the left B1+2 and B3 bronchi, whereas it was quite difficult by conventional bronchoscopy. Transbronchial biopsy revealed squamous cell carcinoma. Further examinations yielded the diagnosis of early-stage lung cancer. Photodynamic therapy was performed and complete response was confirmed. This case indicates the efficacy of autofluorescence bronchoscopy for detecting early-stage lung cancer.
(キーワード): Aged / Bronchoscopy / Carcinoma, Squamous Cell / Fluorescence / Humans / Lung Neoplasms / Male / Photochemotherapy
(徳島大学機関リポジトリ): ● Metadata: 110747
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.51.234
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15460912; ● Search Scopus @ Elsevier (PMID): 15460912; ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.51.234

(徳島大学機関リポジトリ: 110747, DOI: 10.2152/jmi.51.234, PubMed: 15460912) Toyokazu Miki, Seiji Yano, Masaki Hanibuchi, Kanematsu Takanori, Hiroaki Muguruma and Saburo Sone :
Parathyroid hormone-related protein (PTHRP) is responsible for production of bone metastasis, but not visceral metastasis, by human small cell lung cancer SBC-5 cells in natural killer cell-depleted SCID mice.,
International Journal of Cancer, Vol.108, No.4, 511-515, 2004.

(要約): We previously established an osteolytic bone metastasis model with multiorgan dissemination in natural killer (NK) cell-depleted severe combined immunodeficient (SCID) mice using human small cell lung cancer cells (SBC-5), which highly express the parathyroid hormone-related protein (PTHrP). In our present study, we evaluated the role of PTHrP on bone metastasis by SBC-5 cells using anti-PTHrP neutralizing antibody (Ab). Anti-PTHrP Ab did not affect the proliferation or cytokine production of SBC-5 cells in vitro. Repeated intravenous injection with anti-PTHrP Ab inhibited the formation of bone metastasis in a dose-dependent manner, while the same treatment had no significant effect on the metastasis to visceral organs (lung, liver, kidney and lymph node). In addition, treatment with anti-PTHrP Ab improved the elevated serum calcium level, associated with inhibition of osteolytic bone metastasis, suggesting that anti-PTHrP Ab inhibited bone metastasis via suppression of bone resorption probably by neutralizing PTHrP. These findings suggest that PTHrP is essential for bone metastasis, but not visceral metastasis, by small cell lung cancer SBC-5 cells.
(キーワード): Animals / Antibodies, Blocking / Antibodies, Monoclonal / Antineoplastic Agents / Bone Neoplasms / Calcium / Carcinoma, Small Cell / Cell Division / Cytokines / Disease Models, Animal / Dose-Response Relationship, Drug / Humans / Kidney Neoplasms / Killer Cells, Natural / Liver Neoplasms / Lung Neoplasms / Lymphatic Metastasis / Lymphocyte Depletion / Male / Mice / Mice, Inbred ICR / Mice, SCID / Parathyroid Hormone-Related Protein / Tumor Cells, Cultured
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/ijc.11586
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14696114; ● Search Scopus @ Elsevier (PMID): 14696114; ● Search Scopus @ Elsevier (DOI): 10.1002/ijc.11586

(DOI: 10.1002/ijc.11586, PubMed: 14696114) Seiji Yano, Helong Zhang, Masaki Hanibuchi, Toyokazu Miki, Hisatsugu Goto, Hisanori Uehara and Saburo Sone :
Combined therapy with a new bisphosphonate, minodronate (YM529), and chemotherapy for multiple organ metastases of small cell lung cancer cells in severe combined immunodeficient mice.,
Clinical Cancer Research, Vol.9, No.14, 5380-5385, 2003.

(要約): Lung cancer in the advanced stage frequently metastasizes to multiple organs, including the liver, lungs, lymph nodes, and bone. Bisphosphonates have been widely used to treat osteolytic bone metastasis in the past years; however, many studies have implicated that a single use of bisphosphonates could not prolong the survival of patients. In the present study, using a multiple-organ metastasis model of human lung cancer cells, we examined the effect of combined therapy with a new bisphosphonate (YM529) and etoposide (VP-16). Human small cell lung cancer (SBC-5) cells i.v. inoculated into natural killer cell-depleted severe combined immunodeficient mice metastasized to multiple organs, including the lungs, liver, kidneys, lymph nodes, and bone. SBC-5-bearing mice were treated with YM529 and/or VP-16 and sacrificed 5 weeks after tumor cell inoculation. Bone metastasis was assessed by X-ray photographs, and visceral metastasis was evaluated macroscopically. The number of osteoclasts in the bone lesions was examined by tartrate-resistant acid phosphatase staining. Monotherapy with YM529 suppressed the production of bone metastases, but not visceral metastasis. Histological analyses revealed that the number of osteoclasts in bone lesions was lower in YM526-treated mice, compared with control mice. VP-16 inhibited both bone metastasis and visceral (lung and liver) metastasis. However, neither YM529 alone nor VP-16 alone significantly prolonged the survival of SBC-5-bearing mice. Combined use of YM529 and VP-16 further inhibited the production of bone metastasis and significantly prolonged survival. Combined therapy with bisphosphonate and chemotherapy may be useful for small cell lung cancer patients with multiple organ metastases including bone metastasis.
(キーワード): Animals / Antineoplastic Agents, Phytogenic / Bone Neoplasms / Carcinoma, Small Cell / Cell Division / Diphosphonates / Drug Combinations / Etoposide / Humans / Imidazoles / Kidney Neoplasms / Killer Cells, Natural / Liver Neoplasms / Lung Neoplasms / Lymphatic Metastasis / Male / Mice / Mice, Inbred ICR / Mice, SCID / Osteoclasts / Parathyroid Hormone-Related Protein / Survival Rate / Tumor Cells, Cultured / Vascular Endothelial Growth Factor A
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14614023; ● Search Scopus @ Elsevier (PMID): 14614023

(PubMed: 14614023) 埴淵昌毅, 島田玲香, 西岡安彦, 篠原勉, 曽根三郎 :
三尖弁感染症心内膜炎および化膿性脊椎炎に併発した敗血症性肺塞栓症の1例(症例報告),
日本呼吸器学会雑誌, Vol.41, No.5, 365-369, 2003年. Masaki Hanibuchi, Seiji Yano, Yasuhiko Nishioka, Hiroaki Yanagawa, Toyokazu Miki and Saburo Sone :
Immunological circumvention of multiple organ metastases of multidrug resistant human small cell lung cancer cells by mouse-human chimeric anti-ganglioside GM2 antibody KM966.,
Clinical & Experimental Metastasis, Vol.18, No.5, 353-360, 2001.

(要約): serum against SBC-3/DOX cells to a similar extent compared with parental SBC-3 cells. Pretreatment of human effector cells with various cytokines induced further enhancement of the KM966-dependent ADCC against SBC-3/DOX cells. Intravenous injection of SBC-3 or SBC-3/DOX cells into natural killer (NK) cell-depleted severe combined immunodeficient (SCID) mice developed metastases in multiple organs (liver, kidneys and lymph nodes). Interestingly, SBC-3/DOX cells produced metastases more rapidly than SBC-3 cells, suggesting more aggressive phenotype of SBC-3/DOX cells than their parental cells in vivo. Systemic treatment with KM966, given on days 2 and 7, drastically inhibited the formation of multiple-organ metastases produced by both SBC-3 and SBC-3/DOX cells, indicating that KM966 can eradicate metastasis by SCLC cells irrespective of MDR phenotype. These findings suggest that the mouse-human chimeric KM966 targets the GM2 antigen, and might be useful for the immunological circumvention of multiple-organ metastases of refractory SCLC.
(キーワード): Animals / Antibodies, Monoclonal / Antineoplastic Agents / Carcinoma, Small Cell / Cytokines / Doxorubicin / Drug Resistance, Multiple / Drug Resistance, Neoplasm / G(M2) Ganglioside / Humans / Lung Neoplasms / Male / Mice / Mice, SCID
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11467766; ● Search Scopus @ Elsevier (PMID): 11467766

(PubMed: 11467766) Tsutomu Shinohara, Naoki Nishimura, Masaki Hanibuchi, Hiroshi Nokihara, Toyokazu Miki, Hirofumi Hamada and Saburo Sone :
Transduction of KAI1/CD82 cDNA promotes hematogenous spread of human lung-cancer cells in natural killer cell-depleted SCID mice,
International Journal of Cancer, Vol.94, No.1, 16-23, 2001.

(要約): KAI1, which is identical to CD82, was initially identified as a metastasis-suppressor gene for human prostate cancer, and its expression is reported to be a favorable prognostic factor for operable human lung cancer. In this study, we examined the functional role of KAI1/CD82 in the late phase of metastatic spread of human lung-cancer cells. For this, KAI1/CD82 cDNA was introduced into KAI1/CD82 low-expressing human lung-cancer cell lines, SBC-3 and PC-14, and then the metastatic potential of the transformants was analyzed by i.v. inoculation of KAI1/CD82-transduced cells, SBC-3/KAI1 and PC-14/KAI1, into NK cell-depleted SCID mice. Contrary to our expectations, KAI1/CD82 gene transfer promoted multiorgan metastasis of i.v.-inoculated human lung-cancer cells, while s.c. tumor growth was unaffected. Cancer cells from metastatic tumors of NK cell-depleted SCID mice injected i.v. with SBC-3/KAI1 expressed appreciable cell-surface KAI1/CD82, and cells not expressing KAI1/CD82 (revertants) were not detected in the tumors. Our findings indicate that under conditions where the host's natural cytotoxicity is suppressed, KAI1/CD82 may enhance the formation of tumors by circulating lung-cancer cells at metastatic sites.
(キーワード): Animals / Antigens, CD / Antigens, CD82 / Cell Adhesion / Cell Line / Cytotoxicity, Immunologic / Endothelium, Vascular / Killer Cells, Natural / Lung Neoplasms / Male / Membrane Glycoproteins / Mice / Mice, SCID / Neoplastic Cells, Circulating / Proto-Oncogene Proteins / Transduction, Genetic
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/ijc.1445
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11668473; ● Search Scopus @ Elsevier (PMID): 11668473; ● Search Scopus @ Elsevier (DOI): 10.1002/ijc.1445

(DOI: 10.1002/ijc.1445, PubMed: 11668473) Prahlad Parajuli, Hiroaki Yanagawa, Masaki Hanibuchi, Eiji Takeuchi, Toyokazu Miki, Seiji Yano and Saburo Sone :
Humanized anti-ganglioside GM2 antibody is effective to induce antibody-dependent cell-mediated cytotoxicity in mononuclear cells from lung cancer patirnts,
Cancer Letters, Vol.165, No.2, 179-184, 2001.

(要約): Ganglioside GM2 is one of the major gangliosides expressed on the cell surface of human tumors including lung cancer. We have previously reported that a mouse-human chimeric monoclonal antibody (mAb), KM966, against GM2 promotes the lysis of lung cancer cells by human blood mononuclear cells (MNC) of healthy donors. In this study, we examined antibody-dependent cell-mediated cytotoxicity (ADCC) of MNC, using KM966 mAb and its humanized counterpart, KM8969, in 16 lung cancer patients and 18 control patients. The ADCC activity was assessed by 4-h (51)Cr release from GM2 positive SBC-3 small cell lung cancer cells. MNC from lung cancer patients exhibited similar ADCC activity to those from control patients when KM966 and KM8969 were used as mAb. Moreover, effective ADCC activity was observed even in MNC from advanced lung cancer patients. These observations suggest the potential activity of humanized anti-GM2 mAb (KM8969), as well as chimeric KM966, in biological therapy for lung cancer patients.
(キーワード): Aged / Aged, 80 and over / Animals / Antibodies, Monoclonal / Carcinoma, Small Cell / Case-Control Studies / Chromium / G(M2) Ganglioside / Humans / Leukocytes, Mononuclear / Lung Neoplasms / Mice / Middle Aged / Time Factors / Tumor Cells, Cultured
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/S0304-3835(01)00427-X
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11275367; ● Search Scopus @ Elsevier (PMID): 11275367; ● Search Scopus @ Elsevier (DOI): 10.1016/S0304-3835(01)00427-X

(DOI: 10.1016/S0304-3835(01)00427-X, PubMed: 11275367) Singh Mahendra Sukh, Hiroaki Yanagawa, Masaki Hanibuchi, Toyokazu Miki, Okamura Haruki and Saburo Sone :
Augmentation by interleukin-18 of MHC-nonrestricted killer activity of human peripheral blood mononuclear cells in response to interleukin-12,
International Journal of Immunopharmacology, Vol.22, No.1, 35-43, 2000.

(要約): Interleukin (IL)-18 is a novel cytokine with pleiotropic functions. In the present study, we examined the induction of the killer activity of peripheral blood mononuclear cells (MNC) against lung cancer cell lines upon treatment with IL-18 in combination with IL-12. Cytotoxic activity was measured by standard (51)Cr release assay. IL-18 (100 ng/ml) was found to significantly augment IL-12-induced killer activity in a MHC-nonrestricted manner against allogeneic NK-resistant Daudi cells and lung cancer cell lines: SBC-3, RERF-LC-AI and A549. IL-18 could augment IL-12-induced killer activity both at the optimal as well as suboptimal doses of the latter. However, IL-18 was found to have little effect on the killer activity of MNC induced by optimal or suboptimal dose of IL-2 or IL-15. Treatment of MNC with IL-18 in combination with IL-12 for a period of more than 4 days was observed to optimally induce the killer activity. As for induction of IFN-gamma production by MNC, IL-18 augmented that induced by IL-2 and IL-15, as well as that induced by IL-12. These results show the potential of IL-18 in combination with IL-12 for clinical application in treatment of cancer.
(キーワード): Interleukin-18 / Mononuclear cell / Tumor cytotoxicity / Interleukin-12 / Lung cancer
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/S0192-0561(99)00062-4
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10684987; ● Search Scopus @ Elsevier (PMID): 10684987; ● Search Scopus @ Elsevier (DOI): 10.1016/S0192-0561(99)00062-4

(DOI: 10.1016/S0192-0561(99)00062-4, PubMed: 10684987) Toyokazu Miki, Seiji Yano, Masaki Hanibuchi and Saburo Sone :
Bone metastasis model with multi-organ dissemination of human small cell lung cancer (SBC-5) cells in nutural killer-cell depleted SCID mice,
Oncology Research, Vol.12, No.5, 209-217, 2000.

(要約): Lung cancer is commonly associated with multiorgan metastasis, and bone is a frequent metastatic site for lung cancer. Nevertheless, no bone metastasis model of lung cancer with multiorgan dissemination is available, which could provide opportunity to study the molecular pathogenesis. We examined the abilities of eight human lung cancer cell lines injected intravenously into natural killer (NK) cell-depleted SCID mice to generate metastatic nodules in bone and multiple organs, and explored the correlation of the parathyroid hormone-related protein (PTHrP) with the bone metastasis. Although all the small-cell carcinoma cell lines (SBC-5, SBC-3, SBC-3/ADM, H69, H69/VP) formed metastatic nodules in multiple organs (liver, kidney, and lymph nodes), only SBC-5 cells reproducibly developed bone metastases. Squamous cell carcinoma (RERF-LC-AI) cells metastasized mainly into the liver and kidneys, whereas adenocarcinoma (PC-14, A549) mainly produced colonies in the lungs. As assessed by X-ray photography, the osteolytic bone metastases produced by SBC-5 cells were detected as early as on day 28, and all recipient mice developed bone metastasis by day 35. The expression of PTHrP in eight cell lines was directly correlated with the formation of bone metastasis. No correlation was observed between the formation of bone metastasis and the expression of other metastasis-related cytokines (IL-1, IL-6, IL-8, IL-10, IL-11, TNF-alpha, VEGF, M-CSF). Consistent with the formation of bone metastasis by SBC-5 cells, the levels of PTHrP and calcium in the mouse serum were increased in a time-dependent manner, suggesting that PTHrP produced by human lung cancer may play a crucial role in the formation of bone metastasis and hypercalcemia. These findings indicate that a bone metastasis model of SBC-5 cells may be useful for clarifying the molecular aspects of the metastatic processes in different organ microenvironments and the development of therapeutic modalities for lung cancer patients with bone metastases.
(キーワード): Animals / Body Weight / Bone Neoplasms / Calcium / Carcinoma, Small Cell / Carcinoma, Squamous Cell / Cytokines / Disease Models, Animal / Humans / Hypercalcemia / Kidney Neoplasms / Killer Cells, Natural / Liver Neoplasms / Lung Neoplasms / Lymphocyte Depletion / Male / Mice / Mice, SCID / Parathyroid Hormone-Related Protein / Proteins / Severe Combined Immunodeficiency / Time Factors / 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): 11417746; ● Search Scopus @ Elsevier (PMID): 11417746

(PubMed: 11417746) Masaki Hanibuchi, Yasuhiko Nishioka, Hiroaki Yanagawa, Seiji Yano, Parajuli Prahlad, Bando Masashi and Saburo Sone :
Human interferon-gamma enhances expression of ganglioside GM2 on human lung cancer cells and their susceptibility for antiganglioside GM2 monoclonal antibody-dependent cellular cytotoxicity.,
Oncology Research, Vol.12, No.4, 173-179, 2000.

(要約): Interferons are known to modulate several cellular functions by the induction of various proteins. In this study, we demonstrated that human interferon-gamma (HuIFN-gamma) enhanced the expression of ganglioside GM2 (GM2), which is a kind of tumor-associated antigen substantially expressed in human lung cancer and that human lung cancer cells expressing GM2 became more susceptible to anti-GM2 monoclonal antibody (mAb)-dependent tumor cell killing mediated by human effector cells after HuIFN-gamma treatment. GM2 expression on human lung cancer cells treated with or without HuIFN-gamma was measured by flow cytometry. The antibody-dependent cellular cytotoxicity (ADCC) activity was assessed by 4-h 51Cr release assay. HuIFN-gamma enhanced GM2 expression on human small-cell lung cancer (SCLC), SBC-3, and human non-small-cell lung cancer (NSCLC), A549 cells in a dose-dependent manner. The optimal concentration of HulIFN-gamma was 1,000 U/ml. The effect of HulFN-gamma reached maximum after 4 days of culture. HulFN-gamma did not have any effect to enhance the expression of other gangliosides in SBC-3 cells. No other cytokines used in this study modulated GM2 expression in SBC-3 cells. Anti-GM2 mAb-dependent ADCC activities induced by lymphocytes and monocytes were more potent against IFN-gamma-treated SBC-3 and A549 cells than nontreated cells. Taken together, HulFN-gamma combined with anti-GM2 mAb may be useful for immunotherapy against GM2-positive human lung cancer.
(キーワード): Antibodies, Monoclonal / Carcinoma, Non-Small-Cell Lung / Carcinoma, Small Cell / Dose-Response Relationship, Drug / Flow Cytometry / G(M2) Ganglioside / Humans / Immunotherapy / Interferon-gamma / Lung Neoplasms / Lymphocytes / Monocytes / Time Factors / Tumor Cells, Cultured
(出版サイトへのリンク): ● Publication site (DOI): 10.3727/096504001108747657
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11341466; ● Summary page in Scopus @ Elsevier: 2-s2.0-0034574911

(DOI: 10.3727/096504001108747657, PubMed: 11341466, Elsevier: Scopus) Nakamura Kazuyasu, Masaki Hanibuchi, Seiji Yano, Tanaka Yuko, Fujino Ikuko, Inoue Miho, Takezawa Toshiaki, Shitara Kenya, Saburo Sone and Hanai Nobuo :
Apoptosis induction of human lung cancer cell line in multicellular heterospheroids with humanized antiganglioside GM2 monoclonal antibody.,
Cancer Research, Vol.59, No.20, 5323-5330, 1999.

(要約): The chimeric antiganglioside GM2 monoclonal antibody (MAb) KM966, which showed high effector functions such as complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity (ADCC), potently suppressed growth and metastases of GM2-positive human cancer cells inoculated into mice. To further improve the therapeutic efficacy of the anti-GM2 MAb in humans, we constructed a humanized anti-GM2 MAb, KM8969. The humanized KM8969 was more efficient in supporting ADCC against GM2-positive human cancer cell lines than the chimeric KM966, whereas complement-dependent cytotoxicity was slightly reduced in the humanized KM8969. In addition, the humanized KM8969 was shown to exert potent ADCC mediated by both lymphocytes and monocytes. To investigate the effect of the humanized KM8969 on the biological function of GM2 in the condition physiologically mimicking formation and growth of cancer masses, the heterospheroids composed of normal human dermal fibroblasts and GM2-positive human lung cancer cells were developed. Interestingly, the humanized KM8969 gave rise to growth inhibition of heterospheroids without dependence of the effector functions. Morphological and immunocytochemical analysis suggested that the inhibitory effect was due to the apoptosis of GM2-positive cancer cells in the heterospheroids. The result indicates that GM2 captured by the antibody on the cell surface loses its physiological function that plays a critical role in maintaining the three-dimensional growth of cancer cells in contact with its own cells or other type of cells in a microenvironment. The humanized KM8969, which can destroy the cancer cells via blocking functional GM2 on the cell surface as well as the effector functions, would have extraordinary potential in human cancer therapy.
(キーワード): Animals / Antibodies, Monoclonal / Antibody-Dependent Cell Cytotoxicity / Apoptosis / Complement System Proteins / G(M2) Ganglioside / Humans / Lung Neoplasms / Mice / Recombinant Fusion Proteins / Spheroids, Cellular / 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): 10537316; ● Summary page in Scopus @ Elsevier: 2-s2.0-0032720632

(PubMed: 10537316, Elsevier: Scopus) Seiji Yano, Masaki Hanibuchi, Yasuhiko Nishioka, Hiroshi Nishihara, Naoki Nishimura, Takashi Tsuruo and Saburo Sone :
Combined therapy with anti-p-glycoprotein antibody and macrophage colony-stimulating factor gene transduction for multiorgan metastases of multidrug-resistant human small cell lung cancer in nk cell-depleted scid mice,
International Journal of Cancer, Vol.82, No.1, 105-111, 1999.

(要約): Our aim was to determine the antimetastatic potential of anti-P-glycoprotein (P-gp) antibodies (Abs) against multidrug-resistant (MDR) human small cell lung cancer (SCLC) cells expressing P-gp. Human SCLC cells H69 (P-gp negative) and its etoposide-resistant variant H69/YP (P-gp positive) were used. H69 and H69/VP cells injected i.v. metastasized to the liver, kidneys and systemic lymph nodes of NK cell-depleted severe combined immunodeficient (SCID) mice. H69/VP cells, but not H69 cells, were resistant to treatments with vindesine. Treatment with mouse-human chimeric anti-P-gp Ab (MH162) and its mouse counterpart (MRK-16) reduced metastasis of H69/VP cells in various organs and prolonged the survival of tumor-bearing mice, although they were less effective if injected at late times (after 28 days). Treatment with another mouse anti-Pgp Ab, MRK-17, was effective only against liver metastasis. MH162 and MRK-16 efficiently induced Ab-dependent cellular cytotoxicity (ADCC) by peritoneal macrophages against H69/VP cells in vitro, but MRK-17 was less effective, in accordance with their in vivo antimetastatic potential. Gene transfection of macrophage colony-stimulating factor (M-CSF) into H69/VP cells to augment macrophage-mediated ADCC resulted in inhibition of metastasis to the liver and lymph nodes, but not kidneys. Combined treatment with a low dose of MRK-16 completely cured metastasis of M-CSF transfectant, but not of the mock transfectant. Our findings suggest that while anti-P-gp Abs had antimetastatic potential against SCLC cells expressing P-gp, combined treatment with M-CSF gene transduction to augment the therapeutic efficacy of anti-P-gp Abs may be beneficial for eradicating metastatic MDR SCLC in humans.
(キーワード): Animals / Antibodies, Monoclonal / Antibody-Dependent Cell Cytotoxicity / Carcinoma, Small Cell / Combined Modality Therapy / Drug Resistance, Multiple / Gene Therapy / Humans / Killer Cells, Natural / Lung Neoplasms / Macrophage Colony-Stimulating Factor / Male / Mice / Mice, SCID / Neoplasm Metastasis / P-Glycoprotein / Tumor Cells, Cultured
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/(SICI)1097-0215(19990702)82:1<105::AID-IJC18>3.0.CO;2-C
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10360828; ● Search Scopus @ Elsevier (PMID): 10360828; ● Search Scopus @ Elsevier (DOI): 10.1002/(SICI)1097-0215(19990702)82:1<105::AID-IJC18>3.0.CO;2-C

(DOI: 10.1002/(SICI)1097-0215(19990702)82:1<105::AID-IJC18>3.0.CO;2-C, PubMed: 10360828) Prahlad Parajuli, Yasuhiko Nishioka, Naoki Nishimura, Sukh Mahendra Singh, Masaki Hanibuchi, Hiroshi Nokihara, Hiroaki Yanagawa and Saburo Sone :
Cytolysis of human dendritic cells by autologous lymphokine-activated killer cells: participation of both T cells and NK cells in the killing.,
Journal of Leukocyte Biology, Vol.65, No.6, 764-760, 1999.

(要約): Dendritic cells (DC) play a key role in the initiation of immune response by stimulating the naive T cells. The fate of DC after the initiation of immune response is not clearly understood. Although there are few reports implicating natural killer (NK) cells in the elimination of DC, killing of DC by LAK cells, and specifically by T cells, has not been studied. In this study, we observed that DC, generated from monocytes, in vitro in the presence of granulocyte-macrophage colony-stimulating factor, interleukin-4 (IL-4), and tumor necrosis factor alpha were susceptible to cytolysis by lymphokine-activated killer (LAK) cells induced in the presence of IL-2 and IL-15 but not IL-12 alone. However, LAK cells induced by a combination of IL-12 and suboptimal dose of IL-2 were cytotoxic to DC. When purified lymphocytes were activated with IL-2, the CD8+/CD57- fraction (T-LAK), but not the CD8-/CD57+ fraction (NK-LAK) was cytotoxic to autologous DC. However, when unseparated peripheral blood mononuclear cells were used to generate LAK cells, both T-LAK and NK-LAK fractions showed equal cytotoxicity against autologous DC. Monoclonal antibodies against CD54, CD11a, and CD18 significantly inhibited the cytolysis, indicating that the killing involves the engagement of CD54 with its ligands.
(キーワード): Antibodies, Blocking / Antibodies, Monoclonal / CD18 Antigens / Cytotoxicity, Immunologic / Dendritic Cells / Humans / Intercellular Adhesion Molecule-1 / Interleukin-12 / Interleukin-2 / Killer Cells, Lymphokine-Activated / Killer Cells, Natural / Leukocytes, Mononuclear / Lymphocyte Function-Associated Antigen-1 / Macrophages / Tリンパ球 (T lymphocytes)
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/jlb.65.6.764
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10380897; ● Summary page in Scopus @ Elsevier: 2-s2.0-0033003373

(DOI: 10.1002/jlb.65.6.764, PubMed: 10380897, Elsevier: Scopus) Saburo Sone, Seiji Yano, Masaki Hanibuchi, Hiroshi Nokihara, Naoki Nishimura, Toyokazu Miki, Yasuhiko Nishioka and Tsutomu Shinohara :
Heterogeneity of multiorgan metastases of human lung cancer cells genetically engineered to produce cytokines and reversal using chimeric monoclonal antibodies in natural killer cell-depleted severe combined immunodeficient mice,
Cancer Chemotherapy and Pharmacology, Vol.43, No.Supplement 1, S26-S31, 1999.

(要約): Lung cancer is a major cause of cancer deaths, most of which can be attributed to distant multiorgan metastases. To examine the cellular and molecular mechanisms of lung cancer metastasis to distant organs, we have established novel models of human lung cancer (small cell and non-small cell lung cancer) metastasis in natural killer cell-depleted severe combined immunodeficient (SCID) mice. We investigated whether local production of the cytokines responsible for regulation of macrophage function at tumor growth sites affects the pattern of lung cancer metastasis in distant organs. Several lung cancer cell lines were genetically engineered to produce human macrophage colony-stimulating factor (M-CSF) and monocyte chemoattractant protein-1 (MCP-1), and their metastatic potentials were assessed. Interestingly, M-CSF gene transduction had an antimetastatic effect for the liver and lymph nodes, but not the kidneys. In contrast, MCP-1 gene-modified lung cancer cells and their parent cells had identical metastatic potentials. These findings indicate a possible role for cytokines and suggest that lung cancer has metastatic heterogeneity. Examining ways of controlling human lung cancer metastases, we investigated the antimetastatic effect of chimeric monoclonal antibodies (MAbs) against P-glycoprotein and ganglioside GM2 (MH162 and KM966, respectively). Both MAbs, when given on days 2 and 7, inhibited the development of distant metastases of lung cancer in a dose-dependent fashion. Combined use of anti-P-glycoprotein MAb with M-CSF or MCP-1 gene transduction caused complete inhibition of metastasis of H69/VP cells. The antimetastatic effect of these MAbs in vivo was mainly due to an antibody-dependent cell-mediated cytotoxicity reaction mediated by mouse macrophages. These findings suggest that the mouse-human chimeric MAb in combination with cytokine gene transduction may be useful for the eradication of lung cancer metastases in humans.
(キーワード): Animals / Antibodies, Monoclonal / Carcinoma, Non-Small-Cell Lung / Carcinoma, Small Cell / Chemokine CCL2 / Cytokines / G(M2) Ganglioside / Granulocyte-Macrophage Colony-Stimulating Factor / Humans / Kidney Neoplasms / Killer Cells, Natural / Liver Neoplasms / Lung Neoplasms / Lymphatic Metastasis / Mice / Mice, SCID / Neoplasm Transplantation / P-Glycoprotein / Recombinant Fusion Proteins / Transduction, Genetic / 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): 10357555; ● Search Scopus @ Elsevier (PMID): 10357555

(PubMed: 10357555) Masaki Hanibuchi, Seiji Yano, Yasuhiko Nishioka, Hiroaki Yanagawa, Tetsuya Kawano and Saburo Sone :
Therapeutic efficacy of mouse-human chimeric anti-ganglioside GM2 monoclonal antibody against multiple organ micrometastases of human lung cancer in NK cell-depleted SCID mice,
International Journal of Cancer, Vol.78, No.4, 480-485, 1998.

(要約): The development of distant metastases to multiple organs is a critical problem in the treatment of human lung cancer. In this study, we evaluated the therapeutic efficacy of a mouse-human chimeric anti-ganglioside GM2 (GM2) monoclonal antibody (MAb), KM966 against metastasis formation of GM2-positive human lung cancer cells inoculated intravenously (i.v.) into natural killer (NK) cell-depleted severe combined immunodeficient (SCID) mice. GM2-positive human small cell lung cancer (SCLC), SBC-3 cells (1 x 10(6)), injected through a tail vein into NK cell-depleted SCID mice, formed large number of metastatic colonies in the liver, kidneys and lymph nodes by 42 days after inoculation (day 42). KM966, but not control MAb, given on days 2 and 7, almost completely inhibited metastasis formation of SBC-3 cells in the liver, kidneys and lymph nodes in a dose-dependent fashion. Moreover, treatment with KM966 at advanced stages of metastasis (even from day 28) significantly suppressed multiple organ metastases of SBC-3 cells. The anti-metastatic effect of KM966 in vivo was mainly due to an antibody-dependent cell-mediated cytotoxicity (ADCC) reaction mediated by macrophages of the SCID mice. Our findings suggest that the mouse-human chimeric anti-GM2 MAb, KM966 may be useful for eradicating multiple organ micrometastases of lung cancer in humans.
(キーワード): Animals / Antibodies, Monoclonal / Antibody-Dependent Cell Cytotoxicity / Carcinoma, Small Cell / G(M2) Ganglioside / Humans / Immunotherapy / Killer Cells, Natural / Lung Neoplasms / Male / Mice / Mice, SCID / Neoplasm Invasiveness / Neoplasm Staging / Neoplasm Transplantation / Recombinant Fusion Proteins
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/(SICI)1097-0215(19981109)78:4<480::AID-IJC14>3.0.CO;2-A
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9797137; ● Search Scopus @ Elsevier (PMID): 9797137; ● Search Scopus @ Elsevier (DOI): 10.1002/(SICI)1097-0215(19981109)78:4<480::AID-IJC14>3.0.CO;2-A

(DOI: 10.1002/(SICI)1097-0215(19981109)78:4<480::AID-IJC14>3.0.CO;2-A, PubMed: 9797137) Punya Shrivastava, Masaki Hanibuchi, Seiji Yano, Prahlad Parajuli, Takashi Tsuruo and Saburo Sone :
Circumvention of multidrug resistance by a quinoline derivative, MS-209, in multidrug-resistant human small-cell lung cancer cells and its synergistic interaction with cyclosporin A or verapamil,
Cancer Chemotherapy and Pharmacology, Vol.42, No.6, 483-490, 1998.

(要約): To develop a clinically useful approach to circumvent P-glycoprotein (P-gp)-mediated multidrug resistance (MDR) in MDR human small-cell lung cancer (SCLC), we examined the ability of a novel quinoline compound, MS-209, to reverse MDR by inhibition of P-gp function in combination with other MDR-reversing drugs using a cytotoxicity assay. We established MDR human SCLC cells by culture in medium with gradually increasing concentrations of adriamycin (ADM). Compared with the parental human SCLC cells, SBC-3, the MDR variant SBC-3 cells obtained (SBC-3/ADM) were highly resistant to various chemotherapeutic agents due to P-gp expression. MS-209 reversed the resistance to ADM and vincristine (VCR) of SBC-3/ADM and H69/VP cells in a dose-dependent manner. Moreover, MS-209 in combination with cyclosporin A (CsA) or verapamil (VER) synergistically enhanced the antitumor effects of ADM and VCR on SBC-3/ADM cells. MS-209 restored ADM incorporation and this effect was enhanced by CsA and VER, suggesting that these synergistic effects were due to competitive inhibition of P-gp function. MS-209 in combination with CsA or VER might increase the efficacy of these chemotherapeutic agents against MDR human SCLC cells.
(キーワード): Antineoplastic Agents / Carcinoma, Small Cell / Cyclosporine / Drug Resistance, Multiple / Drug Resistance, Neoplasm / Drug Synergism / Humans / Lung Neoplasms / P-Glycoprotein / Quinolines / Tumor Cells, Cultured / Verapamil
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9788575; ● Search Scopus @ Elsevier (PMID): 9788575

(PubMed: 9788575) Seiji Yano, Hiroaki Yanagawa, Masaki Hanibuchi, Kalpana Pai, Yasuhiko Nishioka, Takashi Tsuruo and Saburo Sone :
The role of cyclosporin A on antibody-dependent monocyte-mediated cytotoxicity against human multidrug-resistant cancer cells,
The Journal of Medical Investigation : JMI, Vol.44, No.3-4, 185-191, 1998.

(要約): A P-glycoprotein (P-gp) inhibitor, cyclosporin A (CsA) was found to enhance the susceptibility of multidrug resistant (MDR) cancer cells to anti-P-gp antibody-dependent cellular cytolysis (ADCC) by monocytes, but the exact mechanism is unknown. In this study, we examined whether CsA enhanced the susceptibility of MDR cells through its inhibitory effect of P-gp function by using anti-ganglioside GM2 (GM2) monoclonal antibody (Ab), KM966, instead of anti-P-gp Ab, MRK16. Monocyte-ADCC induced by both KM966 and MRK16 against P-gp positive human MDR ovarian cancer cells was significantly augmented by addition of CsA. KM966, but not MRK16, induced monocyte-ADCC against P-gp negative human ovarian cancer cells and CsA enhanced this ADCC activity, indicating that suppressive effect of P-gp function by CsA was not essential to the enhancement of ADCC. Moreover, pretreatment of tumor cells with CsA augmented their susceptibility to monocyte-ADCC irrespective of P-gp expression. Interestingly, KM966 or MRK16 induced monocyte-ADCC against various human lung cancer cells expressing either GM2 or P-gp, but CsA did not affect these ADCC. These findings suggest that CsA may enhance the susceptibility to the monocyte-ADCC of ovarian cancer cells, but not of lung cancer cells, irrespective of its suppressive effect of P-gp function.
(キーワード): Antibodies, Monoclonal / Cell Line / Cyclosporine / Cytotoxicity, Immunologic / Drug Resistance, Multiple / Humans / Monocytes / Neoplasms
(徳島大学機関リポジトリ): ● Metadata: 110665
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9597807; ● Search Scopus @ Elsevier (PMID): 9597807

(徳島大学機関リポジトリ: 110665, PubMed: 9597807) Prahlad Parajuli, Seiji Yano, Masaki Hanibuchi, Hiroshi Nokihara, Tsutomu Shinohara and Saburo Sone :
Effect of clarythromycin on the distant metastases of human lung cancer cells in SCID mice,
The Journal of Medical Investigation : JMI, Vol.44, No.3-4, 205-210, 1998.

(要約): Recently, the use of macrolides is suggested to be therapeutically effective in prolonging the survival of patients with inoperable non-small cell lung cancer. The purpose of this study was to examine therapeutic effects of a macrolide, clarythromycin (CAM) on the metastastic developments of two different human non-small cell lung cancers (squamous cell lung carcinoma RERF-LC-AI, and adenocarcinoma PC-14) in severe combined immunodeficient (SCID) mice depleted or undepleted of natural killer (NK) cells, respectively. CAM, injected subcutaneously at doses of 5 and 10 mg/kg body weight/day from day 7 to 41 after i.v. inoculation of human lung cancer cells, was not effective in inhibiting their distant organ metastases in SCID mice. CAM at concentrations of less than 10 micrograms/ml did not have a direct influence on the proliferation of these tumor cells in vitro. Although CAM alone was not effective in augmenting NK activity, it augmented the IL-2-induced killer (LAK) activity against Daudi cells in vitro. These results suggest that CAM alone may not be enough to control the spread of non-small cell lung cancer in the patient with T cell dysfunction.
(キーワード): Animals / Anti-Bacterial Agents / Humans / Lung Neoplasms / Macrolides / Mice / Mice, SCID / Neoplasm Metastasis / Neoplasm Transplantation / Neoplasms, Experimental
(徳島大学機関リポジトリ): ● Metadata: 110668
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9597810; ● Search Scopus @ Elsevier (PMID): 9597810

(徳島大学機関リポジトリ: 110668, PubMed: 9597810) Hiroaki Yanagawa, Takashi Haku, K Hiramatsu, Hiroshi Nokihara, Eiji Takeuchi, Seiji Yano, Masaki Hanibuchi and Saburo Sone :
Intrapleural instillation of interferon gamma in patients with malignant pleurisy due to lung cancer,
Cancer Immunology, Immunotherapy, Vol.45, No.2, 93-99, 1997.

(要約): The effect of intrapleural instillation of recombinant human interferon gamma (IFN gamma) at increasing doses of (1-12) x 10(6) U was examined in six patients with cytologically positive pleural effusion due to lung cancer. Intrapleural instillation was repeated up to three times. Clinically, no reaccumulation of pleural effusion was observed in one patient and disappearance of lung cancer cells from the pleural effusion was seen in two other patients. No severe side-effects were observed. Considerable levels of IFN gamma remained in the pleural effusion as well as in patients' serum up to 7 days after instillation of 2 x 10(6) U and higher doses. The total cell number showed a transient decrease on day 1 of therapy. Levels of pro-inflammatory cytokines, such as tumor necrosis factor alpha, interleukin(IL)-1 beta and IL-6, in the pleural effusion remained almost stable after IFN gamma instillation. On the other hand, intrapleural IL-1 receptor antagonist levels were remarkably elevated by the instillation of IFN gamma. IL-2- and IL-12-inducible killer activity of pleural mononuclear cells tended to increase slightly. Despite the inability of IFN gamma to control pleural effusion in this treatment schedule, IFN gamma instilled by an intrapleural route had a potential local antitumor activity. Moreover, since IFN gamma persists in pleural effusions for a long time after a single instillation, such a therapy in combination with other fibrogenic biological response modifiers can be promising.
(キーワード): Aged / Cytokines / Cytotoxicity, Immunologic / Female / Humans / Interferon-gamma, Recombinant / Lung Neoplasms / Male / Middle Aged / Pleura / Pleurisy
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s002620050407
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9390200; ● Search Scopus @ Elsevier (PMID): 9390200; ● Search Scopus @ Elsevier (DOI): 10.1007/s002620050407

(DOI: 10.1007/s002620050407, PubMed: 9390200) Seiji Yano, Hiroshi Nokihara, Masaki Hanibuchi, Prahlad Parajuli, Tsutomu Shinohara, Tetsuya Kawano and Saburo Sone :
Model of malignant pleural effusion of human lung adenocarcinoma in SCID mice,
Oncology Research, Vol.9, No.11-12, 573-579, 1997.

(要約): Malignant pleural effusion (PE) is a frequent problem in lung cancer. In this study, we established a model of malignant PE of human adenocarcinoma cells, PC-14, in SCID mice. Intravenously injected PC-14 cells formed colonies in the lungs as early as week 4 after tumor inoculation, and produced bloody PE in all recipient SCID mice by week 8. Pretreatment of SCID mice with anti-mouse IL-2 receptor beta chain antibody (TM-beta 1) to deplete natural killer (NK) cells markedly promoted the production of bloody PE and metastases to multiple organs, such as the lungs, liver, kidneys, and lymph nodes 4 weeks after tumor inoculation. Histological studies indicated that PC-14 cells formed colonies in the lungs, and then invaded the pleura and spread to the pleural cavity. To establish cell lines with a high potential to produce PE, we harvested PE, expanded the tumor cells in vitro, and injected them into SCID mice again. By four in vivo selection cycles in this way we obtained PC-14-PM4 cells, which produce lung metastases and PE earlier than PC-14 cells. The survival of SCID mice inoculated with PC-14-PM4 cells was significantly shorter than that of mice inoculated with PC-14 cells. The expressions of adhesion molecules, such as CD44, CD49d, ICAM-1, and MHC class I, on PC-14-PM4 cells tended to increase compared with PC-14 cells. These changes of adhesion molecules seem to be one of possible mechanisms involved in higher metastatic potential of PC-14-PM4 cells. PE models with PC-14 and PC-14-PM4 cells should be useful for biological and preclinical studies on malignant PE produced by human lung cancer.
(キーワード): Adenocarcinoma / Animals / Cell Adhesion Molecules / Disease Models, Animal / Flow Cytometry / Humans / Lung Neoplasms / Male / Mice / Mice, SCID / Neoplasm Transplantation / Pleural Effusion, Malignant / 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): 9563004; ● Search Scopus @ Elsevier (PMID): 9563004

(PubMed: 9563004) Masaki Hanibuchi, Seiji Yano, Yasuhiko Nishioka, Hiroaki Yanagawa and Saburo Sone :
Anti-ganglioside GM2 monoclonal antibody-dependent killing of human lung cancer cells by lymphocytes and monocytes,
Japanese Journal of Cancer Research, Vol.87, No.5, 497-504, 1996.

(要約): Ganglioside GM2 (GM2) frequently appears on the cell surface of human cancers of neuroendocrine origin. A mouse-human chimeric monoclonal antibody (mAb), KM966, against GM2 was previously found to promote the lysis of various cancer cells by human blood mononuclear cells (MNC). In this study, we analyzed the effector cells responsible for the chimeric mAb-dependent cell-mediated cytotoxicity (ADCC) against small cell lung cancer (SCLC) cells and examined the enhancing effect of various cytokines on the ADCC activity. The ADCC activity was assessed by 4-h 51Cr release assay. Highly purified lymphocytes (> 99%) and monocytes (> 90%) were separated by centrifugal elutriation from peripheral blood MNC of the same healthy donor. KM966 induced lysis of SCLC cells mediated by both lymphocytes and monocytes to similar extents, in a dose-dependent manner. Pretreatment of lymphocytes with various cytokines [interleukin (IL)-2, IL-12 and interferon-gamma] and that of monocytes with macrophage-colony-stimulating factor significantly augmented the killer activity against SCLC cells in the presence of KM966 mAb. KM966 was also effective for the lysis of non-small cell lung cancer cells in direct proportion to the GM2 expression levels. These findings suggest that combined treatment of KM966 mAb with cytokines may be therapeutically useful for in vivo killing of lung cancer cells expressing GM2 through the ADCC reaction.
(キーワード): Adenocarcinoma / Antibodies, Monoclonal / Antibody-Dependent Cell Cytotoxicity / Carcinoma, Small Cell / Carcinoma, Squamous Cell / Female / G(M2) Ganglioside / Humans / Interferon-gamma / Interleukin-2 / Lung Neoplasms / Lymphocytes / Macrophage Colony-Stimulating Factor / Monocytes / Ovarian Neoplasms / Tumor Cells, Cultured
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/j.1349-7006.1996.tb00251.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 8641987; ● Search Scopus @ Elsevier (PMID): 8641987; ● Search Scopus @ Elsevier (DOI): 10.1111/j.1349-7006.1996.tb00251.x

(DOI: 10.1111/j.1349-7006.1996.tb00251.x, PubMed: 8641987) Takashi Haku, Hiroaki Yanagawa, Y Ohmoto, Eiji Takeuchi, Seiji Yano, Masaki Hanibuchi, Hiroshi Nokihara, Naoki Nishimura and Saburo Sone :
Systemic chemotherapy alters interleukin-1 beta and its receptor antagonist production by human alveolar macrophages in lung cancer patients,
Oncology Research, Vol.8, No.12, 519-526, 1996.

(要約): The purpose of this study was to determine whether cytotoxic chemotherapy influences the number and function of alveolar macrophages (AM) in patients with lung cancer. AM were obtained by bronchoalveolar lavage from 24 patients with lung cancer and 17 control patients. The functional integrity of AM was determined by their ability to produce interleukin-1 beta (IL-1 beta) and interleukin-1 receptor antagonist (IL-1ra) before and after platinum-containing systemic chemotherapy. The productions of IL-1 beta and IL-1ra were quantitated by enzyme immunoassays. The proportions of multinucleated cells among AM were significantly decreased after systemic chemotherapy in lung cancer patients. No significant difference in spontaneous and lipopolysaccharide (LPS)-stimulated IL-1 beta or IL-1ra production by AM was observed between lung cancer patients and control patients. Significant increase of IL-1 beta and significant decrease of IL-1ra production by AM were demonstrated in patients with small cell lung cancer who experienced response to systemic chemotherapy. These results suggest that systemic chemotherapy may influence functional roles of AM in the lung, and consideration of influence of systemic chemotherapy on host functions is important in cancer treatment.
(キーワード): Adult / Aged / Antineoplastic Agents / Bronchoalveolar Lavage Fluid / Female / Humans / Interleukin 1 Receptor Antagonist Protein / Interleukin-1 / Lung Neoplasms / Macrophages, Alveolar / Male / Middle Aged / Sialoglycoproteins
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9160356; ● Search Scopus @ Elsevier (PMID): 9160356

(PubMed: 9160356) Roustem Nabioullin, Hiroaki Yanagawa, Takashi Haku, K Hiramatsu, Seiji Yano, Masaki Hanibuchi, Kalpana Pai, Takashi Tsuruo and Saburo Sone :
Influence of systemic chemotherapy on anti-P-glycoprotein antibody-dependent cell-mediated cytotoxicity in patients with small cell lung cancer,
Japanese Journal of Clinical Oncology, Vol.25, No.4, 124-130, 1995.

(要約): Anti-P-glycoprotein antibody (MRK-16)-dependent cell-mediated cytotoxicity (ADCC) by blood mononuclear cells (MNC) was examined in patients with small cell lung cancer (SCLC) before and after systemic chemotherapy. The effect of in vitro treatment of MNC with interleukin (IL)-2 and macrophage-colony-stimulating factor (M-CSF) was also examined. The ADCC reaction was assessed by a 6 h 51Cr-release assay using a multidrug-resistant (MDR) SCLC cell line (H69/VP cells). The MRK-16 monoclonal antibody was able to augment spontaneous cytotoxicity by MNC, even in SCLC patients. Pretreatment of MNC with IL-2 significantly augmented their ADCC ability in SCLC patients, while M-CSF had no effect on ADCC activity. After the first cycle of systemic chemotherapy, the ADCC activity tended to decline, but ADCC of MNC pretreated with IL-2 was not affected. The results suggest that anti-P-glycoprotein antibody, in combination with a cytokine such as IL-2, may be therapeutically useful against human SCLC resistant to chemotherapeutic drugs.
(キーワード): Antibodies, Monoclonal / Antibody-Dependent Cell Cytotoxicity / Antineoplastic Combined Chemotherapy Protocols / Carboplatin / Carcinoma, Non-Small-Cell Lung / Cisplatin / Doxorubicin / Drug Resistance, Multiple / Etoposide / Humans / Interleukin-2 / Lung Neoplasms / Macrophage Colony-Stimulating Factor / P-Glycoprotein / 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): 7666588; ● Search Scopus @ Elsevier (PMID): 7666588

(PubMed: 7666588)

MISC

矢葺洋平, 大塚憲司, 竹内栄治, 葉久貴司, 兼松貴則, 西村直樹, 豊田優子, 埴淵昌毅, 軒原浩, 西岡安彦 :
高齢者進行・再発非小細胞肺癌に対する Pemetrexed + Bevacizumab 併用療法の有効性と安全性の検討,
第62回日本肺癌学会学術集会, 2021年.

総説・解説

埴淵昌毅, 西岡安彦 :
特集 COPD合併肺癌: 病因論から治療まで. COPDにおける肺癌合併の分子機構,
呼吸と循環, Vol.64, No.8, 743-747, 2016年8月.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390565159920348544

(CiNii: 1390565159920348544) 埴淵昌毅, 西岡安彦 :
Current topics from major journals―英文抄読会から ALK陽性非小細胞肺癌に対する1次治療でのクリゾチニブと化学療法の比較試験,
日本胸部臨床, Vol.74, No.6, 717, 2015年6月. 埴淵昌毅, 西岡安彦 :
抗がん剤の副作用と支持療法―より適切な抗がん剤の安全使用をめざして― III. 抗がん剤の副作用に対する評価と処置 4.抗がん剤の副作用の予防的治療,
日本臨牀, Vol.73, No.Suppl. 2, 93-97, 2015年2月. 西岡安彦, 後東久嗣, 埴淵昌毅, 柿内聡司 :
呼吸器抄読会,
呼吸, Vol.34, No.2, 233, 2015年2月. 埴淵昌毅 :
COPD―病態の理解とマネジメントの実際―,
小松島市医師会会報, Vol.49, No.1, 31-33, 2015年1月. 埴淵昌毅 :
気管支喘息の日常臨床,
小松島市医師会会報, Vol.48, No.1, 23, 2014年1月. 埴淵昌毅, 西岡安彦 :
特集がんの分子病態診断-免疫染色と遺伝子診断の進歩- トピックス肺がんと炎症,
最新医学, Vol.67, No.3, 479-484, 2012年3月. 埴淵昌毅 :
QOL評価法としてのpatient-reported outcome (PRO) とは,
CRITICAL EYES on Clinical Oncology, Vol.40, 11, 2011年9月. 埴淵昌毅, 柿内聡司, 佐藤正大, 曽根三郎 :
癌の浸潤・転移における分子メカニズムと標的分子,
呼吸器内科, Vol.3, No.17, 212-219, 2010年3月.

(キーワード): 肺癌 (lung cancer) / 浸潤 / 転移 (metastasis) / 標的分子

埴淵昌毅, 曽根三郎 :
原発性肺癌の遠隔転移および転移性肺腫瘍, --- がん転移:臨床と研究の羅針盤 ---,
細胞工学, 58-62, 2010年1月. 矢野聖二, 埴淵昌毅, 曽根三郎 :
肺癌患者の診断およびモニタリング,
呼吸, Vol.24, No.2, 149-155, 2005年. 埴淵昌毅, 曽根三郎 :
ニューロン特異性エノラーゼ(NSE),
Modern Physician, Vol.24, No.5, 978-979, 2004年. 埴淵昌毅, 曽根三郎 :
サイトケラチン19フラグメント(CYFRA 21-1),
Modern Physician, Vol.24, No.5, 976-977, 2004年. 埴淵昌毅, 合田正和, 真鍋和義, 兼松貴則, 矢野聖二, 曽根三郎 :
口蓋扁桃転移を来した非小細胞肺癌の2例,
肺癌, Vol.43, No.4, 319-324, 2003年. 兼松貴則, 埴淵昌毅, 曽根三郎 :
肺癌の薬物療法,
臨床と免疫, Vol.80, No.7, 1234-1237, 2003年. 埴淵昌毅, 曽根三郎 :
肺癌の診断と治療ー最新の研究動向ー, --- III．肺癌の発癌機構 3 肺癌原性物質と発癌機構 ---,
株式会社日本臨牀社, Vol.60, No.5, 63-66, 2002年5月. 埴淵昌毅, 矢野聖二, 曽根三郎 :
癌治療における抗体療法の歴史的変遷,
Surgery Frontier, Vol.9, No.3, 194-198, 2002年. 埴淵昌毅, 曽根三郎 :
診断ー肺癌を見のがさないために, --- 肺癌の臨床診断のすすめ方 ---,
月刊臨牀と研究, Vol.79, No.5, 735-739, 2002年.

講演・発表

Yabuki Yohei, Kenji Otsuka, Hirokazu Ogino, Takeuchi Eiji, Haku Takashi, Takanori Kanematsu, Nishimura Naoki, Yuko Toyoda, Masaki Hanibuchi, Atsushi Mitsuhashi, Tsukazaki Yuki, Ryohiko Ozaki, Hiroto Yoneda, Hiroshi Nokihara and Yasuhiko Nishioka :
A multicenter, open-label, phase II trial of pemetrexed plus bevacizumab in elderly patients with advanced or recurrent non-squamous non-small cell lung cancer,
APSR 2022, Seoul, Nov. 2022. Kazuya Koyama, Sakamoto Susumu, Homma Sakae, Seidai Satou, Masaki Hanibuchi, Masuda Kiyoshi, Imoto Isei, Yuko Toyoda, Isshiki Takuma, Miyoshi Shion, Kato Motoyasu, Takahashi Kazuhisa, Kataoka Kensuke, Kondoh Yasuhiro and Yasuhiko Nishioka :
The Relationship Between Single-Nucleotide Polymorphisms Within Tollip and the Efficacy of Inhaled N-Acetylcysteine Therapy in Idiopathic Pulmonary Fibrosis,
ATS 2020 VIRTUAL, WEB, Aug. 2020.

(出版サイトへのリンク): ● Publication site (DOI): 10.1164/ajrccm-conference.2020.201.1_MeetingAbstracts.A1494
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.1164/ajrccm-conference.2020.201.1_MeetingAbstracts.A1494

(DOI: 10.1164/ajrccm-conference.2020.201.1_MeetingAbstracts.A1494) Koyama Kazuya, Sakamoto Susumu, Homma Sakae, Seidai Satou, Masaki Hanibuchi, Masuda Kiyoshi, Issei Imoto, Yuko Toyoda, Isshiki Takuma, Miyoshi Shion, Kato Motoyasu, Takahashi Kazuhisa, Kataoka Kensuke, Kondoh Yasuhiro and Yasuhiko Nishioka :
Single-nucleotide polymorphisms within TOLLIP and the efficacy of inhaled N-acetylcysteine therapy in idiopathic pulmonary fibrosis.,
ERS International Congress 2019, Madrid, Sep. 2019.

(出版サイトへのリンク): ● Publication site (DOI): 10.1183/13993003.congress-2019.PA2243
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.1183/13993003.congress-2019.PA2243

(DOI: 10.1183/13993003.congress-2019.PA2243) Hirokazu Ogino, Hisatsugu Goto, Okano Yoshio, Machida Hisanori, Hatakeyama Nobuo, Ogushi Fumitaka, Haku Takashi, Takanori Kanematsu, Tomoyuki Urata, Souji Kakiuchi, Masaki Hanibuchi, Saburo Sone and Yasuhiko Nishioka :
Phase II study of S-1 with patient-reported outcome evaluation in elderly patients with previously untreated advanced non-small cell lung cancer.,
ERS International Congress 2017, Milan, Italy, Sep. 2017. Atsuro Saijo, Hisatsugu Goto, Mayuri Nakano, Mitsuhashi Atsushi, Hirokazu Ogino, Makoto Tobiume, Kenji Ohtsuka, Hiroto Yoneda, Masaki Hanibuchi and Yasuhiko Nishioka :
Bone Marrow-Derived Fibrocytes Promote Stem Cell-Like Properties of Lung Cancer Cells.,
ATS 2017 International Conference, Washington, D.C., May 2017. Hisatsugu Goto, Mitsuhashi Atsushi, Atsuro Saijo, Hirokazu Ogino, Kenji Ohtsuka, Makoto Tobiume, Hiroto Yoneda, Masaki Hanibuchi and Yasuhiko Nishioka :
Fibrocytes as a Possible Cellular Biomarker for Anti-Angiogenic Therapy in Lung Cancer.,
ATS 2017 International Conference, Washington, D.C., May 2017. Masaki Hanibuchi, Akira Kanoh, Takuya Kuramoto, Hisatsugu Goto, Atsuro Saijo, Hirokazu Ogino and Yasuhiko Nishioka :
Assessment of clinical usability of a cfDNA-based assay detecting EGFR T790M mutation in EGFR-TKI refractory NSCLC patients,
The IASLC 17th World Conference on Lung Cancer, Dec. 2016. S Morizumi, S Sato, Shinji Abe, H Okazaki, C Yanjuan, Hisatsugu Goto, Masaki Hanibuchi, Yoshinori Aono, Hirohisa Ogawa, Masaki Hanibuchi, Hisanori Uehara and Yasuhiko Nishioka :
Anti-fibrotic efficacy of nintedanib on pulmonary fibrosis via suppression of fibrocyte activity.,
ERS2016 International Conference, Sep. 2016. Hirokazu Ogino, Hisatsugu Goto, Souji Kakiuchi, Atsuro Saijo, Satoshi Sakaguchi, Makoto Tobiume, Kenji Otsuka, Hiroto Yoneda, Masaki Hanibuchi and Yasuhiko Nishioka :
Receptor tyrosine kinase-like orphan receptor 2, ROR2, regulates the proliferation of malignant pleural mesothelioma cells,
ATS 2016 International Conference, May 2016. Seidai Satou, Hisatsugu Goto, Shun Morizumi, Hiroyasu Okazaki, Yajuan Chen, Hiroshi Kawano, Yuko Toyoda, Masaki Hanibuchi, Masahiko Azuma and Yasuhiko Nishioka :
Effect of blockade of fibroblast growth factor receptor signaling in experimental pulmonary fibrosis in mice,
ATS 2016 International Conference, May 2016. Atsuro Saijo, Hisatsugu Goto, Atsushi Mitsuhashi, Mayuri Nakano, Hirokazu Ogino, Yoshinori Aono, Satoshi Sakaguchi, Makoto Tobiume, Kenji Otsuka, Masaki Hanibuchi and Yasuhiko Nishioka :
Bone-marrow derived fibrocytes maintain stem cell-like properties of lung cancer,
ATS 2016 International Conference, May 2016. Hisatsugu Goto, Atsushi Mitsuhashi, Atsuro Saijo, Takuya Kuramoto, Sho Tabata, Yoshinori Aono, Hisanori Uehara, Masaki Hanibuchi and Yasuhiko Nishioka :
Fibrocytes mediate acquired resistance to anti-angiogenic therapy with bevacizumab in thoracic tumors,
ATS 2016 International Conference, May 2016. Hisatsugu Goto, Mitsuhashi Atsushi, Atsuro Saijo, Yoshinori Aono, Hirokazu Ogino, Hirohisa Ogawa, Souji Kakiuchi, Masaki Hanibuchi and Yasuhiko Nishioka :
The role of fibrocytes in the resistance to anti-angiogenic therapy in malignant pleural mesothelioma and lung cancer,
International Conference of Cancer Immunotherapy and Macrophages 2015, Tokyo, Jul. 2015. Hirokazu Ogino, Mitsuhashi Atsushi, Hisatsugu Goto, Atsuro Saijo, Kuramoto Takuya, Tabata Sho, Hisanori Uehara, Souji Kakiuchi, Masaki Hanibuchi and Yasuhiko Nishioka :
Characterization of sphere-forming stem-like population of lung cancer cell line in multi-organ metastasis model,
ATS 2015 International Conference, Denver, May 2015. Hisatsugu Goto, Mitsuhashi Atsushi, Atsuro Saijo, Kuramoto Takuya, Tabata Sho, Yoshinori Aono, Hisanori Uehara, Souji Kakiuchi, Masaki Hanibuchi and Yasuhiko Nishioka :
The role of fibrocytes in the acquired resistance to anti-angiogenic therapy with bevacizumab in malignant pleural mesothelioma,
ATS 2015 International Conference, Denver, May 2015. Seidai Satou, Hisatsugu Goto, Abe Shuichi, Yoshijima Terumi, Okazaki Hiroyasu, Takezaki Akio, Yoshinori Aono, Masaki Hanibuchi and Yasuhiko Nishioka :
Effect of kinase inhibitors for growth factor receptors on the differentiation of human fibrocytes,
ATS 2015 International Conference, Denver, May 2015. Yasuhiko Nishioka, Shuichi Abe, Seidai Satou, Yoshinori Aono, Hisatsugu Goto, Masami Kishi, Terumi Yoshijima, Hiroyasu Okazaki and Masaki Hanibuchi :
Role of human fibrocytes in regulating pulmonary fibrosis: comprehensive analysis of their gene expression profile and growth factor production,
The 18th International Colloquium on Lung and Airway Fibrosis, Mont-Tremblant, Quebec Canada, Sep. 2014. Hisatsugu Goto, Atsushi Mitsuhashi, Atsuro Saijo, Trung The Van, Yoshinori Aono, Hirohisa Ogawa, Soji Kakiuchi, Masaki Hanibuchi, Seiji Yano, Keisuke Izumi and Yasuhiko Nishioka :
The role of fibrocytes in the resistance to anti-angiogenic therapy in malignant pleural mesothelioma and lung cancer,
ATS 2014 International Conference (Mini-symposium), San Diego, May 2014. Seidai Satou, Hisatsugu Goto, Shuichi Abe, Masami Kishi, Katsuhiro Kinoshita, Momoyo Azuma, Akio Takezaki, Jun Kishi, Yoshinori Aono, Masaki Hanibuchi and Yasuhiko Nishioka :
Effect of Nintedanib (BIBF1120) on fibrocyte-induced fibroblast activation,
ATS 2014 International Conference, San Diego, May 2014. Hisatsugu Goto, Ogushi Fumitaka, Haku Takashi, Tomoyuki Urata, Takanori Kanematsu, Souji Kakiuchi, Masaki Hanibuchi, Saburo Sone and Yasuhiko Nishioka :
Phase study of S-1 with patient-reported outcome evaluation in elderly patients with advanced non-small cell lung cancer.,
18th Congress of the Asian Pacific Society of Respirology, Yokohama, Nov. 2013. Masaki Hanibuchi, Kim Sun-Jin, Otsuka Kenji, Mitsuhashi Atsushi, Hisatsugu Goto, Yasuhiko Nishioka and Fidler J. Isaiah :
Therapeutic efficacy of endothelin receptor blockade on experimental brain metastases of human non-small cell lung cancer.,
18th Congress of the Asian Pacific Society of Respirology, Yokohama, Nov. 2013. Mitsuhashi Atsushi, Hisatsugu Goto, Kuramoto Takuya, Tabata Sho, Yukishige Sawaka, Masaki Hanibuchi, Souji Kakiuchi, Atsuro Saijo, Yoshinori Aono, Hisanori Uehara, Seiji Yano, Ledford G Julie, Saburo Sone and Yasuhiko Nishioka :
Surfactant protein A suppresses progression of human lung adenocarcinoma in nude mice via modulating host immune response.,
18th Congress of the Asian Pacific Society of Respirology, Yokohama, Nov. 2013. Yasuhiko Nishioka, Abe Shuichi, Yoshinori Aono, Katsuhiro Kinoshita, Makino Hideki, Kishi Masami and Masaki Hanibuchi :
Fibrocytes regulate function of lung fibroblasts by producing profibrotic growth factors.,
ATS 2013 Conference, Philadelphia, May 2013. Hisatsugu Goto, Mitsuhashi Atsushi, Kuramoto Takuya, Tabata Sho, Yukishige Sawaka, Masaki Hanibuchi, Souji Kakiuchi, Atsuro Saijo, Yoshinori Aono, Hisanori Uehara, Seiji Yano, Ledford G. Julie, Saburo Sone and Yasuhiko Nishioka :
Surfactant protein A suppresses lung cancer progression by regulating tumor-associated macrophage polarization.,
ATS 2013 Conference, Philadelphia, May 2013. Huang Jun, Liu Dai-Shun, Souji Kakiuchi, Hisatsugu Goto, Masaki Hanibuchi and Yasuhiko Nishioka :
Therapeutic efficacy of RNA interference targeting focal adhesion kinase against orthotropic xenograft of human malignant pleural mesothelioma in SCID mice.,
AACR Annual Meeting 2013, Washington, D.C., Apr. 2013. Atsushi Mitsuhashi, Hisatsugu Goto, Trung The Van, Takuya Kuramoto, Sho Tabata, Masaki Hanibuchi, Souji Kakiuchi, Atsuro Saijo, Yoshinori Aono, Hisanori Uehara, Seiji Yano, Saburo Sone and Yasuhiko Nishioka :
Acquired resistance to anti-VEGF therapy via angiogenic switch in orthotopically implanted human malignant pleural mesothelioma in SCID mice.,
Ninth AACR-Japanese Cancer Association Joint Conference: Breakthroughs in Basic and Translational Cancer Research, Maui, Feb. 2013. Sawaka Yukishige, Hisatsugu Goto, Atsushi Mitsuhashi, Takuya Kuramoto, Sho Tabata, Masaki Hanibuchi, Souji Kakiuchi, Atsuro Saijo, Yoshinori Aono, Hisanori Uehara, Seiji Yano, Julie G. Ledford, Saburo Sone and Yasuhiko Nishioka :
Surfactant protein A suppresses lung cancer progression by regulating tumor-associated macrophage polarization.,
Ninth AACR-Japanese Cancer Association Joint Conference: Breakthroughs in Basic and Translational Cancer Research, Maui, Feb. 2013. Atsushi Mitsuhashi, Hisatsugu Goto, Takuya Kuramoto, Sho Tabata, Sawaka Yukishige, Shinji Abe, Masaki Hanibuchi, Souji Kakiuchi, Atsuro Saijo, Yoshinori Aono, Hisanori Uehara, Seiji Yano, Julie G Ledford, Saburo Sone and Yasuhiko Nishioka :
Surfactant protein A suppresses progression of human lung adenocarcinoma in nude mice via modulating host immune response,
Joint Meeting to Seoul National University, Seoul, Dec. 2012. Masaki Hanibuchi, Sun-Jin Kim, Kenji Otsuka, Sho Tabata, Takuya Kuramoto, Hisatsugu Goto, Yasuhiko Nishioka and Isaiah J Fidler :
Eradication of experimental brain metastases of human non-small cell lung cancer by macitentan, a dual antagonist of the endothelin A and B receptor, combined with paclitaxel,
A Joint Meeting by ASCO, EORTC, and NCI on Markers in Cancer, Hollywood, Oct. 2012. Takuya Kuramoto, Hisatsugu Goto, Atsushi Mitsuhashi, Sho Tabata, Hirohisa Ogawa, Hisanori Uehara, Atsuro Saijo, Souji Kakiuchi, Masaki Hanibuchi, Yoichi Maekawa, Koji Yasutomo, Shin-ichi Akiyama, Saburo Sone and Yasuhiko Nishioka :
Dll4-Fc, an inhibitor of Dll4-notch signaling, suppresses liver metastasis of small cell lung cancer cells through down-regulation of NF-kappa-B activity,
14th International Biennial Congress of the Metastasis Research Society, Brisbane, Sep. 2012. Hisatsugu Goto, Atsushi Mitsuhashi, Takuya Kuramoto, Masaki Hanibuchi, Souji Kakiuchi, Sho Tabata, Atsuro Saijo, Jo R Wright, Saburo Sone and Yasuhiko Nishioka :
Surfactant protein A suppresses progression of human lung adenocarcinoma in an experimental lung metastasis model,
14th International Biennial Congress of the Metastasis Research Society, Brisbane, Sep. 2012. Yasuhiko Nishioka, Shinji Abe, Yuki Morita, Mika K Kaneko, Masaki Hanibuchi, Hisatsugu Goto, Souji Kakiuchi, Yoshinori Aono, Jun Huang, Atsushi Mitsuhashi, Seidai Sato, Kazuo Minakuchi and Yukinari Kato :
Antitumor effects of anti-podoplanin antibody NZ-1 against malignant mesothelioma,
14th International Biennial Congress of the Metastasis Research Society, Brisbane, Sep. 2012. Hisatsugu Goto, Atsushi Mitsuhashi, Takuya Kuramoto, Masaki Hanibuchi, Souji Kakiuchi, Sho Tabata, Atsuro Saijo, Shin-ichi Akiyama, Jo R Wright, Saburo Sone and Yasuhiko Nishioka :
Surfactant protein A suppresses progression of human lung adenocarcinoma in an experimental lung metastasis model,
ATS 2012 International Conference, San Francisco, May 2012. Yasuhiko Nishioka, Shinji Abe, Mika K Kaneko, Yoshinori Aono, Jun Huang, Hisatsugu Goto, Masatoshi Kishuku, Masaki Hanibuchi, Saburo Sone, Kazuo Minakuchi and Yukinari Kato :
Antitumor effects of anti-podoplanin antibody NZ-1 against malignant mesothelioma via ADCC,
ATS 2012 International Conference, San Francisco, May 2012. Takuya Kuramoto, Hisatsugu Goto, Atsushi Mitsuhashi, Sho Tabata, Hirohisa Ogawa, Hisanori Uehara, Seidai Sato, Souji Kakiuchi, Masaki Hanibuchi, Yoichi Maekawa, Koji Yasutomo, Shin-ichi Akiyama, Saburo Sone and Yasuhiko Nishioka :
Dll4-Fc, an inhibitor of Dll4-notch signaling, suppresses liver metastasis of small cell lung cancer cells through down-regulation of NF-kappa-B activity,
AACR Annual Meeting 2012, Chicago, Apr. 2012. Masaki Hanibuchi, Shinji Abe, Masatoshi Kishuku, Souji Kakiuchi, Kazuyoshi Kawazoe, Kazuo Minakuchi, Mika K. Kaneko, Yukinari Kato and Yasuhiko Nishioka :
Targeted therapy for mesothelioma using anti-podoplanin antibody NZ-1 via ADCC,
5th EORTC-NCI-ASCO Annual Meeting on 'Molecular Markers in Cancer', Brussels, Belgium, Oct. 2011. Yasuhiko Nishioka, Hisatsugu Goto, Souji Kakiuchi, Masaki Hanibuchi, Yano Seiji and Saburo Sone :
Bone metastasis of lung cancer and its molecular-targeted therapy.,
Joint Metastasis Research Society-AACR Conference, Philadelphia, Sep. 2010. Trung The Van, Masaki Hanibuchi, Hisatsugu Goto, Souji Kakiuchi, Kuramoto Takuya, Sato Seidai, Tobiume Makoto, Atsuro Saijo, Tabata Sho, Yasuhiko Nishioka, Shin-ichi Akiyama and Saburo Sone :
TS-1 suppresses the growth of malignant pleural mesithelioma cells co-expressing dihydropyrimidine dehydrogenase and thymidine phosphorylase in an orthotopic model.,
The 10th International Conference of the International Mesothelioma Interest Group, Sep. 2010. Atsushi Mitsuhashi, Hisatsugu Goto, Hirokazu Ogino, Takuya Kuramoto, Seidai Sato, Makoto Tobiume, Masaki Hanibuchi, Souji Kakiuchi, Seiji Yano, Hisanori Uehara, Yasuhiko Nishioka and Saburo Sone :
Novel therapeutic strategy with E7080, an orally active inhibitor of multiple recepter tyrosine kinase, for controllong experomental metastasis by lung cancer in immunodeficient mice.,
第9回アジア臨床腫瘍学会学術集会, Gifu, Aug. 2010. Trung The Van, Hisatsugu Goto, Masaki Hanibuchi, Souji Kakiuchi, Kuramoto Takuya, Sato Seidai, Tobiume Makoto, Shin-ichi Akiyama, Yasuhiko Nishioka and Sone Saburo :
Therapeutic efficacy of TS-1 on the progression of human malignant pleural mesothelioma in severe combined immunodeficient mice.,
第9回アジア臨床腫瘍学会学術集会, Gifu, Aug. 2010. 坂東紀子, 坂東弘基, 土師恵子, 美馬正人, 福家麻美, 内藤伸仁, 尾崎領彦, 荻野広和, 佐藤正大, 河野弘, 坂口暁, 埴淵昌毅, 西岡安彦 :
当科における重症喘息に対する生物学的製剤の治療効果の検討,
第268回徳島医学会学術集会, 2024年3月. Yuki Tsukazaki, Hirokazu Ogino, Yoshio Okano, Soji Kakiuchi, Shoko Harada, Yugo Matumura, Seiya Ichihara, Takeshi Imakura, Ryohiko Ozaki, Ei Ogawa, Yutaka Morita, Atsushi Mitsuhashi, Yohei Yabuki, Hiroto Yoneda, Masaki Hanibuchi, Yuko Toyoda, Kayoko Hase, Eiji Takeuchi, Takashi Haku and Yasuhiko Nishioka :
The impacts of G-CSF on the therapeutic efficacy of chemo-immunotherapy for extensive-stage small cell lung cancer.,
2024 the Japanese Society of Medical Oncology Annual Meeting (JSMO2024), Feb. 2024. Hirokazu Ogino, Nguyen Na Thi, Hiroyuki Kozai, Atsushi Mitsuhashi, Yuki Tsukazaki, Yohei Yabuki, Ryohiko Ozaki, Hiroshi Nokihara, Masaki Hanibuchi and Yasuhiko Nishioka :
Fluoropyrimidine has a potential to be an immunologically optimal partner ofimmunotherapy for thoracic malignancies.,
024 the Japanese Society of Medical Oncology Annual Meeting (JSMO2024), Feb. 2024. 鈴江涼子, 坂東弘基, 土師恵子, 尾崎領彦, 米田浩人, 荻野広和, 佐藤正大, 埴淵昌毅, 西岡安彦 :
抗横紋筋抗体陽性の重症irAE筋炎・心筋炎に対して早期の集学的治療が奏効した肺扁平上皮癌の1例,
第69回日本呼吸器学会中国・四国地方会, 2023年12月. 寺澤翠, 坂東弘基, 土師恵子, 米田浩人, 荻野広和, 岡田直子, 川中崇, 佐藤正大, 埴淵昌毅, 西岡安彦 :
ペプチド受容体放射性核種療法が奏効した左下葉原発進行期非定型カルチノイドの1例,
第69回日本呼吸器学会中国・四国地方会, 2023年12月. 青井優, 坂東弘基, 土師恵子, 高橋啓輝, 米田浩人, 阿部あかね, 佐藤正大, 東桃代, 埴淵昌毅, 西岡安彦 :
気管支鏡検査で診断したCOVID-19関連肺アスペルギルス症の1例,
第32回日本呼吸器内視鏡学会中国四国支部会, 2023年12月. 中西渓介, 坂東弘基, 土師恵子, 小倉祐一郎, 美馬正人, 内藤伸仁, 阿部あかね, 川真田純, 杉浦宏, 佐藤正大, 東桃代, 埴淵昌毅, 西良浩一, 西岡安彦 :
結核性脊椎炎の治療中にparadoxical responseとして皮下膿瘍が出現した1例,
第74 回日本結核・非結核性抗酸菌症学会中国四国支部会, 2023年12月. 宮本憲哉, 埴淵昌毅, 坂東弘基, 米田浩人, 荻野広和, 佐藤正大, 西岡安彦 :
気管支鏡後の呼吸器感染症のリスク因子および予防的抗菌薬投与の有用性についての検討,
第32回日本呼吸器内視鏡学会中国四国支部会, 2023年12月. 磯村祐太, 坂東弘基, 土師恵子, 内藤伸仁, 佐藤正大, 埴淵昌毅, 西岡安彦 :
悪性リンパ腫の治療経過中に発症したβ-Dグルカン陰性ニューモシスチス肺炎の1例,
第129回日本内科学会四国地方会, 2023年12月. 山本浩生, 坂東弘基, 土師恵子, 山下雄也, 内藤伸仁, 佐藤正大, 河野弘, 埴淵昌毅, 西岡安彦 :
ステロイド抵抗性の気道病変に対してシクロホスファミドが著効した再発性多発軟骨炎の1例,
第129回日本内科学会四国地方会, 2023年12月. 塚﨑佑貴, 飛梅亮, 三橋惇志, 尾崎領彦, 矢葺洋平, 米田浩人, 荻野広和, 埴淵昌毅, 小川博久, 滝沢宏光, 西岡安彦 :
非小細胞肺癌症例における腫瘍浸潤線維細胞の走化因子と疾患予後との関連性についての解析,
第64回日本肺癌学会学術集会, 2023年11月. 荻野広和, 香西博之, 三橋惇志, 塚﨑佑貴, 矢葺洋平, 尾崎領彦, 米田浩人, 埴淵昌毅, 軒原浩, 西岡安彦 :
フッ化ピリミジンは胸部腫瘍の免疫原性細胞死を誘導し免疫チェックポイント阻害薬の至適併用薬となり得る,
第64回日本肺癌学会学術集会, 2023年11月. 佐藤正大, 埴淵昌毅, 三橋惇志, 西岡安彦 :
咳喘息治療における効果予測バイオマーカーの探索,
第72回日本アレルギー学会学術大会, 2023年10月. 矢葺洋平, 三橋惇志, 荻野広和, Na T. Nguyen, 米田浩人, 尾崎領彦, 塚﨑佑貴, 埴淵昌毅, 軒原浩, 西岡安彦 :
HIF1A 阻害による腫瘍細胞由来 CXCL10/11 制御を介した抗 PDL1 抗体への耐性克服,
第82回日本癌学会学術総会, 2023年9月. 原田紗希, 坂東弘基, 土師恵子, 内藤伸仁, 佐藤正大, 埴淵昌毅, 西岡安彦 :
当院において外科治療を施行した肺Mycobacterium avium complexの検討,
第267回徳島医学会学術集会, 2023年8月. 寺澤翠, 坂東弘基, 土師恵子, 小路貴俊, 米田浩人, 佐藤正大, 河野弘, 埴淵昌毅, 西岡安彦 :
シクロスポリンが有効であった血清IL-18高値の重症成人発症スティル病の1例,
第128回日本内科学会四国地方会, 2023年7月. 中西渓介, 坂東弘基, 土師恵子, 松村有悟, 稲葉香織, 米田浩人, 荻野広和, 佐藤正大, 埴淵昌毅, 西岡安彦 :
Carboplatin+etoposideや放射線治療に不応もnab-paclitaxelが奏効した肺原発大細胞神経内分泌癌の1例,
第128回日本内科学会四国地方会, 2023年7月. 山本浩生, 坂東弘基, 土師恵子, 國重道大, 梶本達也, 小山壱也, 香川耕造, 佐藤正大, 埴淵昌毅, 西岡安彦 :
自然経過で嚢胞性画像変化および呼吸機能の改善を認めた重症COVID-19の1例,
第68回日本呼吸器学会中国・四国地方会, 2023年7月. 多田里穂, 坂東弘基, 土師恵子, 新居香織, 米田浩人, 荻野広和, 佐藤正大, 埴淵昌毅, 西岡安彦 :
抗PD-L1抗体投与により腫瘍随伴性小脳変性症が顕在化した小細胞肺癌の1例,
第61回日本肺癌学会中国・四国支部学術集会, 2023年7月. 遠藤裕美, 坂東弘基, 土師恵子, 高橋啓輝, 米田浩人, 荻野広和, 佐藤正大, 埴淵昌毅, 西岡安彦 :
包括的ゲノムプロファイリングにより診断し得たEGFR Exon19欠失変異陽性肺腺癌の1例,
第61回日本肺癌学会中国・四国支部学術集会, 2023年7月. 佐藤正大, 埴淵昌毅, 三橋惇志, 西岡安彦 :
咳喘息における呼気中一酸化窒素と血清ペリオスチンの臨床的意義の検討,
第63回日本呼吸器学会学術講演会, 2023年4月. 埴淵昌毅, 三橋惇志, 西條敦郎, 佐藤正大, 西岡安彦 :
スクリーニング質問票を用いたCOPD検診システムの有用性の検討,
第63回日本呼吸器学会学術講演会, 2023年4月. 松村有悟, 土師恵子, 鈴江涼子, 米田浩人, 香川耕造, 荻野広和, 佐藤正大, 小川博久, 埴淵昌毅, 西岡安彦 :
血清Krebs von den Lungen-6 が高値を示した悪性胸膜中皮腫の1例,
第127回日本内科学会四国地方会, 2022年12月. 新居香織, 土師恵子, 青井優, 山下雄也, 内藤伸仁, 荻野広和, 河野弘, 佐藤正大, 埴淵昌毅, 西岡安彦 :
関節炎を呈したACTH 単独欠損症の1例,
第127回日本内科学会四国地方会, 2022年12月. 宮本憲哉, 土師恵子, 原田紗希, 鈴江涼子, 阿部あかね, 東桃代, 佐藤正大, 埴淵昌毅, 西岡安彦 :
当院における肺MAC症に対するアジスロマイシン併用療法の有効性・安全性の検討,
第73回日本結核・非結核性抗酸菌症学会中国四国支部会, 2022年12月. 森彩花, 土師恵子, 青井優, 宮本憲哉, 村上行人, 塚崎佑貴, 坂東弘基, 尾崎領彦, 香川耕造, 荻野広和, 佐藤正大, 埴淵昌毅, 西岡安彦 :
免疫チェックポイント阻害薬使用後に肺胞出血をきたした1例,
第31回日本呼吸器内視鏡学会中国四国支部会, 2022年12月. 寺澤翠, 土師恵子, 市原聖也, 山下雄也, 福家麻美, 内藤伸仁, 米田浩人, 香川耕造, 荻野広和, 河野弘, 佐藤正大, 埴淵昌毅, 西岡安彦 :
抗PD-L1抗体投与後に顕在化した抗ARS抗体陽性間質性肺炎の1例,
第67回日本呼吸器学会中国・四国地方会, 2022年12月. 中西颯斗, 土師恵子, 松村有悟, 三橋惇志, 小川瑛, 今倉健, 美馬正人, 尾崎領彦, 米田浩人, 荻野広和, 坂口暁, 佐藤正大, 埴淵昌毅, 西岡安彦 :
同時に異なる3つの組織型を認めた多発性肺癌の1例,
第67回日本呼吸器学会中国・四国地方会, 2022年12月. 内藤伸仁, 西村春佳, 山下雄也, 村上行人, 土師恵子, 小山壱也, 荻野広和, 佐藤正大, 河野弘, 埴淵昌毅, 西岡安彦 :
ブレオマイシン誘発肺線維症モデルマウスを用いたJAK阻害薬の抗線維化効果についての検討,
第50回日本臨床免疫学会総会, 2022年10月. 中西颯斗, 土師恵子, 矢葺洋平, 新居香織, 高丸利加子, 米田浩人, 荻野広和, 佐藤正大, 埴淵昌毅, 西岡安彦 :
セルペルカチニブが奏功したRET融合遺伝子陽性肺腺癌の1例,
第265回徳島医学会学術集会, 2022年7月. 小倉佑一朗, Keiko Haji, 近藤健介, Kenji Otsuka, Hirokazu Ogino, Kazuya Koyama, 村上行人, Hiroki Bandoh, Seidai Satou, Masaki Hanibuchi and Yasuhiko Nishioka :
間質性肺炎への治療反応性から肝肺症候群の併存が顕在化した一例,
第66回日本呼吸器学会中国・四国地方会, Jul. 2022. 松村有悟, 土師恵子, 美馬正人, 矢葺洋平, 大塚憲司, 米田浩人, 軒原浩, 荻野広和, 尾崎領彦, 塚崎佑貴, 佐藤正大, 埴淵昌毅, 西岡安彦 :
小細胞肺癌への形質転換を認めたEGFR遺伝子変異陽性肺腺癌の3例,
第60回日本肺癌学会中国・四国支部学術集会, 2022年7月. 新居香織, Yohhei Yabuki, Keiko Haji, 高丸利加子, Hiroto Yoneda, Hirokazu Ogino, Seidai Satou, Masaki Hanibuchi and Yasuhiko Nishioka :
セルペルカチニブが奏効したRET融合遺伝子陽性肺腺癌の1例,
第60回日本肺癌学会中国・四国支部学術集会, Jul. 2022. 矢葺洋平, 大塚憲司, 竹内栄治, 葉久貴司, 兼松貴則, 西村直樹, 豊田優子, 埴淵昌毅, 軒原浩, 西岡安彦 :
再発非小細胞肺癌に対するPemetrexed + Bevacizumab 併用療法の有効性と安全性の検討,
第264回徳島医学会学術集会, 2022年2月. 小山壱也, 埴淵昌毅, 豊田優子, 一色琢磨, 三好嗣臣, 坂本晋, 加藤元康, 髙橋和久, 片岡健介, 近藤康博, 西岡安彦, 本間栄 :
特発性肺線維症におけるTOLLIP遺伝子多型とN-アセチルシステイン吸入療法の有効性の検討,
第61回日本呼吸器学会学術講演会, 2021年4月. 大塚憲司, 後東久嗣, 埴淵昌毅, 荻野広和, 西條敦郎, 香西博之, 米田浩人, 飛梅亮, 西岡安彦 :
化学療法は腫瘍内の骨髄由来抑制細胞を減少させることにより抗PD-1抗体の抗腫瘍効果を増強する,
第28回日本がん転移学会学術集会・総会, 2019年7月. Hiroshi Nokihara, Masaki Hanibuchi, Souji Kakiuchi, Atagi Shinji, Ogushi Fumitaka, Shimizu Eiji, Haku Takashi, Yuko Toyoda, Masahiko Azuma, Mayo Kondou, Hiroshi Kawano, Kenji Otsuka, Satoshi Sakaguchi, Hisatsugu Goto and Yasuhiko Nishioka :
A multicenter, open-label, phase II trial of S-1 plus carboplatin in advanced NSCLC patients with interstitial lung disease,
The 59th Annual Meeting of the Japanese Respiratory Society, Apr. 2019. 埴淵昌毅, 安宅信二, 大串文隆, 山崎章, 葉久貴司, 軒原浩, 西岡安彦 :
間質性肺炎合併未治療進行非小細胞肺癌に対する TS-1+CBDCA 併用療法の第 II 相臨床試験,
第59回日本肺癌学会学術集会, 2018年11月. 髙橋直希, 荻野広和, 埴淵昌毅, 西條敦郎, 飛梅亮, 香西博之, 米田浩人, 福家麻美, 三橋惇志, 宮本憲哉, 軒原浩, 後東久嗣, 西岡安彦 :
当科における高齢者肺癌の臨床的検討,
第257回徳島医学会学術集会, 2018年8月. 荻野広和, 埴淵昌毅, 柿内聡司, 安宅信二, 大串文隆, 清水英治, 葉久貴司, 大塚憲司, 西條敦郎, 軒原浩, 後東久嗣, 西岡安彦 :
間質性肺炎合併未治療進行非小細胞肺癌に対するTS-1+CBDCA併用療法の第Ⅱ相臨床試験,
第16回日本臨床腫瘍学会学術集会, 2018年7月. 荻野広和, 後東久嗣, 大塚憲司, 西條敦郎, 埴淵昌毅, 西岡安彦 :
線維細胞が腫瘍免疫に及ぼす影響についての検討,
第22回日本がん分子標的治療学会学術集会, 2018年5月. 大塚憲司, 後東久嗣, 荻野広和, 西條敦郎, 埴淵昌毅, 西岡安彦 :
肺癌・悪性胸膜中皮腫マウスモデルにおける免疫チェックポイント阻害薬と化学療法の併用効果,
第22回日本がん分子標的治療学会学術集会, 2018年5月. 荻野広和, 埴淵昌毅, 西條敦郎, 大塚憲司, 豊田優子, 後東久嗣, 西岡安彦 :
徳島大学病院の肺癌症例において高齢者と若年者を比較した後ろ向き研究．,
第115回日本内科学会総会・講演会, 2018年4月. 豊田優子, 埴淵昌毅, 柿内聡司, 安宅信二, 大串文隆, 清水英治, 葉久貴司, 軒原浩, 後東久嗣, 西岡安彦 :
間質性肺炎合併未治療進行非小細胞肺癌に対するTS-1+CBDCA併用療法の第Ⅱ相臨床試験．,
第115回日本内科学会総会・講演会, 2018年4月. 西條敦郎, 埴淵昌毅, 荻野広和, 軒原浩, 豊田優子, 後東久嗣, 西岡安彦 :
再発小細胞肺癌に対するpaclitaxel療法の検討,
第58回日本肺癌学会学術集会, 2017年10月. 荻野広和, 埴淵昌毅, 西條敦郎, 手塚敏史, 後東久嗣, 西岡安彦 :
徳島大学病院における高齢者肺癌と若年者肺癌の臨床的特徴に関する比較検討,
第15回日本臨床腫瘍学会学術集会, 2017年7月. 西條敦郎, 荻野広和, 大塚憲司, 手塚敏史, 後東久嗣, 埴淵昌毅, 西岡安彦 :
Clinical efficacy of bevacizumab for non-squamous non-small cell lung cancer patients with malignant pleural effusion.,
第15回日本臨床腫瘍学会学術集会, 2017年7月. 後東久嗣, 西條敦郎, 中野万有里, 飛梅亮, 大塚憲司, 米田浩人, 埴淵昌毅, 西岡安彦 :
がん幹細胞化の誘導を介したfibrocyteの肺がん進展・転移促進メカニズム,
第26回日本がん転移学会学術集会・総会, 2017年7月. 後東久嗣, 三橋惇志, 西條敦郎, 埴淵昌毅, 西岡安彦 :
線維細胞(fibrocyte)を標的としたがん転移・進展メカニズムの解明と血管新生阻害薬耐性克服の試み．,
第26回日本がん転移学会学術集会・総会, 2017年7月. 大塚憲司, 埴淵昌毅, 後東久嗣, 西岡安彦 :
肺癌・悪性胸膜中皮腫に対する抗PD-1抗体，抗PD-L1抗体と化学療法の併用効果の基礎的検討,
第21回日本がん分子標的学会学術集会, 2017年6月. 山子泰斗, 後東久嗣, 西條敦郎, 埴淵昌毅, 西岡安彦 :
肺がん骨転移におけるRANKL標的治療の限界と可能性,
第21回日本がん分子標的学会学術集会, 2017年6月. 和泉俊尋, 阿部真治, 荻野広和, 後東久嗣, 埴淵昌毅, 加藤幸成, 西岡安彦 :
悪性胸膜中皮腫同所移植マウスモデルに対する新規マウス抗ポドプラニン抗体LpMab-21による抗腫瘍効果の検討,
第21回日本がん分子標的学会学術集会, 2017年6月. 西村春佳, 手塚敏史, 西條敦郎, 河野弘, 後東久嗣, 岸潤, 軒原浩, 埴淵昌毅, 吾妻雅彦, 西岡安彦 :
肺扁平上皮癌治療後の空洞病変に認めた肺アスペルギルス症の1例,
第116回日本内科学会四国地方会, 2017年5月. 近藤真代, 手塚敏史, 河野弘, 後東久嗣, 岸潤, 埴淵昌毅, 吾妻雅彦, 土師正太郎, 梶龍兒, 西岡安彦 :
小脳浮腫および水頭症を認め開頭減圧術を要したNPSLEの1例,
第116回日本内科学会四国地方会, 2017年5月. 手塚敏史, 小川博久, 近藤真代, 豊田優子, 佐藤正大, 後東久嗣, 岸潤, 吾妻雅彦, 埴淵昌毅, 西岡安彦 :
ダニ抗原誘導性のアレルギー性気道炎症および気道リモデリングはPAR-2 antagonistの投与により抑制される,
第57回日本呼吸器学会学術講演会, 2017年4月. 埴淵昌毅, 中瀬勝則, 豊崎纏, 木下成三, 島田久夫, 鶴尾美穂, 原田和代, 水井研治, 葉久貴司, 西岡安彦 :
徳島市におけるCOPD早期発見を目的とした検診システム,
第57回日本呼吸器学会学術講演会, 2017年4月. Hirokazu Ogino, Masaki Hanibuchi, Souji Kakiuchi, Atsuro Saijo, Toshifumi Tezuka, Yuko Toyoda, Satoshi Sakaguchi, Hisatsugu Goto, Kokichi Arisawa and Yasuhiko Nishioka :
Analysis of the Prognostic Factors of Extensive Disease Small-Cell Lung Cancer Patients in Tokushima University Hospital.,
The 57th Annual Meeting of the Japanese Respiratory Society, Apr. 2017. Atsuro Saijo, Hisatsugu Goto, Mayuri Nakano, Mitsuhashi Atsushi, Hirokazu Ogino, Makoto Tobiume, Kenji Ohtsuka, Hiroto Yoneda, Masaki Hanibuchi and Yasuhiko Nishioka :
Bone marrow-derived fibrocytes promote stem cell-like properties of lung cancer cells.,
The 57th Annual Meeting of the Japanese Respiratory Society, Apr. 2017. 豊田優子, 岸潤, 河野弘, 森住俊, 小山壱也, 西村春佳, 香川耕造, 手塚敏史, 後東久嗣, 埴淵昌毅, 吾妻雅彦, 西岡安彦 :
当院における全身性エリテマトーデス合併間質性肺炎の臨床的検討,
第57回日本呼吸器学会学術講演会, 2017年4月. 河野弘, 豊田優子, 岸潤, 森住俊, 近藤真代, 山下雄也, 手塚敏史, 後東久嗣, 埴淵昌毅, 吾妻雅彦, 西岡安彦 :
当院における間質性肺炎合併全身性エリテマトーデス症例の臨床的検討,
第61回日本リウマチ学会総会・学術集会, 2017年4月. 埴淵昌毅, 加納亮, 倉本卓哉, 後東久嗣, 西岡安彦 :
癌患者血漿中遊離DNAを用いた遺伝子変異検査技術の比較,
第114回日本内科学会総会・講演会, 2017年4月. 髙島拓也, 手塚敏史, 近藤真代, 飛梅亮, 河野弘, 後東久嗣, 岸潤, 吾妻雅彦, 埴淵昌毅, 西岡安彦 :
Exon19とexon21の遺伝子変異を同時に認めた肺腺癌の1例,
第56回日本呼吸器学会中国・四国地方会, 2016年12月. 菊地高史, 手塚敏史, 近藤真代, 荻野広和, 河野弘, 後東久嗣, 岸潤, 吾妻雅彦, 埴淵昌毅, 西岡安彦 :
Stevens-Johnson 症候群後に発症した閉塞性細気管支炎にステロイドおよびタクロリムスが有効であった1例,
第56回日本呼吸器学会中国・四国地方会.岡山.2016年12月23, 2016年12月. 杉峯優人, 手塚敏史, 香川耕造, 米田浩人, 大塚憲司, 河野弘, 後東久嗣, 岸潤, 吾妻雅彦, 埴淵昌毅, 西岡安彦 :
EBUS-TBNA後に縦隔炎を発症した縦隔原発セミノーマの1例,
第25回日本呼吸器内視鏡学会中国四国支部会, 2016年12月. 原倫世, 手塚敏史, 近藤真代, 河野弘, 後東久嗣, 岸潤, 吾妻雅彦, 埴淵昌毅, 西岡安彦 :
EBによる末梢神経障害を呈した結核性胸膜炎の1例,
第67回日本結核病学会中国四国支部会, 2016年12月. 埴淵昌毅, 手塚敏史, 西條敦郎, 荻野広和, 後東久嗣, 西岡安彦 :
当科における高齢者肺癌の若年者との比較検討,
第57回日本肺癌学会学術集会, 2016年12月. 荻野広和, 後東久嗣, 西條敦郎, 柿内聡司, 埴淵昌毅, 西岡安彦 :
徳島大学病院における進展型小細胞肺癌患者の予後因子に関する後ろ向き研究,
第57回日本肺癌学会学術集会, 2016年12月. 西條敦郎, 手塚敏史, 荻野広和, 豊田優子, 後東久嗣, 埴淵昌毅, 西岡安彦 :
悪性胸水を伴った非扁平上皮非小細胞肺癌に対する Bevacizumab 併用化学療法の検討,
第57回日本肺癌学会学術集会, 2016年12月. 豊田優子, 山下雄也, 森住俊, 近藤真代, 荻野広和, 河野弘, 手塚敏史, 岸潤, 後東久嗣, 埴淵昌毅, 埴淵昌毅, 西岡安彦 :
当院における膠原病関連間質性肺炎の急性憎悪の臨床的検討,
第27回日本リウマチ学会中国・四国支部学術集会, 2016年12月. 荻野広和, 岸潤, 河野弘, 手塚敏史, 豊田優子, 後東久嗣, 埴淵昌毅, 吾妻雅彦, 西岡安彦 :
関節リウマチの薬物療法における栄養状態の変化の検討,
第27回日本リウマチ学会中国・四国支部学術集会, 2016年12月. 山下雄也, 豊田優子, 荻野広和, 河野弘, 手塚敏史, 岸潤, 後東久嗣, 埴淵昌毅, 吾妻雅彦, 西岡安彦 :
当院におけるループス腎炎に対するIVCYとMMFの治療経験,
第27回日本リウマチ学会中国・四国支部学術集会, 2016年12月. 田中こころ, 荻野広和, 宮田淳也, 山下雄也, 森住俊, 近藤真代, 河野弘, 手塚敏史, 豊田優子, 岸潤, 後東久嗣, 埴淵昌毅, 吾妻雅彦, 西岡安彦 :
15年前より認める慢性腎機能障害に対してステロイド加療が奏功した腎サルコイドーシスの1例,
第27回日本リウマチ学会中国・四国支部学術集会, 2016年12月. 米田浩人, 手塚敏史, 山下雄也, 西條敦郎, 河野弘, 後東久嗣, 岸潤, 吾妻雅彦, 埴淵昌毅, 西岡安彦 :
多発性胃十二指腸潰瘍を伴ったMTX関連リンパ増殖性疾患の1例,
第115回日本内科学会四国地方会, 2016年11月. 香西博之, 手塚敏史, 山下雄也, 西條敦郎, 河野弘, 後東久嗣, 岸潤, 吾妻雅彦, 埴淵昌毅, 西岡安彦 :
Gefitinib投与中にAchromobacter Xylosoxidansによる菌血症を発症した肺腺癌の1例,
第115回日本内科学会四国地方会, 2016年11月. 藤本陸史, 前京子, 阿部日登美, 元木由美, 埴淵昌毅, 武久洋三 :
アミカシン適正投与設計による有効性，安全性の検討,
第24回日本慢性期医療学会, 2016年10月. 元木由美, 大寺誠, 阿部日登美, 武久洋三, 小川真司, 埴淵昌毅, 髙田信二郎 :
慢性期人工呼吸管理における呼吸リハビリテーションの効果,
第24回日本慢性期医療学会, 2016年10月. 藤本陸史, 宮﨑輝, 藤坂輝代, 秋田美樹, 元木由美, 武久敬洋, 埴淵昌毅, 武久洋三 :
多剤内服薬の改善に向けた取り組み,
第13回日本病院総合診療医学会学術総会, 2016年9月. 元木由美, 大寺誠, 阿部日登美, 武久洋三, 小川真司, 埴淵昌毅, 髙田信二郎 :
慢性期人工呼吸管理における呼吸リハビリテーションの効果,
第13回日本病院総合診療医学会学術総会, 2016年9月. 荻野広和, 埴淵昌毅, 大塚憲司, 西條敦郎, 坂口暁, 手塚敏史, 柿内聡司, 後東久嗣, 西岡安彦 :
徳島大学病院における進展型小細胞肺癌患者の予後因子についての検討,
第14回日本臨床腫瘍学会学術集会, 2016年7月. 山本清成, 手塚敏史, 荻野広和, 後東久嗣, 岸潤, 吾妻雅彦, 埴淵昌毅, 西岡安彦 :
下顎歯肉癌治療後に発生した放射線誘発血管肉腫の1例,
第253回徳島医学会学術集会, 2016年7月. 藤本陸史, 宮﨑輝, 梅井康広, 西内優, 藤坂輝代, 秋田美樹, 元木由美, 武久敬洋, 埴淵昌毅, 武久洋三 :
多剤内服薬の改善に向けた取り組み,
第253回徳島医学会学術集会, 2016年7月. 荻野広和, 後東久嗣, 西條敦郎, 大塚憲司, 埴淵昌毅, 西岡安彦 :
受容体チロシンキナーゼROR2は悪性胸膜中皮腫細胞の増殖を制御する,
第25回日本がん転移学会学術集会・総会, 2016年7月. 西條敦郎, 後東久嗣, 三橋惇志, 中野万有里, 大塚憲司, 荻野広和, 坂口暁, 埴淵昌毅, 西岡安彦 :
骨髄由来線維細胞(fibrocyte)は肺癌のがん幹細胞様特性を促進する,
第25回日本がん転移学会学術集会・総会, 2016年7月. 大塚憲司, 埴淵昌毅, 後東久嗣, 西岡安彦 :
肺癌，悪性胸膜中皮腫に対する免疫チェックポイント阻害剤の有効性の基礎的検討,
第25回日本がん転移学会学術集会・総会, 2016年7月. 香川耕造, 手塚敏史, 大塚憲司, 森住俊, 後東久嗣, 岸潤, 吾妻雅彦, 埴淵昌毅, 西岡安彦 :
CrizotinibによるILDを発症後にAlectinibの投与が可能であったALK融合遺伝子陽性肺腺癌の1例,
第55 回日本肺癌学会中国・四国支部会, 2016年7月. 近藤真代, 手塚敏史, 米田浩人, 豊田優子, 後東久嗣, 岸潤, 吾妻雅彦, 埴淵昌毅, 村上太一, 土井俊夫, 河北直也, 滝沢宏光, 西岡安彦 :
腹腔シンチグラフィにより診断し横隔膜縫合閉鎖術を行った横隔膜交通症の1例,
第55 回日本呼吸器学会中国・四国地方会, 2016年7月. 元木由美, 大寺誠, 阿部日登美, 武久洋三, 小川真司, 埴淵昌毅, 髙田信二郎 :
慢性期人工呼吸管理における呼吸リハビリテーションの効果,
第66回日本病院学会, 2016年6月. 藤本陸史, 前京子, 阿部日登美, 元木由美, 埴淵昌毅, 武久洋三 :
アミカシンの適正投与設計による有効性，安全性の検討,
第66回日本病院学会, 2016年6月. 阿部真治, 加藤幸成, 後東久嗣, 埴淵昌毅, 西岡安彦 :
ポドプラニンを標的とした抗体療法とペメトレキセドの併用による悪性胸膜中皮腫に対する抗腫瘍効果の検討,
第20回日本がん分子標的治療学会学術集会, 2016年5月. 森住俊, 佐藤正大, 荻野広和, 河野弘, 坂口暁, 後東久嗣, 岸潤, 埴淵昌毅, 吾妻雅彦, 西岡安彦 :
当院におけるニンテダニブの特発性肺線維症に対する使用経験,
第114回日本内科学会四国地方会, 2016年5月. 山下雄也, 西條敦郎, 佐藤正大, 手塚敏史, 坂口暁, 後東久嗣, 岸潤, 埴淵昌毅, 吾妻雅彦, 西岡安彦 :
当院における膠原病合併肺癌の検討,
第114回日本内科学会四国地方会, 2016年5月. 豊田優子, 佐藤正大, 岸潤, 河野弘, 森住俊, 岸昌美, 手塚敏史, 坂口暁, 後東久嗣, 埴淵昌毅, 西岡安彦 :
当院における膠原病関連間質性肺炎の急性増悪に関する臨床的検討,
第56回日本呼吸器学会学術講演会, 2016年4月. 埴淵昌毅, 中瀬勝則, 豊﨑纏, 木下成三, 島田久夫, 鶴尾美穂, 吾妻雅彦, 葉久貴司, 西岡安彦 :
徳島市におけるCOPD検診の現状,
第56回日本呼吸器学会学術講演会, 2016年4月. 手塚敏史, 小川博久, 近藤真代, 吾妻雅彦, 豊田優子, 佐藤正大, 岡崎弘泰, 河野弘, 岸潤, 後東久嗣, 埴淵昌毅, 西岡安彦 :
RAS阻害剤 (XRP44X) を用いた喘息モデルマウスにおける検討,
第56回日本呼吸器学会学術講演会, 2016年4月. 阿部真治, 加藤幸成, 金子美華, 後東久嗣, 埴淵昌毅, 西岡安彦 :
悪性胸膜中皮腫に対する新規抗ポドプラニン抗体NZ-12の効果,
第56回日本呼吸器学会学術講演会, 2016年4月. 小山広士, 佐藤正大, 近藤真代, 手塚敏史, 後東久嗣, 岸潤, 埴淵昌毅, 西岡安彦 :
胸膜炎や心外膜炎を契機に診断された成人Still病の2例,
第252回徳島医学会学術集会, 2016年2月. 四宮由貴, 佐藤正大, 竹﨑彰夫, 近藤真代, 瀧倉輝実, 坂口暁, 豊田優子, 後東久嗣, 岸潤, 埴淵昌毅, 西岡安彦 :
サルコイドーシス経過観察中に発症した結核性胸膜炎の1例,
第24回日本呼吸器内視鏡学会中国四国支部会, 2015年12月. 曽我部洋平, 佐藤正大, 西條敦郎, 中野万有里, 河野弘, 坂口暁, 豊田優子, 後東久嗣, 岸潤, 埴淵昌毅, 西岡安彦 :
癌性髄膜炎に対しアファチニブが奏効した2例,
第54回日本呼吸器学会中国・四国地方会, 2015年12月. 猪子未希, 荻野広和, 中野万有里, 岡崎弘泰, 大塚憲司, 後東久嗣, 岸潤, 埴淵昌毅, 坂東良美, 常山幸一, 西岡安彦 :
脳，口蓋垂，喉頭および小腸への遠隔転移を形成する稀な臨床経過をたどった右上葉原発多形癌の一剖検例,
第54回日本呼吸器学会中国・四国地方会, 2015年12月. 米田浩人, 佐藤正大, 香川耕造, 荻野広和, 坂口暁, 豊田優子, 東桃代, 後東久嗣, 岸潤, 埴淵昌毅, 西岡安彦 :
骨髄異形成症候群に播種性結核症を合併し治療に難渋した一例,
第66回日本結核病学会中国四国支部会, 2015年12月. 森住俊, 佐藤正大, 荻野広和, 近藤真代, 手塚敏史, 豊田優子, 後東久嗣, 岸潤, 埴淵昌毅, 西岡安彦 :
当科で施行された胸膜癒着術におけるタルク製剤とOK-432の使用成績の比較,
第113回日本内科学会四国地方会, 2015年12月. 近藤真代, 佐藤正大, 手塚敏史, 豊田優子, 飛梅亮, 後東久嗣, 岸潤, 埴淵昌毅, 西岡安彦 :
胸膜炎・心外膜炎を契機に診断された成人Still病の2例,
第113回日本内科学会四国地方会, 2015年12月. 山下雄也, 荻野広和, 岸潤, 豊田優子, 森住俊, 近藤真代, 瀧倉輝実, 佐藤正大, 河野弘, 手塚敏史, 後東久嗣, 埴淵昌毅, 西岡安彦 :
強膜炎，ネフローゼ症候群および僧房弁腱索断裂による重症僧房弁閉鎖不全症を呈した全身性エリテマトーデスの1例,
第26回日本リウマチ学会中国・四国支部学術集会, 2015年12月. 埴淵昌毅, 加納亮, 倉本卓哉, 後東久嗣, 坂口暁, 豊田優子, 手塚敏史, 西條敦郎, 西岡安彦 :
癌患者血漿中遊離DNAを用いた遺伝子変異検査技術の比較,
第56回日本肺癌学会学術集会, 2015年11月. 西條敦郎, 坂口暁, 手塚敏史, 柿内聡司, 豊田優子, 後東久嗣, 埴淵昌毅, 西岡安彦 :
当科における膠原病に合併した肺癌の検討,
第56回日本肺癌学会学術集会, 2015年11月. 荻野広和, 三橋惇志, 後東久嗣, 西條敦郎, 佐藤正大, 坂口暁, 手塚敏史, 倉本卓哉, 田畑祥, 上原久典, 埴淵昌毅, 西岡安彦 :
Sphere形成癌幹細胞様分画のヒト肺癌多臓器転移モデルマウスにおける役割についての解析,
第74回日本癌学会学術総会, 2015年10月. 阿部真治, 加藤幸成, 金子美華, 大塚憲司, 後東久嗣, 埴淵昌毅, 西岡安彦 :
新規ヒトキメラ型抗ポドプラニン抗体NZ-12の悪性胸膜中皮腫に対する抗腫瘍効果,
第74回日本癌学会学術総会, 2015年10月. 梶田敬介, 佐藤正大, 豊田優子, 坂口暁, 手塚敏史, 後東久嗣, 埴淵昌毅, 西岡安彦 :
PS不良ALK融合遺伝子陽性の若年者肺腺癌に対しクリゾチニブが奏効した1例,
第251回徳島医学会学術集会, 2015年8月. 西條敦郎, 後東久嗣, 三橋惇志, 中野万有里, 山子泰斗, 坂口暁, 柿内聡司, 埴淵昌毅, 西岡安彦 :
Fibrocyteはがん幹細胞性維持により肺癌進展を促進する,
第24回日本がん転移学会学術集会・総会, 2015年7月. 猪子未希, 荻野広和, 坂口暁, 岸昌美, 豊田優子, 近藤真代, 中野万有里, 岸潤, 埴淵昌毅, 西岡安彦 :
Nocardia wallacei感染症の1例,
第53回日本呼吸器学会中国・四国地方会, 2015年7月. 香川耕造, 坂口暁, 塚﨑佑貴, 佐藤正大, 飛梅亮, 米田浩人, 竹﨑彰夫, 手塚敏史, 後東久嗣, 埴淵昌毅, 西岡安彦 :
癌性髄膜炎にafatinibが奏効したEGFR exon 18 G718A変異をもつ肺腺癌の1例,
第54回日本肺癌学会中国・四国支部会, 2015年7月. 前京子, 阿部日登美, 石塚智子, 元木由美, 埴淵昌毅, 武久洋三 :
感染対策テストによる職員教育,
第65回日本病院学会, 2015年6月. 元木由美, 阿部日登美, 田中千勢, 平井真美, 濱本由実子, 正木宏典, 太田智樹, 埴淵昌毅, 武久洋三 :
嚥下内視鏡による唾液誤嚥予防効果の検討,
第65回日本病院学会, 2015年6月. 藤本陸史, 宮﨑輝, 梅井康広, 西内優, 藤坂輝代, 秋田美樹, 元木由美, 武久敬洋, 埴淵昌毅, 武久洋三 :
多剤内服薬の改善に向けた取り組み,
第65回日本病院学会, 2015年6月. 近藤育美, 元木由美, 埴淵昌毅, 武久洋三 :
医師クラークにおける医療安全への取り組み,
第65回日本病院学会, 2015年6月. 元木由美, 阿部日登美, 田中千勢, 平井真美, 濱本由実子, 正木宏典, 太田智樹, 藤川和也, 埴淵昌毅, 武久洋三 :
嚥下内視鏡による唾液誤嚥予防効果の検討,
第6回日本プライマリ・ケア連合学会学術大会, 2015年6月. 藤本陸史, 宮﨑輝, 梅井康広, 西内優, 藤坂輝代, 久米美弥子, 田原萌子, 大和薫, 秋田美樹, 藤川和也, 元木由美, 武久敬洋, 埴淵昌毅, 武久洋三 :
多剤内服薬の改善に向けた取り組み,
第6回日本プライマリ・ケア連合学会学術大会, 2015年6月. 大塚憲司, 埴淵昌毅, 後東久嗣, 西岡安彦 :
肺癌に対する抗PD-L1抗体治療の基礎的検討,
第19回日本がん分子標的治療学会学術集会, 2015年6月. 三橋惇志, 後東久嗣, 西條敦郎, 埴淵昌毅, 西岡安彦 :
線維細胞 (fibrocytes) が関わる血管新生阻害に対する獲得耐性メカニズム,
第19回日本がん分子標的治療学会学術集会, 2015年6月. 坂口暁, 豊田優子, 手塚敏史, 竹﨑彰夫, 中野万有里, 瀧倉輝実, 佐藤正大, 岡崎弘泰, 大塚憲司, 柿内聡司, 後東久嗣, 岸潤, 埴淵昌毅, 西岡安彦 :
肺胞出血をきたした11症例の検討,
第38回日本呼吸器内視鏡学会学術集会, 2015年6月. 武井美貴子, 近藤真代, 佐藤正大, 河野弘, 豊田優子, 埴淵昌毅, 西岡安彦, 三木浩和, 田中久美子, 高山哲治 :
好酸球性胆管炎を合併した全身性エリテマトーデスの1例,
第112回日本内科学会四国地方会, 2015年6月. 瀧倉輝実, 坂口暁, 森住俊, 大塚憲司, 岸昌美, 手塚敏史, 西條敦郎, 柿内聡司, 埴淵昌毅, 西岡安彦 :
N-acetylcysteine吸入が有効であったピルフェニドン抵抗性特発性肺線維症の1例,
第112回日本内科学会四国地方会, 2015年6月. 村上尚嗣, 野々木理子, 井上広基, 別宮佳奈子, 岩崎優, 桑山泰治, 金崎淑子, 新谷保実, 佐藤幸一, 埴淵昌毅 :
加湿器使用が原因と考えられた過敏性肺炎の2例,
第112回日本内科学会四国地方会, 2015年6月. 豊田優子, 瀧倉輝実, 近藤真代, 佐藤正大, 尾崎領彦, 岸潤, 手塚敏史, 河野弘, 後東久嗣, 埴淵昌毅, 西岡安彦 :
膠原病に合併した血球貪食性リンパ組織球症の4症例,
第59回日本リウマチ学会総会・学術集会, 2015年4月. 佐藤正大, 後東久嗣, 森住俊, 阿部秀一, 吉嶋輝実, 岡﨑弘泰, 埴淵昌毅, 西岡安彦 :
肺線維芽細胞に対するfibrocyteの作用とnintedanibの抑制効果,
第55回日本呼吸器学会学術講演会, 2015年4月. 埴淵昌毅, 中瀬勝則, 豊﨑纏, 木下成三, 島田久夫, 鶴尾美穂, 吾妻雅彦, 葉久貴司, 西岡安彦 :
徳島市におけるCOPD検診システムの構築,
第55回日本呼吸器学会学術講演会, 2015年4月. 手塚敏史, 小川博久, 豊田優子, 竹﨑彰夫, 佐藤正大, 岡﨑弘泰, 吉嶋輝実, 後東久嗣, 埴淵昌毅, 西岡安彦 :
Plasminogen Activator Inhibitor-1阻害剤 (IMD-4690) の慢性喘息モデルマウスにおける検討,
第55回日本呼吸器学会学術講演会, 2015年4月. 柿内聡司, 荻野広和, 大塚憲司, 坂口暁, 西條敦郎, 後東久嗣, 埴淵昌毅, 西岡安彦 :
当科における間質性肺炎合併肺癌の治療の現状,
第55回日本呼吸器学会学術講演会, 2015年4月. 中野万有里, 吉嶋輝実, 埴淵昌毅, 中村信元, 三木浩和, 賀川久美子, 西岡安彦 :
Pneumocystis jiroveciに対しST合剤の脱感作療法を行った4症例の検討,
第89回日本感染症学会総会, 2015年4月. 岩坂麻衣子, 佐藤正大, 荻野広和, 坂口暁, 豊田優子, 中野万有里, 森住俊, 小川博久, 柿内聡司, 後東久嗣, 埴淵昌毅, 西岡安彦 :
Idiopathic pleuroparenchymal fibroelastosis (IPPFE) における間質性肺炎マーカーの検討,
第112回日本内科学会講演会, 2015年4月. 荻野広和, 豊田優子, 中野万有里, 東桃代, 埴淵昌毅, 西岡安彦 :
皮膚筋炎に対してステロイドおよび免疫抑制剤による加療中に発症した播種性Mycobacterium avium症の1例,
第90回日本結核病学会総会, 2015年3月. 中野万有里, 東桃代, 瀧倉輝実, 坂口暁, 豊田優子, 上回紗代, 安倍秀斉, 埴淵昌毅, 土井俊夫, 西岡安彦 :
長期間ステロイド投与が発症の契機となったMycobacterium intracellulareによる関節炎と骨髄炎の2症例,
第65回日本結核病学会中国四国支部会, 2015年2月. 尾崎領彦, 坂口暁, 手塚敏史, 大塚憲司, 森積俊, 岸潤, 後東久嗣, 埴淵昌毅, 西岡安彦 :
胸膜直下に帯状に分布するすりガラス陰影で発症した，自己免疫性肺胞蛋白症の一例,
第23回日本呼吸器内視鏡学会中国四国支部会, 2015年2月. 宇山直人, 大塚秀樹, 音見暢一, 原田雅史, 生島仁史, 山子泰斗, 豊田優子, 埴淵昌毅, 西岡安彦, 滝沢宏光, 坂東良美 :
特異な経過を示した肺原発滑膜肉腫の一例,
第7回呼吸機能イメージング研究会学術集会, 2015年2月. 稲垣太造, 荻野広和, 坂口暁, 豊田優子, 中野万有里, 森住俊, 佐藤正大, 小川博久, 後東久嗣, 埴淵昌毅, 西岡安彦 :
Idiopathic pleuroparenchymal fibroelastosisにおける間質性肺炎マーカーの検討,
第250回徳島医学会学術集会, 2015年2月. 岩佐あゆみ, 佐藤正大, 坂口暁, 豊田優子, 田島壮一郎, 櫻田巧, 後東久嗣, 柿内聡司, 埴淵昌毅, 西岡安彦 :
UGT1A1遺伝子のヘテロ接合体 (*6または*28) を持つ患者における塩酸イリノテカン投与に関する検討,
第52回日本呼吸器学会中国・四国地方会, 2014年12月. 板東智子, 荻野広和, 坂口暁, 手塚敏史, 森住俊, 吉嶋輝実, 岸潤, 後東久嗣, 埴淵昌毅, 西岡安彦 :
鳥特異的抗体が高値を呈した鳥関連過敏性肺炎の一例,
第52回日本呼吸器学会中国・四国地方会, 2014年12月. 埴淵昌毅, 西岡安彦 :
徳島大学病院の進捗状況,
第2回国際遠隔医療教育ネットワークに関する担当医師及び技術担当者全国合同会議, 2014年12月. 近藤真代, 佐藤正大, 豊田優子, 岸潤, 手塚敏史, 吉嶋輝実, 岸昌美, 河野弘, 後東久嗣, 埴淵昌毅, 西岡安彦 :
血小板減少を契機として診断された高齢者のSLEの2例,
第25回日本リウマチ学会中国・四国支部学術集会, 2014年12月. 栗原健士, 吉嶋輝実, 坂口暁, 豊田優子, 中野万有里, 岸潤, 手塚敏史, 後東久嗣, 埴淵昌毅, 西岡安彦 :
経過中に血球貪食症候群を発症し，シクロホスファミド間歇大量静注療法が奏効した重症SLEの1例,
第111回日本内科学会四国地方会, 2014年11月. 森住俊, 佐藤正大, 坂口暁, 豊田優子, 岸昌美, 小川博久, 柿内聡司, 後東久嗣, 埴淵昌毅, 西岡安彦 :
Idiopathic pleuroparenchymal fibroelastosisにおける間質性肺炎マーカーの検討,
第111回日本内科学会四国地方会, 2014年11月. 元木由美, 阿部日登美, 寺内翔, 十河紀美子, 埴淵昌毅, 武久洋三 :
抗菌薬適正使用ラウンドへの取り組み,
第22回日本慢性期医療学会, 2014年11月. 柿内聡司, 大塚憲司, 佐藤正大, 西條敦郎, 坂口暁, 後東久嗣, 埴淵昌毅, 西岡安彦 :
当院における間質性肺炎合併肺癌の治療の現状,
第55回日本肺癌学会学術集会, 2014年11月. 後東久嗣, 三橋敦志, 西條敦郎, 柿内聡司, 埴淵昌毅, 上原久典, 矢野聖二, 西岡安彦 :
ベバシズマブに対する獲得耐性メカニズムとしての線維細胞 (fibrocytes) の役割,
第73回日本癌学会学術総会, 2014年9月. 埴淵昌毅, 中曽亜佐美, 藤原範子, 東桃代, 西岡安彦 :
徳島大学病院における結核対策の現状,
第8回日本結核病学会中国四国支部研究会 (シンポジウム), 2014年9月. 坂口暁, 後東久嗣, 大串文隆, 葉久貴司, 兼松貴則, 浦田知之, 柿内聡司, 埴淵昌毅, 曽根三郎, 西岡安彦 :
高齢者進行NSCLC患者を対象としてPRO評価を取り入れたTS-1療法の臨床第Ⅱ相試験,
第52回日本癌治療学会学術集会, 2014年8月. 山下雄也, 荻野広和, 阿河弘和, 岸昌美, 坂口暁, 吉嶋輝実, 佐藤正大, 柿内聡司, 後東久嗣, 岸潤, 埴淵昌毅, 西岡安彦 :
鳥特異的抗体が高値を呈した鳥関連過敏性肺炎の一例,
第249回徳島医学会学術集会, 2014年7月. 大塚憲司, 後東久嗣, 葉久貴司, 兼松貴則, 浦田知之, 柿内聡司, 埴淵昌毅, 大串文隆, 曽根三郎, 西岡安彦 :
高齢者進行非小細胞肺癌患者を対象としてPRO評価を取り入れたTS-1療法の臨床第Ⅱ相試験,
第12回日本臨床腫瘍学会学術集会, 2014年7月. 塚﨑佑貴, 大塚憲司, 岸昌美, 近藤真代, 吉嶋輝実, 佐藤正大, 岡埼弘泰, 竹﨑彰夫, 東桃代, 埴淵昌毅, 坂下直美, 福田悠, 西岡安彦 :
Acute Fibrinous and Organizing Pneumonia (AFOP) の一剖検例,
第51回日本呼吸器学会中国・四国地方会, 2014年7月. 松本康平, 尾崎領彦, 豊田優子, 中野万有里, 森住俊, 河野弘, 岸潤, 柿内聡司, 埴淵昌毅, 西岡安彦 :
高Ca血症にて発症した多臓器サルコイドーシスの1例,
第51回日本呼吸器学会中国・四国地方会, 2014年7月. 阿河弘和, 佐藤正大, 近藤真代, 塚﨑佑貴, 手塚敏史, 豊田優子, 坂口暁, 柿内聡司, 後東久嗣, 埴淵昌毅, 西岡安彦 :
当科における悪性胸水貯留例に対するタルク製剤の使用経験,
第53回日本肺癌学会中国・四国支部会, 2014年7月. 荻野広和, 西條敦郎, 大塚憲司, 坂口暁, 手塚敏史, 柿内聡司, 後東久嗣, 埴淵昌毅, 西岡安彦 :
Lambert-Eaton筋無力症候群を契機に発見された小細胞肺癌の一例,
第53回日本肺癌学会中国・四国支部会, 2014年7月. 後東久嗣, 三橋惇志, 倉本卓哉, 田畑祥, 西條敦郎, 柿内聡司, 埴淵昌毅, 上原久典, 西岡安彦 :
肺癌多臓器転移モデルにおけるsphere形成癌幹細胞様分画の役割,
第23回日本がん転移学会学術集会・総会, 2014年7月. 山子泰斗, 後東久嗣, 三橋敦志, 倉本卓哉, 田畑祥, 西條敦郎, 柿内聡司, 埴淵昌毅, 小川博久, 上原久典, 西岡安彦 :
ヒト小細胞肺癌骨転移に対するRANKL標的治療におけるIGF-1の関与,
第23回日本がん転移学会学術集会・総会, 2014年7月. 元木由美, 阿部日登美, 寺内翔, 十河紀美子, 埴淵昌毅, 武久洋三 :
抗菌薬適正使用ラウンドへの取り組み,
第64回日本病院学会, 2014年7月. 後東久嗣, 三橋惇志, 西條敦郎, 倉本卓哉, 田畑祥, 埴淵昌毅, 柿内聡司, 青野純典, 上原久典, 西岡安彦 :
ベバシズマブに対する獲得耐性メカニズムとしての線維細胞 (fibrocytes) の役割,
第18回日本がん分子標的治療学会学術集会 (シンポジウム), 2014年6月. 大塚憲司, 阿部真治, 埴淵昌毅, 木宿昌俊, 川添和義, 加藤幸成, 西岡安彦 :
胸膜中皮腫同所移植モデルにおける抗ポドプラニン抗体の抗腫瘍効果,
第18回日本がん分子標的治療学会学術集会, 2014年6月. 中野万有里, 高橋直希, 吉嶋輝実, 西條敦郎, 手塚敏史, 東桃代, 埴淵昌毅, 西岡安彦 :
当院で経験した重症熱性血小板減少症候群(severe fever with thrombocytopenia syndrome: SFTS)の1例,
第88回日本感染症学会学術講演会, 2014年6月. 近藤真代, 森住俊, 坂口暁, 西條敦郎, 吉嶋輝実, 中野万有里, 柿内聡司, 後東久嗣, 埴淵昌毅, 西岡安彦 :
PemetrexedとBevacizumabの併用療法が有効であった高齢者非小細胞肺癌の1例,
第110回日本内科学会四国地方会, 2014年6月. 尾崎領彦, 豊田優子, 岸潤, 木下勝弘, 岸昌美, 佐藤正大, 柿内聡司, 埴淵昌毅, 西岡安彦 :
左腎動脈閉塞等により結節性多発動脈炎が疑われた血管内膜肉腫の1剖検例,
第110回日本内科学会四国地方会, 2014年6月. 佐藤正大, 岸昌美, 木下勝弘, 後東久嗣, 埴淵昌毅, 西岡安彦 :
血清 SP-D 上昇を認めた Idiopathic pleuroparenchymal fibroelastosis (IPPFE) 症例の検討,
第54回日本呼吸器学会学術講演会, 2014年4月. 豊田優子, 岸潤, 河野弘, 後東久嗣, 埴淵昌毅, 中島利博, 西岡安彦 :
関節リウマチ患者由来の線維芽細胞様滑膜細胞において thymidine phosphorylaseはCXCL10 を制御する,
第58回日本リウマチ学会総会学術集会, 2014年4月. 柿内聡司, 大塚憲司, 佐藤正大, 西條敦郎, 坂口暁, 後東久嗣, 埴淵昌毅, 西岡安彦 :
当院における間質性肺炎合併肺癌の治療の現状,
第54回日本呼吸器学会学術講演会, 2014年4月. 阿部真治, 加藤幸成, 金子美華, 東満美, 後東久嗣, 埴淵昌毅, 西岡安彦 :
悪性胸膜中皮腫同所移植モデルにおける抗ポドプラニン抗体の抗腫瘍効果,
第54回日本呼吸器学会学術講演会, 2014年4月. 中瀬勝則, 鶴尾美穂, 島田久夫, 木下成三, 豊﨑纏, 杉野聡, 浦聡明, 山下恵美, 古味勝美, 小田芳栄, 服部順子, 西岡安彦, 埴淵昌毅, 吾妻雅彦 :
徳島市医師会のCOPD対策,
第248回徳島医学会学術集会, 2014年2月. 山本聖子, 埴淵昌毅, 森住俊, 岸昌美, 木下勝弘, 河野弘, 竹﨑彰夫, 豊田優子, 東桃代, 後東久嗣, 岸潤, 西岡安彦 :
左上葉無気肺を呈したアレルギー性気管支肺アスペルギルス症の一例,
第248回徳島医学会, 2014年2月. 津保友香, 埴淵昌毅, 滝沢宏光, 吉田光輝, 吉嶋輝実, 大塚憲司, 佐藤正大, 西條敦郎, 豊田優子, 手塚敏史, 柿内聡司, 後東久嗣, 坂東良美, 先山正二, 西岡安彦 :
肺原発滑膜肉腫の一例.,
第248回徳島医学会, 2014年2月. 尾崎領彦, 髙橋直希, 後東久嗣, 豊田優子, 手塚敏史, 大塚憲司, 西條敦郎, 坂口暁, 木下勝弘, 柿内聡司, 小川博久, 川上行奎, 埴淵昌毅, 近藤和也, 先山正二, 泉啓介, 西岡安彦 :
気管支鏡直視下生検にて診断に至ったoncocytic carcinoidの一例.,
第22回日本呼吸器内視鏡学会中国四国支部会, 2014年2月. 是松麻美, 内藤伸仁, 岸昌美, 中野万有里, 吉田光輝, 川上行奎, 木下勝弘, 東桃代, 吉嶋輝実, 佐藤正大, 岸潤, 森河由里子, 松山友理子, 榊美佳, 坂東良美, 渡邉俊介, 上原久典, 泉啓介, 先山正二, 埴淵昌毅, 西岡安彦 :
胸水中に多数のLanghans型巨細胞を認めたMycobacterium avium症に伴う胸膜炎の一例.,
第64回日本結核病学会中国四国支部会, 2014年2月. 高橋直希, 西條敦郎, 柿内聡司, 埴淵昌毅, 滝沢宏光, 西野豪志, 森住俊, 岸昌美, 木下勝弘, 後東久嗣, 音見暢一, 生島仁史, 先山正二, 西岡安彦 :
PET/CTにて集積を認めなかった嚢胞状縦隔リンパ節腫大を伴う肺腺癌の一例,
第6回呼吸機能イメージング研究会学術集会, 2014年1月. 津保友香, 埴淵昌毅, 滝沢宏光, 吉田光輝, 吉嶋輝実, 大塚憲司, 佐藤正大, 西條敦郎, 豊田優子, 手塚敏史, 柿内聡司, 後東久嗣, 坂東良美, 先山正二, 西岡安彦 :
肺原発滑膜肉腫の一例.,
第50回日本呼吸器学会中国・四国地方会, 2013年12月. 山本聖子, 埴淵昌毅, 森住俊, 岸昌美, 木下勝弘, 河野弘, 竹﨑彰夫, 豊田優子, 東桃代, 後東久嗣, 岸潤, 西岡安彦 :
左上葉無気肺を呈したアレルギー性気管支肺アスペルギルス症の一例.,
第50回日本呼吸器学会中国・四国地方会, 2013年12月. 内藤伸仁, 河野弘, 大塚憲司, 豊田優子, 岸潤, 手塚敏史, 木下勝弘, 吉嶋輝実, 岸昌美, 埴淵昌毅, 西岡安彦 :
腹部大動脈周囲炎を伴った多発血管炎性肉芽腫症の2例.,
第24回日本リウマチ学会中国・四国支部学術集会, 2013年12月. 坂東弘基, 埴淵昌毅, 豊田優子, 手塚敏史, 吉嶋輝実, 後東久嗣, 柿内聡司, 岸潤, 西岡安彦, 坂本幸裕 :
気管支拡張症を呈した原発性線毛運動不全症の1例.,
第109回日本内科学会四国地方会, 2013年12月. 矢葺洋平, 西條敦郎, 木下勝弘, 岸昌美, 大塚憲司, 埴淵昌毅, 西岡安彦, 井内新, 青野純典 :
徳島県で発生した重症熱性血小板減少症候群(severe fever with thrombocytopenia syndrome: SFTS)の1例.,
第109回日本内科学会四国地方会, 2013年12月. 手塚敏史, 小川博久, 木下勝弘, 埴淵昌毅, 西岡安彦 :
Calpain inhibitor(Calpeptin)の喘息モデルマウスにおける検討.,
第63回日本アレルギー学会秋季学術大会, 2013年11月. 岡野義夫, 後東久嗣, 葉久貴司, 兼松貴則, 浦田知之, 柿内聡司, 埴淵昌毅, 大串文隆, 曽根三郎, 西岡安彦 :
高齢者進行非小細胞肺癌患者を対象としてPRO評価を取り入れたTS-1療法の臨床第Ⅱ相試験.,
第54回日本肺癌学会総会, 2013年11月. 西條敦郎, 柿内聡司, 手塚敏史, 後東久嗣, 山子泰斗, 大塚憲司, 埴淵昌毅, 西岡安彦 :
当院におけるBevacizumab長期維持投与症例の検討.,
第51回日本癌治療学会学術集会, 2013年10月. 手塚敏史, 豊田優子, 柿内聡司, 大塚憲司, 西條敦郎, 木下勝弘, 後東久嗣, 櫻田巧, 埴淵昌毅, 西岡安彦 :
当科の肺癌化学療法におけるshort-hydration Cisplatinの忍容性に関する検討.,
第51回日本癌治療学会学術集会, 2013年10月. 手塚敏史, 小川博久, 木下勝弘, 埴淵昌毅, 西岡安彦 :
O57-4 Calpain inhibitor (Calpeptin)の喘息モデルマウスにおける検討(O57 気管支喘息病態5,口演,第63回日本アレルギー学会秋季学術大会),
アレルギー, Vol.62, No.9, 1400, 2013年10月.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390001205000905728

(CiNii: 1390001205000905728) 柿内聡司, 大塚憲司, 西條敦郎, 手塚敏史, 豊田優子, 後東久嗣, 埴淵昌毅, 西岡安彦 :
当院における間質性肺炎合併肺癌の治療の現状.,
第11回日本臨床腫瘍学会学術集会, 2013年8月. 矢葺洋平, 西條敦郎, 木下勝弘, 東桃代, 後東久嗣, 柿内聡司, 埴淵昌毅, 西岡安彦, 井内新, 青野純典, 福野天, 朝田完二, 長瀬教夫, 藤田博己, 馬原文彦 :
徳島県で発生した重症熱性血小板減少症候群 (severe fever with thrombocytopenia syndrome: SFTS) の1例,
第247回徳島医学会学術集会, 2013年8月. 中瀬勝則, 鶴尾美穂, 島田久夫, 木下成三, 豊﨑纏, 杉野聡, 浦聡明, 山下恵美, 古味勝美, 服部順子, 西岡安彦, 埴淵昌毅, 吾妻雅彦 :
徳島市医師会のCOPD対策,
第247回徳島医学会学術集会, 2013年8月. 猪子未希, 西條敦郎, 岸昌美, 埴淵昌毅, 青野純典, 豊田優子, 木下勝弘, 手塚敏史, 吉嶋輝実, 河野弘, 岸潤, 西岡安彦, 池田真由美, 吉田光輝, 先山正二, 福田悠 :
肺多発浸潤影と胸膜炎を初発症状とした多発性筋炎の1例,
第247回徳島医学会学術集会, 2013年8月. 埴淵昌毅, 柿内聡司, 後東久嗣, 西岡安彦 :
呼吸器疾患のControversy -Pros & Cons- 高齢者肺癌にベバシズマブは必要か? -Proの立場から-,
第49回日本呼吸器学会中国・四国地方会 (第20回呼吸器セミナー), 2013年7月. 長瀬紗季, 豊田優子, 阿部秀一, 岸潤, 河野弘, 手塚敏史, 埴淵昌毅, 池田真由美, 先山正二, 西岡安彦 :
サルコイドーシスの経過観察中に肺腺癌を合併した1例,
第49回日本呼吸器学会中国・四国地方会, 2013年7月. 是松麻美, 岸昌美, 青野純典, 竹﨑彰夫, 東桃代, 木下勝弘, 阿部秀一, 埴淵昌毅, 吉田光輝, 先山正二, 福田悠, 西岡安彦 :
徳島大学病院における胸腔鏡 (VATS)下肺生検症例の検討,
第49回日本呼吸器学会中国・四国地方会, 2013年7月. 尾崎領彦, 柿内聡司, 手塚敏史, 西條敦郎, 山子泰斗, 後東久嗣, 埴淵昌毅, 西岡安彦 :
徳島大学病院におけるBevacizumab長期維持投与例の検討,
第52回日本肺癌学会中国・四国支部会, 2013年7月. 西條敦郎, 後東久嗣, 田畑祥, 三橋惇志, 豊田優子, 埴淵昌毅, 柿内聡司, 秋山伸一, 西岡安彦 :
がん細胞の遊走におけるthymidine phosphorylaseとCXCL11の役割,
第22回日本がん転移学会学術集会・総会, 2013年7月. 後東久嗣, 三橋惇志, 倉本卓哉, 田畑祥, 西條敦郎, 埴淵昌毅, 柿内聡司, 青野純典, 上原久典, 曽根三郎, 西岡安彦 :
肺surfactant protein A (SP-A) の肺癌進展における機能解析,
第22回日本がん転移学会学術集会・総会, 2013年7月. 近藤育美, 木下崇史, 元木由美, 埴淵昌毅, 武久洋三 :
慢性期病院での医療クラークの役割について,
第63回日本病院学会, 2013年6月. 大西弘祐, 阿部日登美, 元木由美, 埴淵昌毅, 武久洋三 :
慢性期病棟での喀痰吸引カテーテル管理方法について,
第63回日本病院学会, 2013年6月. 元木由美, 大鹿保香, 阿部日登美, 長尾優子, 埴淵昌毅, 武久洋三 :
胃瘻栄養患者における糖質制限食の有効性について,
第63回日本病院学会, 2013年6月. 三橋惇志, 後東久嗣, 西條敦郎, 倉本卓哉, 田畑祥, 埴淵昌毅, 矢野聖二, 曽根三郎, 西岡安彦 :
悪性胸膜中皮腫同所移植マウスモデルにおける抗VEGF治療耐性化メカニズムの検討,
第17回日本がん分子標的治療学会学術集会, 2013年6月. 黄俊, 田畑祥, 埴淵昌毅, 西岡安彦 :
悪性中皮腫におけるPAPPAの機能解析と分子標的治療法開発の検討,
第17回日本がん分子標的治療学会学術集会, 2013年6月. 埴淵昌毅, 大塚憲司, 後東久嗣, 倉本卓哉, 三橋惇志, 西岡安彦, 曽根三郎, Isaiah J Fidler :
Endothelin受容体拮抗剤による肺癌脳転移抑制効果の検討,
第17回日本がん分子標的治療学会学術集会, 2013年6月. 森住俊, 大塚憲司, 豊田優子, 河野弘, 岸潤, 手塚敏史, 吉嶋輝実, 柿内聡司, 埴淵昌毅, 西岡安彦 :
脳炎と腹部大動脈瘤を合併した多発血管炎性肉芽腫症の1例,
第108回日本内科学会四国地方会, 2013年6月. 高橋直希, 埴淵昌毅, 青野純典, 木下勝弘, 東桃代, 岸昌美, 竹崎彰夫, 西條敦郎, 後東久嗣, 西岡安彦 :
当院におけるidiopathic pleuroparenchymal fibroelastosis (IPPFE) 症例の検討,
第108回日本内科学会四国地方会, 2013年6月. Huang Jun, Liu Dai-Shun, Souji Kakiuchi, Hisatsugu Goto, Masaki Hanibuchi and Yasuhiko Nishioka :
Therapeutic efficacy of RNA interference targeting focal adhesion kinase against orthotropic xenograft of human malignant pleural mesothelioma in SCID mice.,
第53回日本呼吸器学会学術講演会, Apr. 2013. 阿部真治, 加藤幸成, 金子美華, 木宿昌俊, 川添和義, 東満美, 埴淵昌毅, 水口和生, 西岡安彦 :
ヒトNK細胞を介した抗ポドプラニン抗体NZ-8の悪性胸膜中皮腫に対する抗腫瘍効果.,
第53回日本呼吸器学会学術講演会, 2013年4月. 埴淵昌毅, 後東久嗣, 近藤真代, 山子泰斗, 岡﨑弘泰, 手塚敏史, 西岡安彦 :
当院におけるIdiopathic pleuroparenchymal fibroelastosis(IPPFE)症例の検討-IgG4関連疾患との関連性-.,
第110回日本内科学会講演会, 2013年4月. 柿内聡司, 大塚憲司, 山子泰斗, 西條敦郎, 手塚敏史, 後東久嗣, 青野純典, 埴淵昌毅, 西岡安彦 :
当院における間質性肺炎合併肺癌の治療の現状.,
第110回日本内科学会講演会, 2013年4月. 吉嶋輝実, 埴淵昌毅, 東桃代, 豊田優子, 河野弘, 岸潤, 竹﨑彰夫, 岡﨑弘泰, 長尾多美子, 鈴木麗子, 高開登茂子, 先山正二, 西岡安彦 :
徳島大学病院職員における潜在性結核感染症の現状,
第63回日本結核病学会中国四国支部会, 2013年2月. 米田浩人, 手塚敏史, 青野純典, 香川耕造, 西條敦郎, 山子泰斗, 大塚憲司, 柿内聡司, 後東久嗣, 埴淵昌毅, 泉啓介, 西岡安彦 :
胸腔鏡下胸膜生検で診断しえた腎盂癌胸膜転移の1例,
第21回日本呼吸器内視鏡学会中国四国支部会, 2013年2月. 米田浩人, 柿内聡司, 手塚敏史, 後東久嗣, 埴淵昌毅, 西岡安彦 :
当科におけるBevacizumab長期維持投与例の検討,
第8回腫瘍分子標的治療セミナー, 2013年2月. 松田華子, 河野弘, 岸潤, 青野純典, 香川耕造, 米田浩人, 岡崎弘泰, 竹﨑彰夫, 東桃代, 埴淵昌毅, 西岡安彦 :
ステロイド抵抗性器質化肺炎の加療中に気胸・肺血栓塞栓症を合併した1例,
第48回日本呼吸器学会中国・四国地方会, 2012年12月. 森住俊, 豊田優子, 手塚敏史, 柿内聡司, 大塚憲司, 山子泰斗, 西條敦郎, 後東久嗣, 櫻田巧, 埴淵昌毅, 西岡安彦 :
Cisplatinのshort-hydration投与法の忍容性に関する検討,
第48回日本呼吸器学会中国・四国地方会, 2012年12月. 阿部真治, 加藤幸成, 金子美華, 黄俊, 埴淵昌毅, 曽根三郎, 西岡安彦 :
悪性胸膜中皮腫に対するヒトキメラ型抗ポドプラニン抗体療法の検討,
第25回日本バイオセラピィ学会学術集会総会, 2012年12月. 香川耕造, 河野弘, 藤田浩司, 村上永尚, 岸潤, 埴淵昌毅, 梶龍兒, 西岡安彦 :
MPO-ANCA関連肥厚性硬膜炎の1例,
第107回日本内科学会四国地方会, 2012年12月. 米田浩人, 大塚憲司, 青野純典, 豊田優子, 手塚敏史, 柿内聡司, 後東久嗣, 埴淵昌毅, 西岡安彦 :
難治性の腎性・肝性胸水に対して胸腔-腹腔シャントが奏功した1例,
第107回日本内科学会四国地方会, 2012年12月. 三橋惇志, 後東久嗣, Van The Trung, 倉本卓哉, 田畑祥, 埴淵昌毅, 西岡安彦 :
悪性胸膜中皮腫同所移植マウスモデルにおける抗VEGF治療耐性化メカニズムの検討,
感染免疫リトリート, 2012年11月. 元木由美, 阿部日登美, 猪内秀和, 埴淵昌毅, 武久洋三 :
当院での耐性菌に対する取り組み,
第20回日本慢性期医療学会, 2012年11月. 豊田優子, 柿内聡司, 埴淵昌毅, 手塚敏史, 後東久嗣, 西岡安彦 :
Patient-Reported Outcome (PRO) による肺癌薬物療法の有用性の検討,
第53回日本肺癌学会総会, 2012年11月. 埴淵昌毅, 阿部真治, 加藤幸成, 金子美華, 木宿昌俊, 川添和義, 黄俊, 三橋惇志, 水口和生, 西岡安彦 :
抗ポドプラニン抗体NZ-1の悪性胸膜中皮腫に対する抗体依存性細胞障害活性と抗腫瘍効果,
第53回日本肺癌学会総会, 2012年11月. 大塚憲司, 豊田優子, 柿内聡司, 後東久嗣, 埴淵昌毅, 吾妻雅彦, 西岡安彦, 監﨑孝一郎, 福森知治, 坂東良美 :
多発結節影を呈したLangerhans cell histiocytosisの1例,
第105回日本内科学会四国地方会, 2012年11月. 埴淵昌毅 :
気管支喘息の日常臨床―吸入ステロイド治療の有効性について―,
小松島市医師会学術講演会, 2012年10月. 河野弘, 豊田優子, 岸潤, 埴淵昌毅, 西岡安彦 :
抗CCP抗体高値を呈し関節炎を伴わずに発症したステロイド抵抗性器質化肺炎の1例,
第23回日本リウマチ学会中国・四国支部学術集会, 2012年10月. 埴淵昌毅 :
COPD診断・管理・予防のための国際的戦略 (2011年改訂版) について,
ディスカバリーCOPDアドバンスセミナー, 2012年10月. 埴淵昌毅, 長尾多美子, 鈴木麗子, 高開登茂子, 東桃代, 先山正二, 西岡安彦 :
潜在性結核感染症 (latent tuberculosis infection: LTBI) に対する治療の現状と問題点,
第6回日本結核病学会中国四国支部研究会, 2012年9月. 元木由美, 阿部日登美, 猪内秀和, 埴淵昌毅, 武久洋三 :
当院での耐性菌に対する取り組み,
第54回全日本病院学会, 2012年9月. 田畑祥, 池田龍二, 山本雅達, 古川龍彦, 倉本卓哉, 後東久嗣, 埴淵昌毅, 西岡安彦, 曽根三郎, 秋山伸一 :
ヒト癌細胞の生存におけるチミジン異化作用の役割,
第71回日本癌学会学術総会, 2012年9月. 西岡安彦, 阿部真治, 木宿昌俊, 川添和義, 黄俊, 埴淵昌毅, 水口和生, 曽根三郎, 加藤幸成 :
悪性胸膜中皮腫に対するラット-ヒトキメラ型抗ポドプラニン抗体NZ-8の抗腫瘍効果,
第71回日本癌学会学術総会, 2012年9月. 山子泰斗, 柿内聡司, 大塚憲司, 西條敦郎, 手塚敏史, 後東久嗣, 埴淵昌毅, 西岡安彦 :
PNA-LNA PCR Clamp法とCycleave法を用いたEGFR遺伝子変異測定の比較検討,
肺癌分子標的治療セミナー, 2012年9月. 高橋彩加, 岡﨑弘泰, 岸潤, 豊田優子, 手塚敏史, 松立吉弘, 柿内聡司, 後東久嗣, 埴淵昌毅, 久保宜明, 西岡安彦 :
刺青部分に肉芽腫性変化を起こしたサルコイドーシスの1例,
第245回徳島医学会学術集会, 2012年7月. 藤田美香, 河野弘, 近藤真代, 竹﨑彰夫, 岸潤, 藤井達也, 中瀧恵実子, 青野純典, 埴淵昌毅, 武田憲昭, 西岡安彦 :
頸部・縦隔蜂窩織炎で急激に発症し窒息に至った劇症型A群溶血性レンサ球菌感染症 (Streptococcal Toxic Shock-like Syndrome;STSS) の1例,
第245回徳島医学会学術集会, 2012年7月. 中西嘉憲, 河野弘, 阿部秀一, 竹﨑彰夫, 後東久嗣, 青野純典, 埴淵昌毅, 先山正二, 福田悠, 西岡安彦 :
特発性肺骨化症の1例,
第47回日本呼吸器学会中国・四国地方会, 2012年7月. 香川耕造, 西條敦郎, 柿内聡司, 大塚憲司, 山子泰斗, 手塚敏史, 後東久嗣, 埴淵昌毅, 西岡安彦 :
測定法によりEGFR変異の測定結果に乖離がみられた非小細胞肺癌の3例,
第51回日本肺癌学会中国・四国支部会, 2012年7月. 米田浩人, 青野純典, 岸昌美, 豊田優子, 近藤真代, 岡﨑弘泰, 岸潤, 埴淵昌毅, 監﨑孝一郎, 福田悠, 西岡安彦 :
高IgG血症の長期間の経過観察中に多中心性キャッスルマン病の診断に至った1例,
第47回日本呼吸器学会中国・四国地方会, 2012年7月. 倉本卓哉, 後東久嗣, 三橋惇志, 田畑祥, 上原久典, 西條敦郎, 柿内聡司, 埴淵昌毅, 前川洋一, 安友康二, 秋山伸一, 曽根三郎, 西岡安彦 :
小細胞肺がん転移におけるDll4-Notchシグナルの臓器特異性に関する検討,
第21回日本がん転移学会学術集会・総会, 2012年7月. 大塚憲司, 埴淵昌毅, 後東久嗣, 西岡安彦, 曽根三郎, Fidler Isaiah J :
Endothelin受容体拮抗剤による肺癌脳転移抑制効果の検討,
第21回日本がん転移学会学術集会・総会, 2012年7月. 田畑祥, 池田龍二, 山本雅達, 古川龍彦, 倉本卓哉, 後東久嗣, 埴淵昌毅, 西岡安彦, 曽根三郎, 秋山伸一 :
ヒト癌細胞のROS産生および生存におけるチミジン異化作用の役割,
第16回日本がん分子標的治療学会学術集会, 2012年6月. 西岡安彦, 阿部真治, 加藤幸成, 木宿昌俊, 川添和義, 黄俊, 埴淵昌毅, 水口和生, 曽根三郎 :
悪性胸膜中皮腫に対するヒトキメラ型抗ポドプラニン抗体NZ-8の抗腫瘍効果,
第16回日本がん分子標的治療学会学術集会, 2012年6月. 倉本卓哉, 後東久嗣, 佐藤正大, 三橋惇志, 田畑祥, 西條敦郎, 上原久典, Welm Alana L, 埴淵昌毅, 秋山伸一, 曽根三郎, 西岡安彦 :
ヒト肺がん多臓器転移モデルにおけるMacrophage-stimulating proteinの役割に関する検討,
第16回日本がん分子標的治療学会学術集会, 2012年6月. 豊田優子, 埴淵昌毅, 柿内聡司, 櫻田巧, 後東久嗣, 手塚敏史, 岸潤, 青野純典, 西岡安彦 :
当科における終末期の鎮静についての検討,
第17回日本緩和医療学会学術大会, 2012年6月. 田岡志保, 河野弘, 手塚敏史, 柿内聡司, 後東久嗣, 埴淵昌毅, 西岡安彦, 岡本耕一, 高山哲治 :
FDG-PET/CTにより小腸転移を発見した肺癌の2症例．,
第106回日本内科学会四国地方会, 2012年6月. 大塚憲司, 柿内聡司, 後東久嗣, 青野純典, 埴淵昌毅, 西岡安彦 :
高用量のメロぺネムが奏効した細菌性肺炎症例,
徳島感染症講演会, 2012年6月. 大塚憲司, 原知也, 豊田優子, 岸潤, 青野純典, 山口浩司, 埴淵昌毅, 佐田政隆, 西岡安彦 :
心筋炎を合併したChurg-Strauss症候群の1例,
第106回日本内科学会四国地方会, 2012年6月. 西條敦郎, 柿内聡司, 香西博之, 大塚憲司, 山子泰斗, 手塚敏史, 後東久嗣, 埴淵昌毅, 西岡安彦 :
Cycleave法とPCR-Clamp法によるEGFR遺伝子変異測定結果とEGFRチロシンキナーゼ阻害剤の治療効果との相関,
第35回日本呼吸器内視鏡学会学術集会, 2012年5月. Jun Huang, Shinji Abe, Yuki Morita, Shuji Ozaki, Masatoshi Kishuku, Kazuo Minakuchi, Masaki Hanibuchi, Toshio Matsumoto, Saburo Sone and Yasuhiko Nishioka :
Antibody-dependent cellular cytotoxicity against mesothelioma cells mediated by anti-HM 1.24 antibodies,
第52回日本呼吸器学会学術講演会, Apr. 2012. 柿内聡司, 埴淵昌毅, 後東久嗣, 豊田優子, 西條敦郎, 手塚敏史, 田岡隆成, 高橋正幸, 金山博臣, 西岡安彦 :
mTOR阻害剤投与症例における間質性肺障害の臨床的特徴,
第109回日本内科学会講演会, 2012年4月. 近藤真代, 豊田優子, 阿部秀一, 河野弘, 岸昌美, 竹﨑彰夫, 東桃代, 柿内聡司, 後東久嗣, 青野純典, 埴淵昌毅, 西岡安彦 :
病勢に関連してCA19-9の変動を認めた非結核性抗酸菌症の1例,
第20回日本呼吸器内視鏡学会中国四国支部会, 2012年3月. 香西博之, 手塚敏史, 河野弘, 竹﨑彰夫, 東桃代, 柿内聡司, 後東久嗣, 岸潤, 青野純典, 埴淵昌毅, 西岡安彦 :
非結核性抗酸菌症を合併したサルコイドーシスの1例,
第20回日本呼吸器内視鏡学会中国四国支部会, 2012年3月. 竹﨑彰夫, 西條敦郎, 大塚憲司, 岸昌美, 手塚敏史, 柿内聡司, 後東久嗣, 岸潤, 青野純典, 埴淵昌毅, 西岡安彦 :
当科で経験した肺胞出血4症例の臨床的検討,
第20回日本呼吸器内視鏡学会中国四国支部会, 2012年3月. 矢野祖, 近藤真代, 河野弘, 西條敦郎, 豊田優子, 柿内聡司, 岸潤, 埴淵昌毅, 西岡安彦, 古川貴大, 藤田浩司 :
神経サルコイドーシスの1例,
第244回徳島医学会学術集会, 2012年2月. 岡崎弘泰, 豊田優子, 岸潤, 河野弘, 柿内聡司, 後東久嗣, 埴淵昌毅, 吾妻雅彦, 榊美佳, 西岡安彦 :
組織診断が得られた肝サルコイドーシスの2症例,
第22回日本リウマチ学会中国・四国支部学術集会, 2011年12月. 阿部真治, 加藤幸成, 金子美華, 黄俊, 埴淵昌毅, 曽根三郎, 西岡安彦 :
悪性胸膜中皮腫に対する抗ポドプラニン抗体療法の検討,
第24回日本バイオセラピィ学会学術集会総会, 2011年12月. 大塚憲司, 豊田優子, 柿内聡司, 後東久嗣, 埴淵昌毅, 吾妻雅彦, 西岡安彦, 監﨑孝一郎, 福森知治, 坂東良美 :
多発結節影を呈したLangerhans cell histiocytosisの1例,
第105回日本内科学会四国地方会, 2011年11月. 近藤真代, 河野弘, 柿内聡司, 岸潤, 埴淵昌毅, 吾妻雅彦, 近藤絵里, 合田正和, 石丸直澄, 西岡安彦 :
IgG4関連下垂体炎の1例,
第105回日本内科学会四国地方会, 2011年11月. Yasuhiko Nishioka, Yukinari Kato, Masaki Hanibuchi and Saburo Sone :
Antimumor effects of anti-podoplanin antibody NZ-1 against malignant mesothelioma,
70th Annual Meeting of the Japanese Cancer Association, Oct. 2011. Le T. Dat, Taisuke Matsuo, Tetsuro Yoshimaru, Takuya Kuramoto, Masaki Hanibuchi, Hisatsugu Goto, Souji Kakiuchi, Yasuhiko Nishioka, Saburo Sone and Toyomasa Katagiri :
Genome-wide gene expression profiling analysis of bone metastases of human non-smal cell lung cancer (NSCLC) in mice,
70th Annual Meeting of the Japanese Cancer Association, Oct. 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. 高橋直希, 飛梅亮, 手塚敏史, 豊田優子, 東桃代, 後東久嗣, 柿内聡司, 岸潤, 青野純典, 埴淵昌毅, 吾妻雅彦, 曽根三郎, 西岡安彦, 高橋美紀子, 福田悠 :
間質性肺炎の精査により診断されたIgG4関連疾患の1例,
第46回日本呼吸器学会中国・四国地方会, 2011年7月. 香西博之, 豊田優子, 柿内聡司, 竹﨑彰夫, 岸昌美, 大塚憲司, 手塚敏史, 後東久嗣, 埴淵昌毅, 吾妻雅彦, 西岡安彦 :
気胸を合併した肺癌10例についての検討,
第50回日本肺癌学会中国・四国支部会, 2011年7月. 田岡隆成, 岸昌美, 竹﨑彰夫, 木下勝弘, 豊田優子, 柿内聡司, 埴淵昌毅, 井崎博文, 高橋正幸, 福森知治, 金山博臣, 西岡安彦 :
当院におけるmTOR阻害薬投与患者に発症した間質性肺炎の臨床的検討,
第46回日本呼吸器学会中国・四国地方会, 2011年7月. 埴淵昌毅 :
救急対応が必要な呼吸器・アレルギー疾患,
第2回徳島呼吸器・アレルギー研修セミナー, 2011年7月. 後東久嗣, アデルガブル, 埴淵昌毅, 倉本卓哉, 柿内聡司, 佐藤正大, 田畑祥, テバンチュン, 小川博久, 秋山伸一, 西岡安彦, 曽根三郎 :
ヒト肺癌転移モデルにおけるerlotinibの宿主介在性抗腫瘍効果の検討,
第20回日本がん転移学会学術集会, 2011年6月. 西岡安彦, 阿部真治, 加藤幸成, 木宿昌俊, 川添和義, 黄俊, 埴淵昌毅, 水口和夫, 曽根三郎 :
抗ポドプラニン抗体NZ-1の悪性胸膜中皮腫に対する抗体依存性細胞障害活性と抗腫瘍効果,
第15回日本がん分子標的治療学会学術集会, 2011年6月. バンテチュン, 埴淵昌毅, 後東久嗣, 柿内聡司, 倉本卓哉, レタンダー, 矢野聖二, 秋山伸一, 西岡安彦, 曽根三郎 :
血管新生阻害剤TSU-68の悪性胸膜中皮腫同所移植モデルにおける抗腫瘍効果の検討．,
第15回日本がん分子標的治療学会学術集会, 2011年6月. 木下勝弘, 佐藤正大, 後東久嗣, 柿内聡司, 埴淵昌毅, 吾妻雅彦, 西岡安彦, 曽根三郎 :
ベバシズマブが奏功した非小細胞肺癌の2症例,
第104回日本内科学会四国地方会, 2011年5月. 西岡安彦, 後東久嗣, 倉本卓哉, 柿内聡司, 埴淵昌毅, 古垣耕, 曽根三郎 :
骨微小環境でのEGF受容体を標的とした肺癌の骨転移制御の検討．,
第13回癌と骨病変研究会, 2010年11月. Yasuhiko Nishioka, Hisatsugu Goto, Kuramoto Takuya, Souji Kakiuchi, Masaki Hanibuchi, Yano Seiji and Sone Saburo :
Bone metastasis of lung cancer and its molecular-targeted therapy.,
第69回日本癌学会学術総会, Sep. 2010. チュンバンテ, 後東久嗣, 埴淵昌毅, 柿内聡司, レタンダー, 矢野聖二, 秋山伸一, 西岡安彦, 曽根三郎 :
血管新生阻害剤TSU-68の悪性胸膜中皮腫同所移植モデルにおける抗腫瘍効果の検討．,
第14回日本がん分子標的治療学会学術集会, 2010年7月. 後東久嗣, アデルガブル, 埴淵昌毅, 倉本卓哉, チュンバンテ, 小川博久, 柿内聡司, 佐藤正大, 飛梅亮, 秋山伸一, 西岡安彦, 曽根三郎 :
ヒト肺癌転移モデスにおけるerlotinibの宿主介在性腫瘍効果の検討．,
第19回日本がん転移学会学術集会, 2010年6月. 柿内聡司, 組橋由記, 埴淵昌毅, 後東久嗣, 富本英樹, 豊田優子, 坂口暁, 多田浩也, 西岡安彦, 曽根三郎 :
PRO評価に基づいた肺癌薬物療法の有用性の検討.,
第107回日本内科学会総会・講演会, 2010年4月.

研究会・報告書: 後東久嗣, Gabr Gomaa Mohammed Adel, 埴淵昌毅, 倉本卓哉, 小川博久, 田畑祥, Van The Trung, 柿内聡司, 秋山伸一, 曽根三郎, 西岡安彦 :
ヒト肺癌転移モデルにおけるerlotinibの骨転移抑制効果の検討．,
第14回癌と骨病変研究会, 2011年11月.

特許: 研究者総覧に該当データはありませんでした。
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: 肺がん微小環境の新たな標的：線維細胞を基軸とした薬剤耐性克服と革新的治療への展開 (研究課題/領域番号: 16H05309 )
肺癌・中皮腫の微小環境に着目したベバシズマブの耐性関連バイオマーカーの探索 (研究課題/領域番号: 26461191 )
周波数走査型離散フーリエ変換分光法～THz及び近赤外領域における実証と応用展開～ (研究課題/領域番号: 26246031 )
ヒト肺がん脳転移モデルを用いた新規脳転移療法開発のための探索的研究 (研究課題/領域番号: 24591166 )
同所移植ヒト悪性胸膜中皮腫モデルを用いた新規抗血管新生療法の探索 (研究課題/領域番号: 22390166 )
肺癌転移の臓器微小環境特性から見た分子標的治療法の開発 (研究課題/領域番号: 17016051 )
肺癌の悪性化にかかわる複数因子を分子標的とした抗体治療 (研究課題/領域番号: 16790445 )
肺がんの転移・血管新生分子を標的とした生物学的制御法開発 (研究課題/領域番号: 12217099 )
研究者番号（80335794）による検索

その他: 研究者総覧に該当データはありませんでした。

研究者総覧で最新データを確認する

2024年5月17日更新

専門分野・研究分野: 内科学 (Internal Medicine)
呼吸器病学 (Respiratory Disease)
所属学会・所属協会: 社団法人日本内科学会
日本肺癌学会中国・四国支部
日本呼吸器内視鏡学会
日本呼吸器学会中国・四国支部
社団法人日本呼吸器学会
日本内科学会四国支部
日本がん治療認定医機構
日本禁煙学会
日本結核病学会
委員歴・役員歴: 社団法人日本内科学会 (認定内科医 [2001年9月〜2018年3月])
日本肺癌学会中国・四国支部 (評議員 [2004年7月〜2009年7月])
日本呼吸器内視鏡学会 (評議員 [2009年4月〜2011年3月])
日本呼吸器学会中国・四国支部 (代議員 [2004年7月〜2017年7月])
社団法人日本呼吸器学会 (代議員 [2012年4月〜2018年1月])
日本内科学会四国支部 (評議員 [2007年5月〜2016年5月])
社団法人日本内科学会 (総合内科専門医 [2015年12月〜2021年3月])
日本呼吸器内視鏡学会 (気管支鏡専門医 [2003年12月〜2018年12月])
日本呼吸器内視鏡学会 (気管支鏡指導医 [2008年11月〜2018年12月])
社団法人日本呼吸器学会 (呼吸器専門医 [2004年10月〜2017年3月])
社団法人日本呼吸器学会 (指導医 [2011年12月〜2017年3月])
日本がん治療認定医機構 (がん治療認定医 [2008年4月〜2018年3月])
日本がん治療認定医機構 (暫定教育医 [2007年8月〜2017年7月])
日本禁煙学会 (認定指導医 [2013年8月〜2018年8月])
日本結核病学会 (結核・抗酸菌症認定医 [2014年3月〜2019年2月])
社団法人日本内科学会 (指導医 [2003年9月〜2005年8月])
社団法人日本内科学会 (指導医 [2007年9月〜2015年8月])
社団法人日本呼吸器学会 (広報委員会委員 [2008年6月〜2010年4月])
社団法人日本呼吸器学会 (細胞・分子生物学学術部会プログラム委員 [2012年6月〜2014年6月])
日本呼吸器学会中国・四国支部 (幹事 [2016年7月〜2018年7月])
社団法人日本呼吸器学会 (広報委員会委員 [2016年4月〜2018年4月])
社団法人日本呼吸器学会 (専門医制度審議会資格審査委員会委員 [2016年4月〜2018年4月])
日本呼吸器学会中国・四国支部 (事務局 [2011年3月〜2017年3月])
受賞: 1998年1月, 三木康楽賞 (財団法人三木康楽会)
2014年1月, 三木康楽賞 (財団法人三木康楽会)
活動: 予防接種健康被害調査委員会に係る専門医師 (委員 [2012年4月〜2017年3月])
徳島県社会保険診療報酬請求審査委員会 (審査委員 [2005年6月〜9月])
徳島県災害医療コーディネーター (専門部門災害医療コーディネーター [2014年3月〜2018年3月])
徳島県生活習慣病管理指導協議会肺がん部会 (委員 [2015年4月〜2016年3月])
徳島県がん教育総合支援事業協議会 (委員 [2015年7月〜2016年6月])
徳島県生活習慣病管理指導協議会肺がん部会 (委員 [2007年4月〜2009年4月])
徳島県社会保険診療報酬請求審査委員会 (審査委員 [2011年6月〜2014年7月])
阿南市予防接種健康被害調査委員会 (委員 [2015年3月〜2016年3月])
徳島市医師会COPD対策・禁煙推進委員会 (委員 [2013年6月〜2018年6月])
小松島市・勝浦郡1市2町結核対策委員会 (委員 [2006年4月〜12月])
徳島県身体障害者更生相談嘱託医 ( [2004年4月〜2005年3月])
公益社団法人医療系大学間共用試験実施評価機構医学系CBT実施少委員会ブラッシュアップ専門部会 (委員 [2014年6月〜6月])
徳島県がん対策連絡会議 (委員 [2015年9月〜2017年8月])
徳島がん対策センター (センター長 [2015年4月〜2017年3月])
徳島県がん診療連携協議会 (会長 [2015年4月〜2017年3月])
医師・医療関係者とがん患者会等とのネットワーク構築事業 (委員 [2015年6月〜2017年3月])
災害時における在宅酸素療法患者支援体制に関する検討会 (委員 [2015年1月〜2017年3月])
とくしまスクエア会議 (委員 [2012年10月〜2017年3月])
徳島大学病院社会保険委員会医科診療部門専門委員会委員長 (2014年4月〜2015年3月)
徳島大学病院がん診療連携センター長 (2015年4月〜2017年3月)

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更新

2024年5月18日更新

Ｊグローバル

Jグローバル最終確認日: 2024/5/18 01:07
氏名（漢字）: 埴淵昌毅
氏名（フリガナ）: ハニブチマサキ
氏名（英字）: Hanibuchi Masaki
所属機関: 旧所属徳島大学医学部医学科分子制御内科学講師

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2024年5月18日更新

研究者番号: 80335794

所属（現在）: 2024/4/1 : 徳島大学, 大学院医歯薬学研究部(医学域), 特任教授

所属（過去の研究課題 情報に基づく）*注記: 2018/4/1 : 徳島大学, 大学院医歯薬学研究部(医学系), 准教授
2016/4/1 : 徳島大学, 大学院医歯薬学研究部(医学系), 准教授
2015/4/1 – 2016/4/1 : 徳島大学, 大学院医歯薬学研究部, 准教授
2012/4/1 – 2014/4/1 : 徳島大学, ヘルスバイオサイエンス研究部, 准教授
2012/4/1 : 徳島大学, 大学院・ヘスルバイオサイエンス研究部, 准教授
2011/4/1 : 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 准教授
2007/4/1 – 2009/4/1 : 徳島大学, 医学部・歯学部附属病院, 講師
2006/4/1 : 徳島大, 医学部・歯学部附属病院, 講師
2003/4/1 – 2005/4/1 : 徳島大学, 医学部・歯学部附属病院, 講師
2002/4/1 : 徳島大学, 医学部, 助手

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 / 呼吸器内科学

研究代表者以外

生物系 / 医歯薬学 / 内科系臨床医学 / 呼吸器内科学
理工系 / 総合理工 / 応用物理学 / 光工学・光量子科学
生物系

キーワード

研究代表者

モノクローナル抗体療法 / 肺癌多臓器転移モデル / 薬剤耐性因子 / 遠隔転移因子 / PTHrP / 肺がん / 脳転移 / 血管新生 / 宿主因子

研究代表者以外

肺癌 / 血管新生 / PTHrP / VEGF / 癌性胸水 / VEGF受容体 / 骨転移 / 血管標的薬 / 多臓器転移 / 分子標的治療 / EGF受容体 / MMP / 臓器微小環境 / cDNAマイクロアレイ / 浸潤 / 樹状細胞 / 免疫遺伝子治療 / KAI1 / CD82 / ガングリオシド / 抗体療法 / 免疫療法 / 破骨細胞 / 可溶性VEGF受容体 / EGFR阻害薬 / 薬剤耐性 / 肝細胞増殖因子 / 抗HM1.24抗原 / HGF / マルチキナーゼ阻害薬 / 胸膜中皮腫 / organotropism / 抗PTHrP抗体 / ビスフォスフォネート / HM1.24抗原 / ADCC / 耐性 / ゲフィチニブ / マイクロアレイ / プロテオーム解析 / 脳転移 / 蛍光気管支鏡 / MYO18B / Src / CD9 / 非閉塞性肺疾患 / 悪性胸膜中皮腫 / 同所移植モデル / フーリエ変換分光 / テラヘルツ分光 / 赤外分光 / ガス分析 / 応用光学・量子光工学 / リモートセンシング / 量子エレクトロニクス / 血管新生阻害薬 / 血管新生阻害剤 / 線維細胞 / 肺がん / がん幹細胞 / 免疫チェックポイント / がん免疫 / 免疫チェックポイント分子

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研究者を探す

埴淵 昌毅

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研究代表者

研究代表者以外

研究代表者

研究代表者以外

埴淵昌毅