トップ›研究者一覧›成澤裕子

研究者を探す

研究者にアプローチする
更新情報を通知する

成澤裕子

徳島大学

プロフィール
教育活動
研究活動
社会活動
リサーチマップ・
Jグローバル
KAKEN
注目研究

研究者総覧で最新データを確認する

2024年11月15日更新

職名: 講師
電話: 088-633-9062
電子メール: narusawa.yuko@tokushima-u.ac.jp
学歴: 研究者総覧に該当データはありませんでした。
学位: 博士(医学) (香川大学) (2015年3月)
職歴・経歴: 2009/4: 香川大学医学部病理病態・生体防御医学講座腫瘍病理学技能補佐員
2015/12: 香川大学医学部病理病態・生体防御医学講座腫瘍病理学助教
2021/10: 株式会社四国細胞病理センター

専門分野・研究分野: 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11月15日更新

専門分野・研究分野: 研究者総覧に該当データはありませんでした。
担当経験のある授業科目: SIH道場~アクティブ・ラーニング入門~(医・保健) (共通教育)
保健環境学実習 (学部)
検査機器総論 (学部)
病理学Ⅰ(基礎) (学部)
病理学Ⅱ(応用) (学部)
病理検査学実習 (学部)
病理解析学演習 (大学院)
病理解析学特論 (大学院)
細胞診断学実習 (学部)
統合臨床検査学 (学部)
臨床技能実習 (学部)
臨床検査学入門 (共通教育)
臨床検査総論Ⅰ(臨床検査・尿検査・採血) (学部)
臨床検査総論Ⅱ(尿沈渣・便・体液・喀痰検査) (学部)
臨床検査総論実習 (学部)
解剖組織学実習 (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11月15日更新

専門分野・研究分野: 研究者総覧に該当データはありませんでした。

研究テーマ: 研究者総覧に該当データはありませんでした。

著書

研究者総覧に該当データはありませんでした。

論文

Aya Shinomiya, Juanjuan Ye, Keisuke Miyake, Yuko Narusawa, Takehiro Nakamura, Koichi Oshima, Yoko Matsuda and Takashi Tamiya :
Necropsy-confirmed case of cytokeratin-positive interstitial reticulum cell tumor in the skull bone.,
Pathology International, Vol.71, No.12, 856-859, 2021.

(キーワード): Aged, 80 and over / Autopsy / Diagnosis, Differential / Female / Fibroblasts / Humans / Immunohistochemistry / Keratins / Lymph Nodes / Neoplasms / Neoplasms, Bone Tissue / Skull
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/pin.13167
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34592039; ● Search Scopus @ Elsevier (PMID): 34592039; ● Search Scopus @ Elsevier (DOI): 10.1111/pin.13167

(DOI: 10.1111/pin.13167, PubMed: 34592039) Yamato Suemitsu, Yusuke Ono, Yusuke Mizukami, Juanjuan Ye, Keiko Yamakawa, Takeshi Takamoto, Yuko Narusawa, Yuri Mukai, Manabu Takamatsu, Atsuko Nakazawa, Mari Mino-Kenudson, Toshio Kumasaka and Yoko Matsuda :
Mutation and Genetic Heterogeneity.,
Frontiers in Oncology, Vol.11, 2021.

(要約): In conclusion, the clear and basophilic cells of the tumor were supposedly derived from the same clone and subsequently acquired additional mutations. This is the first report of clonal evolution in pancreatoblastoma.
(出版サイトへのリンク): ● Publication site (DOI): 10.3389/fonc.2021.725290
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34513702; ● Search Scopus @ Elsevier (PMID): 34513702; ● Search Scopus @ Elsevier (DOI): 10.3389/fonc.2021.725290

(DOI: 10.3389/fonc.2021.725290, PubMed: 34513702) Yuko Narusawa, Masanao Yokohira, Keiko Yamakawa, Juanjuan Ye, Misa Tanimoto, Linxuan Wu, Yuri Mukai, Katsumi Imaida and Yoko Matsuda :
Relationship between Lung Carcinogenesis and Chronic Inflammation in Rodents.,
Cancers, Vol.13, No.12, 2021.

(要約): mutations) have been widely studied. Animal studies have revealed that chronic inflammation significantly enhances lung carcinogenesis, and inhibition of inflammation suppresses cancer progression. Moreover, the reduction in tumor size by suppression of inflammation in animal experiments suggests that chronic inflammation influences the promotion of tumorigenesis. Here, we review rodent lung tumor models induced by various chemical carcinogens, including tobacco-related carcinogens, and transgenics, and discuss the roles of chronic inflammation in lung carcinogenesis.
(出版サイトへのリンク): ● Publication site (DOI): 10.3390/cancers13122910
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34200786; ● Search Scopus @ Elsevier (PMID): 34200786; ● Search Scopus @ Elsevier (DOI): 10.3390/cancers13122910

(DOI: 10.3390/cancers13122910, PubMed: 34200786) Haiyan Xu, Keizo Hiraishi, Lin-Hai Kurahara, Yuko Narusawa, Xiaodong Li, Yaopeng Hu, Yoko Matsuda, Heping Zhang and Katsuya Hirano :
Probio-M9 on Colitis-Associated Carcinogenesis by Restoration of the Gut Microbiota in a Mouse Model.,
Nutrients, Vol.13, No.4, 2021.

(要約): /day) was orally administered for 7 days. Animals were sacrificed at 20 weeks after AOM administration and immunohistochemical staining and Western blotting was performed. The α-diversity of microflora (Shannon index), principal coordinate analysis, and distribution of intestinal bacterium genera and metabolic pathways were compared. The AOM/DSS group showed weight loss, diarrhea, intestinal shortening, increased number of colon tumors, proliferating tumorigenesis, increased inflammation score, fibrosis, increased CD68+, or CD163+ macrophage cells in the subserosal layer of non-tumor areas. Inflammation and tumorigenesis ameliorated after Probio-M9 treatment. Fecal microbial functions were altered by AOM/DSS treatment. Probio-M9 significantly upregulated the fecal microbial diversity and reversed fecal microbial functions. Thus, Probio-M9 could suppress tumor formation in the large intestine by regulating the intestinal environment and ameliorating inflammation, suggesting its therapeutic potential for treatment of inflammation and colitis-associated tumorigenesis.
(キーワード): 発癌 (carcinogenesis) / Colitis / Colonic Neoplasms / Dextran Sulfate / Gastrointestinal Microbiome / Humans / Inflammation / Lacticaseibacillus rhamnosus / Male / Milk, Human / Neoplasms, Experimental
(出版サイトへのリンク): ● Publication site (DOI): 10.3390/nu13041143
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33808480; ● Search Scopus @ Elsevier (PMID): 33808480; ● Search Scopus @ Elsevier (DOI): 10.3390/nu13041143

(DOI: 10.3390/nu13041143, PubMed: 33808480) Masanao Yokohira, Minoru Oshima, Keiko Yamakawa, Juanjuan Ye, Yuko Narusawa, Reiji Haba, Yuki Fukumura, Kenichi Hirabayashi, Hiroshi Yamaguchi, Motohiro Kojima, Keiichi Okano, Yasuyuki Suzuki and Yoko Matsuda :
Adequate tissue sampling for the assessment of pathological tumor regression in pancreatic cancer.,
Scientific Reports, Vol.11, No.1, 2021.

(要約): Standardized pathological evaluation of the regression assessment of neoadjuvant pancreatic cancer is necessary to improve prognostication and compare treatment outcomes in clinical trials. However, appropriate tissue sampling from surgically resected pancreatic cancer after neoadjuvant therapy has not been elucidated. We compared the tumor regression scores in the largest cancer slide determined macroscopically or histologically. We reviewed all slides and macroscopic photos of cut surfaces from resected pancreas of patients treated with neoadjuvant chemotherapy (n = 137; chemoradiotherapy or chemotherapy). The tumor regression scores (the Evans, College of American Pathologists, Japanese Pancreas Society grading systems, and Area of Residual Tumor [ART] score) were evaluated for the largest tumor slide determined by macroscopy or histologically as well as all slides from the resected pancreas. The largest cancer slides determined macroscopically and histologically were discrepant in 26% of the cases. Cancer cells were not detected in the largest macroscopically defined cut slides in 3%. Only ART scores assessed in the largest histological slides displayed significant difference in overall survival. We recommend obtaining the largest histological slides to provide adequate assessment for regression of neoadjuvant-treated pancreatic cancer. Sufficient sampling to detect the largest histological slides would be mandatory.
(キーワード): Aged / Aged, 80 and over / Biopsy / Clinical Decision-Making / Disease Management / Disease Progression / Female / Humans / Kaplan-Meier Estimate / Male / Middle Aged / Neoplasm Grading / Neoplasm Staging / Pancreatic Neoplasms / Prognosis / Time Factors
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/s41598-021-86152-y
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33753833; ● Search Scopus @ Elsevier (PMID): 33753833; ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-021-86152-y

(DOI: 10.1038/s41598-021-86152-y, PubMed: 33753833) Keiko Yamakawa, Juanjuan Ye, Yuko Narusawa and Yoko Matsuda :
Pathological Changes in Pancreatic Carcinogenesis: A Review.,
Cancers, Vol.13, No.4, 2021.

(要約): Despite advances in diagnostics and therapeutics, the prognosis of pancreatic cancer remains dismal. Because of a lack of early diagnostic methods, aggressive local progression, and high incidence of distant metastasis, most pancreatic cancers are inoperable; therefore, the characteristics of early pancreatic cancer have not been well understood. Autopsy studies revealed the characteristics of prediagnostic pancreatic malignancies, including precancerous lesions, early stage pancreatic cancer, and pancreatic cancer without clinical symptoms (occult cancers). Animal models using hamsters and genetically engineered mice have focused on mechanisms of carcinogenesis, thereby providing insights into risk factors and prevention and serving as a preclinical test for the development of novel diagnostic and treatment modalities. In this review, we have summarized pathological changes in the pancreas of humans and experimental animals during carcinogenesis.
(出版サイトへのリンク): ● Publication site (DOI): 10.3390/cancers13040686
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33567676; ● Search Scopus @ Elsevier (PMID): 33567676; ● Search Scopus @ Elsevier (DOI): 10.3390/cancers13040686

(DOI: 10.3390/cancers13040686, PubMed: 33567676) Keiko Yamakawa, Masanao Yokohira, Yuko Narusawa, Sosuke Kishi, Shohei Kanie and Katsumi Imaida :
Activation of MEK1/2-ERK1/2 signaling during NNK-induced lung carcinogenesis in female A/J mice.,
Cancer Medicine, Vol.5, No.5, 903-913, 2016.

(要約): The extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway is activated by several growth factors and mitogens, and upregulation has been noted in many human cancers, including examples in the lung. In this study, to study the association of ERK1/2 activation with mutation of Kras encoding an upstream activator of ERK1/2 in lung premalignant lesions, we immunohistochemically examined expression of phosphorylated forms of ERK1/2 (pERK1/2) and MAP/ERK kinase 1/2 (pMEK1/2) proteins and correlation between ERK activation and mutation of Kras encoding an upstream activator of ERK1/2, in a mouse lung carcinogenesis model. Female 7-week-old A/J mice were administered a single dose of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), then maintained without additional treatment until sacrifice at week 52. Histopathologically, adenocarcinomas, adenomas and hyperplasias were observed in the lung. pMEK1/2 was expressed mostly in the cell cytoplasm in all three. In contrast, pERK1/2-positive cells were also relatively rare in any histological types as compared with level of pMEK1/2 expression. However, pERK1/2-positive cells in adenocarcinoma were still markedly more common than in hyperplasias and adenomas (~5-fold, ~4-fold; P < 0.01). Activating mutations of Kras gene at codons 12, 13 and 61 were detected in the majority of adenomas and adenocarcinomas, but without any significant relation to pERK1/2 expression. These results suggest that activation of ERK1/2 plays a key role in malignant transformation during lung carcinogenesis featuring Kras mutaion. Activation of ERK1/2 in lung premalignant lesions was little regardless of the mutation of Kras, and ERK1/2 activation in NNK-induced mouse lung carcinogenesis may be regulated not only by Kras mutation but also other signaling pathway or regulatory factor.
(キーワード): Adenocarcinoma / Adenocarcinoma of Lung / Adenoma / Animals / Cell Transformation, Neoplastic / Enzyme Activation / Female / Lung Neoplasms / MAP Kinase Kinase Kinase 1 / MAP Kinase Kinase Kinase 2 / MAP Kinase Signaling System / Mice, Inbred A / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / Mutation / Nitrosamines / Proliferating Cell Nuclear Antigen / Proto-Oncogene Proteins p21(ras)
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/cam4.652
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26864819; ● Search Scopus @ Elsevier (PMID): 26864819; ● Search Scopus @ Elsevier (DOI): 10.1002/cam4.652

(DOI: 10.1002/cam4.652, PubMed: 26864819) Masanao Yokohira, Nozomi Hashimoto, Toshitaka Nakagawa, Yuko Narusawa, Keiko Yamakawa, Sosuke Kishi, Shohei Kanie, Fumiko Ninomiya, Kousuke Saoo and Katsumi Imaida :
Long-Term Chronic Toxicity and Mesothelial Cell Reactions Induced by Potassium Octatitanate Fibers (TISMO) in the Left Thoracic Cavity in A/J Female Mice.,
International Journal of Toxicology, Vol.34, No.4, 325-335, 2015.

(要約): The present study was conducted to examine the chronic effects of potassium octatitanate fibers (trade name TISMO; chemical formula K2O·6TiO2) on the mouse lung and thoracic cavity. This method of infusion was employed to examine the direct effects of the fibers to the pleura. In the present study, 52- and 65-week experiments were employed to examine the long-term chronic effects after infusion of fiber-shaped TISMO into the thoracic cavities of A/J mice. Following this infusion, TISMO fibers were observed in the alveoli, indicating penetration through the visceral pleura. The additional histopathological detection of TISMO fibers in the liver, spleen, kidneys, ovary, heart, bone marrow, and brain of TISMO-infused mice indicated migration of the fibers out from the thoracic cavity. Atypical mesothelial cells with severe pleural proliferation were observed, but malignant mesotheliomas were not detected. This study demonstrated that intrathoracic infusion of TISMO fiber did not cause malignant mesothelioma but did cause severe chronic inflammation and proliferation of pleural mesothelial cells.
(キーワード): Animals / Epithelial Cells / Female / Kidney / Liver / Lung / Lung Neoplasms / Mesothelioma / Mesothelioma, Malignant / Mice / Mice, Inbred A / Organ Size / Pleura / Spleen / Thoracic Cavity / Titanium / Toxicity Tests, Chronic
(出版サイトへのリンク): ● Publication site (DOI): 10.1177/1091581815587744
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26023052; ● Search Scopus @ Elsevier (PMID): 26023052; ● Search Scopus @ Elsevier (DOI): 10.1177/1091581815587744

(DOI: 10.1177/1091581815587744, PubMed: 26023052) Yuko Narusawa, Masanao Yokohira, Nozomi Hashimoto, Keiko Yamakawa, Sosuke Kishi, Fumiko Ninomiya, Shohei Kanie, Kousuke Saoo and Katsumi Imaida :
Rat strain differences in levels and effects of chronic inflammation due to intratracheal instillation of quartz on lung tumorigenesis induced by DHPN.,
Experimental and Toxicologic Pathology, Vol.66, No.8, 391-401, 2014.

(要約): Chronic inflammatory effects of single intratracheal instillation (i.t.) of quartz on rat lung tumorigenesis were examined using 4 different animal models. At first, in order to determine an appropriate dose of quartz i.t. to promote lung tumorigenesis, F344 male rats were administrated single 0, 0.5, 1, 2 or 4 mg quartz/rat after initiation by N-bis(2-hydroxypropyl) nitrosamine (DHPN). Further studies were performed to examine strain differences of the effects of chronic inflammation caused by quartz i.t. in 3 strains of rat, i.e. F344, Wistar-Hannover and SD. Each was instilled with 2mg quartz/rat after DHPN administration and sacrificed in week 24. In addition, strain differences in generation of inflammation were determined at days 1 and 28. Finally, for determination of long-term effects period, F344 and Wistar-Hannover rats were similarly treated, but the experiment was terminated at week 52. In F344 rats, the tumor areas in DHPN treated groups showed a tendency to increase along with the dose of quartz. F344 rats demonstrated the highest and Wistar-Hannover rats the lowest sensitivity to quartz in acute and chronic phases in the 3 strains. In 52 week, in F344 rats, the multiplicity of tumors and the serum concentration of IL-6 in the group treated with DHPN and quartz were significantly increased. The present experiments indicated that chronic inflammation due to quartz instillation exerted promoting effects on lung carcinogenesis in F344, SD and Wistar-Hannover rats. The strain differences in tumor promotion appeared to correlate with inflammatory reactions to quartz and increase of IL-6.
(キーワード): Animals / Carcinogenesis / Carcinogens / Inflammation / Lung / Lung Neoplasms / Male / Nitrosamines / Quartz / Rats / Rats, Inbred F344 / Rats, Sprague-Dawley / Rats, Wistar
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.etp.2014.06.002
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25024166; ● Search Scopus @ Elsevier (PMID): 25024166; ● Search Scopus @ Elsevier (DOI): 10.1016/j.etp.2014.06.002

(DOI: 10.1016/j.etp.2014.06.002, PubMed: 25024166) Masanao Yokohira, Keiko Yamakawa, Yuko Narusawa, Takamasa Numano, Fumio Furukawa, Sosuke Kishi, Fumiko Ninomiya, Shohei Kanie, Hiroko Hitotsumachi, Kousuke Saoo and Katsumi Imaida :
Immunohistochemical characteristics of surfactant proteins a, B, C and d in inflammatory and tumorigenic lung lesions of f344 rats.,
Journal of Toxicologic Pathology, Vol.27, No.3-4, 175-182, 2014.

(要約): Surfactant proteins (SPs), originally known as human lung surfactants, are essential to respiratory structure and function. There are 4 subtypes, SP-A, SP-B, SP-C and SP-D, with SP-A and SP-D having immunological functions, and SP-B and SP-C having physicochemical properties that reduce the surface tension at biological interfaces. In this experiment, the expressions of SP-A, SP-B, SP-C and SP-D in lung neoplastic lesions induced by N-bis (2-hydroxypropyl) nitrosamine (DHPN) and inflammatory lesions due to quartz instillation were examined and compared immunohistochemically. Formalin fixed paraffin embedded (FFPE) lung samples featuring inflammation were obtained with a rat quartz instillation model, and neoplastic lesions, hyperplasias and adenomas, were obtained with the rat DHPN-induced lung carcinogenesis model. In the rat quartz instillation model, male 10-week old F344 rats were exposed by intratracheal instillation (IT) to quartz at a dose of 2 mg/rat suspended in saline (0.2 ml) on day 0, and sacrificed on day 28. Lung tumorigenesis in F344 male rats was initiated by DHPN in drinking water for 2 weeks, and the animals were then sacrificed in week 30. Lung proliferative lesions, hyperplasias and adenomas, were observed with DHPN, and inflammation was observed with quartz. The expressions of SP-A, SP-B, SP-C and SP-D were examined immunohistochemically. SP-B and SP-C showed strong expression in lung hyperplasias and adenomas, while SP-A and SP-D were observed in mucus or exudates in inflammatory alveoli. These results suggest the possibility that SP-B and SP-C are related to lung tumorigenesis.
(出版サイトへのリンク): ● Publication site (DOI): 10.1293/tox.2014-0020
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25378802; ● Search Scopus @ Elsevier (PMID): 25378802; ● Search Scopus @ Elsevier (DOI): 10.1293/tox.2014-0020

(DOI: 10.1293/tox.2014-0020, PubMed: 25378802) Masanao Yokohira, Sosuke Kishi, Keiko Yamakawa, Yuko Narusawa, Fumiko Ninomiya, Shigemi Kinouch, Junko Tanizawa, Kousuke Saoo and Katsumi Imaida :
Napsin A is possibly useful marker to predict the tumorigenic potential of lung bronchiolo-alveolar hyperplasia in F344 rats.,
Experimental and Toxicologic Pathology, Vol.66, No.2-3, 117-123, 2013.

(要約): There are 2 types of bronchiolo-alveolar hyperplasia found in rat lungs. One is 'inflammatory hyperplasia' with a potential to recover in future with removal of the stimulating insult and the other is 'latent tumorigenic hyperplasia' as an independent preneoplastic lesion for adenocarcinoma. In the present experiment, we focused on rat lung bronchiolo-alveolar hyperplasia induced by 4-(methyl-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK), which decreases with time after induction and reverts to normal, or by N-bis(2-hydroxypropyl)nitrosamine (DHPN), with tumorigenic potential to progress to adenoma and adenocarcinoma. Though NNK is a typical carcinogen inducing lung adenocarcinoma in female A/J mice, the tumorigenic potential by NNK in rats is weak. Differences between hyperplasias induced by DHPN and by NNK were here examined immunohistochemically. Formalin fixed paraffin embedded lung samples with hyperplastic and inflammatory lesions were obtained from rats exposed to DHPN or NNK and from lung inflammation models induced with fine particles like CuO, NiO and quartz. The 19 markers were examined immunohistochemically. Napsin A, in the inflammatory lesions and hyperplasia induced by NNK, was positive for macrophages and secretions in the alveoli spaces but less so in the walls of the alveoli. In the proliferative lesions including hyperplasia induced by DHPN, strong positive staining for napsin A was observed in the walls of the alveoli. Thus high expression was suggested to be possibly useful for detecting tumorigenic potential of rat lung hyperplasia.
(キーワード): Adenocarcinoma / Adenocarcinoma of Lung / Adenoma / Animals / Aspartic Acid Endopeptidases / Biomarkers, Tumor / Bronchioles / Hyperplasia / Immunohistochemistry / Lung / Lung Neoplasms / Nitrosamines / Prognosis / Pulmonary Alveoli / Rats / Rats, Inbred F344
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.etp.2013.11.002
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24295539; ● Search Scopus @ Elsevier (PMID): 24295539; ● Search Scopus @ Elsevier (DOI): 10.1016/j.etp.2013.11.002

(DOI: 10.1016/j.etp.2013.11.002, PubMed: 24295539) Fumiko Ninomiya, Masanao Yokohira, Sosuke Kishi, Yuko Narusawa, Keiko Yamakawa, Tatsushi Inoue, Toshiya Kuno and Katsumi Imaida :
Gender-dependent effects of gonadectomy on lung carcinogenesis by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in female and male A/J mice.,
Oncology Reports, Vol.30, No.6, 2632-2638, 2013.

(要約): The present study was conducted to investigate the effects of gonadectomy on lung carcinogenesis in female and male mice, and to determine an association between sex hormone and lung carcinogenesis. Female and male A/J mice were divided into gonadectomized and unoperated control groups and all animals were treated intraperitoneally with 1 or 2 injections of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) at the dose of 2 mg/mouse. The mice were sacrificed 18 or 56 weeks after surgery. Serum levels of estradiol in females and testosterone in males were confirmed to be decreased by gonadectomy. Lung white nodules were detected in all mice of all groups. In the control groups of 18- and 56-week studies, the multiplicities of lung nodules in females were significantly greater than in males. In males in the 56-week study, the multiplicity of macroscopical lung nodules, bronchiolo-alveolar hyperplasias, adenomas and tumors (adenomas and adenocarcinomas) showed significant increase with castration. In females in the 18-week study, the multiplicity of adenomas decreased significantly by ovariectomy. Based on the results of the present study, female A/J mice were confirmed to be more susceptible to NNK-induced lung carcinogenesis than males. Furthermore, it was suggested that the process is inhibited by testosterone and accelerated by estradiol. These findings indicate the possibility that sex hormones play important roles in determining sex differences in lung carcinogenesis in the A/J mice initiated by NNK.
(キーワード): Adenocarcinoma / Adenoma / Animals / Carcinogenesis / Estradiol / Female / Humans / Hyperplasia / Lung / Lung Neoplasms / Male / Mice / Neoplasms, Hormone-Dependent / Nitrosamines / Orchiectomy / Ovariectomy / Sex Characteristics / Testosterone
(出版サイトへのリンク): ● Publication site (DOI): 10.3892/or.2013.2759
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24085151; ● Search Scopus @ Elsevier (PMID): 24085151; ● Search Scopus @ Elsevier (DOI): 10.3892/or.2013.2759

(DOI: 10.3892/or.2013.2759, PubMed: 24085151) Masanao Yokohira, Yuko Narusawa, Keiko Yamakawa, Sosuke Kishi, Fumiko Ninomiya, Kousuke Saoo and Katsumi Imaida :
Strain differences in pleural mesothelial cell reactions induced by potassium octatitanate fibers (TISMO) infused directly into the thoracic cavity.,
Experimental and Toxicologic Pathology, Vol.65, No.6, 925-932, 2013.

(要約): Although we have previously reported that the fiber-shaped TISMO, morphologically similar to asbestos, can induce a severe mesothelial reaction in A/J mice, it is important to clarify any strain differences. In the present study, female A/J, C3H/HeN, ICR and C57BL/6 mice were therefore employed as test strains. At the beginning of the experiment, all mice underwent a left thoracotomy and direct administration of 3mg of TISMO particles suspended in 0.2 ml saline into the left thorax. The experiment was terminated after 21 weeks and all groups were sacrificed and the mesothelium and main organs were examined histopathologically. To contribute to mechanistic analysis, iron staining with Berlin blue and Turnbull's blue, and immunostaining for calretinin were also performed. The present experiment demonstrated only minor strain differences in the degree of pleural reaction to TISMO. However, there was clear variation in the iron and lymphocyte accumulation in the pleura and in the liver. This difference in response to TISMO fibers in vivo is important information when considering the development of mesothelioma as an animal model and the extrapolation to human risk from such animal studies.
(キーワード): Animals / Body Weight / Epithelium / Female / Immunohistochemistry / Infusion Pumps / Kidney / Liver / Lung / Mice / Organ Size / Particle Size / Pleural Cavity / Species Specificity / Titanium
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.etp.2013.01.006
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23375775; ● Search Scopus @ Elsevier (PMID): 23375775; ● Search Scopus @ Elsevier (DOI): 10.1016/j.etp.2013.01.006

(DOI: 10.1016/j.etp.2013.01.006, PubMed: 23375775) Masanao Yokohira, Yuko Narusawa, Nozomi Hashimoto, Keiko Yamakawa, Fumiko Ninomiya, Sosuke Kishi, Kousuke Saoo and Katsumi Imaida :
Toxicity of nicotine by repeated intratracheal instillation to f344 rats.,
Journal of Toxicologic Pathology, Vol.25, No.4, 257-263, 2012.

(要約): In vivo, nicotine in cigarette smoke induces various effects not only on the respiratory system but also the central and peripheral nerve systems, circulatory organs and digestive organs, and there is a possibility of promotion of lung tumorigenesis. The present experiment was conducted to examine histopathological changes caused by nicotine in the lung with repeated intratracheal instillation (i.t.). Six-week-old male F344 rats were administered nicotine by i.t. at doses of 0.05, 0.1 and 0.2 mg nicotine/rat every 3 weeks beginning at week 4, for up to a total of 9 times and were then sacrificed at week 30. The total number of administrations, total dose of nicotine and effective number of rats were 9 times, 0.45 mg and 5 rats and 4 times, 0.20 mg and 5 rats for the 0.05 mg nicotine/rat group; 3 times, 0.30 mg and 5 rats and 4 times, 0.40 mg and 3 rats for the 0.1 mg group; and 3 times, 0.60 mg and 3 rats for the 0.2 mg group, respectively. As a control group, 5 rats were administered 0.2 ml saline/rat 9 times. Some rats administered 0.1 and 0.2 mg nicotine suffered convulsions just after administration. Histopathologically, though proliferative changes were not observed, neutrophil infiltration, edema and fibrosis in the lung were induced by nicotine. In conclusion, repeated treatment of nicotine promoted neurologic symptoms in the acute phase, and strong inflammation in the lungs in the chronic phase, even at a low dose. Toxicity of nicotine is suggested to depend not on total dose of nicotine in the experiment but rather on repeated injury with consecutive administration.
(出版サイトへのリンク): ● Publication site (DOI): 10.1293/tox.25.257
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23345928; ● Search Scopus @ Elsevier (PMID): 23345928; ● Search Scopus @ Elsevier (DOI): 10.1293/tox.25.257

(DOI: 10.1293/tox.25.257, PubMed: 23345928) Satoshi Suzuki, Masanao Yokohira, Nozomi Hashimoto, Kousuke Saoo, Yoko Matsuda, Keiko Yamakawa, Yuko Narusawa, Toshiya Kuno and Katsumi Imaida :
Different threshold levels for 2-amino-3,8 dimethylimidazo[4,5-f]quinoxaline (MelQx) initiation of lung and colon carcinogenesis and the effects of an additional initiation by 4 (methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in A/J mice.,
Molecular Medicine Reports, Vol.3, No.2, 301-307, 2010.

(要約): The existence of possible threshold dose levels of genotoxic carcinogens for carcinogenesis is of particular interest for human risk assessment. Recently, no observed effect levels (NOELs) for various hepatocarcinogens have been reported. However, reports on threshold levels for lung carcinogenesis have hitherto been lacking. In the present study, we first investigated low dose response lung and colon carcinogenesis with a food-derived genotoxic carcinogen, 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) (0, 0.01, 0.1, 1, 10 and 100 ppm in the diet) alone for 32 weeks using female A/J mice. The endpoints were histopathologically diagnosed hyperplasias and adenomas in the lung, and aberrant crypt foci (ACF) in the colon. The results showed NOELs of 100 and 1 ppm, respectively. We next investigated the effect of additional pre-treatment with 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) (2 mg/mouse, single dose, intraperitoneal injection) prior to the low-dose application of MeIQx (0, 0.01, 0.1, 1, 10, 100 and 600 ppm in the diet) for 32 weeks. Lung lesions were significantly increased in the NNK + MeIQx (1 ppm) group, but not in the NNK + MeIQx (10 ppm) groups. Since the dose-response curve was not of so-called 'hockey stick type', it was not possible to determine a NOEL for lung tumorigenesis. Significant increase in the mRNA expression of CYP2A5, a major metabolic enzyme for NNK, was also observed in the NNK + MeIQx (1 ppm) group, and a similar pattern was noted for O6-methylguanine DNA methyltransferase (MGMT). By contrast, the formation of colon ACF showed a dose-dependent increase. The NOEL for the formation of colon ACF was considered to be 10 ppm MeIQx with NNK. These results suggest that MeIQx may have different threshold dose levels for the induction of lung tumorigenic lesions and ACF formation in the colon. Pre-treatment with NNK, a potent lung carcinogen, concealed the effects of MeIQx in the lung, but exerted minimal influence in the colon. CYP2A5 and MGMT expression may be of importance, particularly in the lung. The present study provides critical suggestions for the human risk assessment of genotoxic carcinogens.
(出版サイトへのリンク): ● Publication site (DOI): 10.3892/mmr_00000255
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21472237; ● Search Scopus @ Elsevier (PMID): 21472237; ● Search Scopus @ Elsevier (DOI): 10.3892/mmr_00000255

(DOI: 10.3892/mmr_00000255, PubMed: 21472237) Keiko Yamakawa, Toshiya Kuno, Nozomi Hashimoto, Masanao Yokohira, Satoshi Suzuki, Yuko Narusawa, Kousuke Saoo and Katsumi Imaida :
Molecular analysis of carcinogen-induced rodent lung tumors: Involvement of microRNA expression and Krαs or Egfr mutations.,
Molecular Medicine Reports, Vol.3, No.1, 141-147, 2010.

(要約): Genetic and epigenetic alterations play a key role in lung carcinogenesis, and a high frequency of KRAS and epidermal growth factor receptor (EGFR) mutations have been observed in human lung cancers. Recent evidence indicates that the expression of specific microRNAs (miRNAs) may be involved. In rodent lung carcinogenesis models, Kras mutations are frequently observed, whereas genetic alteration of the Egfr gene is generally rare. Since little is known regarding the involvement of miRNAs in rodent lung carcinogenesis, the present study of miRNA expression levels in the liver and lung during 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)- and 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx)-induced lung tumorigenesis in A/J mice was conducted. In addition, incidences of Egfr and Kras gene mutations in rat and mouse lung tumors induced by the chemical carcinogens NNK, MeIQx and N-bis(2?hydroxypropyl)nitrosamine (DHPN) were examined. Three miRNAs, let-7a, miR-34c and miR-125a-5p, were selected for attention. In rat lung tumors, one silent mutation was detected in the Egfr gene exon 20 (AAC↷AAT; N772). Activating mutations of the Krαs gene at codon 12 were detected in neoplastic lesions induced by NNK (5/6, 83%), MeIQx (1/1, 100%) and DHPN (7/15, 47%), all resulting in G/C↷A/T transitions. NNK or MeIQx administration reduced the expression of miR-125a-5p (MeIQx alone group, 86.3%; MeIQx + NNK group, 83.6%; p<0.05, at day 15) and let-7a (MeIQx + NNK group, 56.3%; p<0.001, at day 22) in the liver. miR-34c was up-regulated 3.5-fold with NNK treatment as compared to the control group (p<0.001). These findings raise the possibility that aberrant expression of miRNA is involved in lung tumorigenesis, at least in its early stages.
(出版サイトへのリンク): ● Publication site (DOI): 10.3892/mmr_00000231
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21472213; ● Search Scopus @ Elsevier (PMID): 21472213; ● Search Scopus @ Elsevier (DOI): 10.3892/mmr_00000231

(DOI: 10.3892/mmr_00000231, PubMed: 21472213)

MISC

研究者総覧に該当データはありませんでした。

総説・解説: 研究者総覧に該当データはありませんでした。
講演・発表: Hiroto Nishio, Yuko Narusawa, Kensaku Aki, Motoki Sugasaki, Takayuki Nakao, Takeshi Oya and Michiko Yamashita :
Efficacy of Aether AIHema in Teaching Clinical Hematology to Undergraduate Medical Laboratory Science Students,
ASCPaLM 2024, Seoul, Sep. 2024. 山下菜々美, 瀧井友梨恵, 大原菜摘, 成澤裕子, 小野晃代, 中西一世, 渡邉俊介, 笠井孝彦, 桑山泰治, 片㘴諒, 森河由里子, 坂東良美, 上原久典, 山下理子 :
原発不明癌の腹膜播種と考えらえた一例,
徳島臨床細胞学会学術集会抄録集, 2024年3月.

研究会・報告書: 重清咲良, 米澤彩花, 髙尾正一郎, 成澤裕子, 山下理子 :
Bz-X800 Analyzerを用いた骨髄脂肪細胞の定量的解析の試み,
徳島県臨床衛生検査技師会誌, 19, 2023年12月. 米澤彩花, 重清咲良, 成澤裕子, 山下理子 :
骨髄外脂肪における膠様変性の検討,
徳島県臨床衛生検査技師会誌, 18, 2023年12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: 研究者総覧に該当データはありませんでした。

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11月15日更新

専門分野・研究分野: 研究者総覧に該当データはありませんでした。
所属学会・所属協会: 日本癌学会
日本臨床衛生検査技師会
日本臨床細胞学会
日本毒性病理学会
社団法人日本病理学会
社団法人日本獣医学会
委員歴・役員歴: 研究者総覧に該当データはありませんでした。
受賞: 研究者総覧に該当データはありませんでした。
活動: 研究者総覧に該当データはありませんでした。

リサーチマップで最新データを確認するＪグローバルで最新データを確認する

2024年11月10日更新

2024年11月9日更新

Ｊグローバル

Jグローバル最終確認日: 2024/11/9 01:11
氏名（漢字）: 成澤裕子
氏名（フリガナ）: ナルサワユウコ
氏名（英字）: Nakano-narusawa Yuko
所属機関: 徳島大学講師

リサーチマップ

researchmap最終確認日: 2024/11/10 01:26
氏名（漢字）: 成澤裕子
氏名（フリガナ）: ナルサワユウコ
氏名（英字）: Nakano-narusawa Yuko
プロフィール: リサーチマップAPIで取得できませんでした。
登録日時: 2017/6/16 15:12
更新日時: 2024/2/1 16:56
アバター画像URI: リサーチマップAPIで取得できませんでした。
ハンドル: リサーチマップAPIで取得できませんでした。
eメール: リサーチマップAPIで取得できませんでした。
eメール（その他）: リサーチマップAPIで取得できませんでした。
携帯メール: リサーチマップAPIで取得できませんでした。
性別: リサーチマップAPIで取得できませんでした。
没年月日: リサーチマップAPIで取得できませんでした。
所属ID: 0344000000
所属: 徳島大学
部署: 大学院医歯薬学研究部　病理解析学分野
職名: 講師
学位: 博士（医学）
学位授与機関: 香川大学
URL: リサーチマップAPIで取得できませんでした。
科研費研究者番号: リサーチマップAPIで取得できませんでした。
Google Analytics ID: リサーチマップAPIで取得できませんでした。
ORCID ID: リサーチマップAPIで取得できませんでした。
その他の所属ID: リサーチマップAPIで取得できませんでした。
その他の所属名: リサーチマップAPIで取得できませんでした。
その他の所属部署: リサーチマップAPIで取得できませんでした。
その他の所属職名: リサーチマップAPIで取得できませんでした。
最近のエントリー: リサーチマップAPIで取得できませんでした。
Read会員ID: リサーチマップAPIで取得できませんでした。
経歴
受賞: リサーチマップAPIで取得できませんでした。
Misc
論文
講演・口頭発表等: リサーチマップAPIで取得できませんでした。
書籍等出版物: リサーチマップAPIで取得できませんでした。
研究キーワード
研究分野
所属学協会
担当経験のある科目: リサーチマップAPIで取得できませんでした。
その他: リサーチマップAPIで取得できませんでした。
Works: リサーチマップAPIで取得できませんでした。
特許: リサーチマップAPIで取得できませんでした。
学歴
委員歴: リサーチマップAPIで取得できませんでした。
社会貢献活動: リサーチマップAPIで取得できませんでした。

ＫＡＫＥＮで最新データを確認する

2024年11月9日更新

研究者番号: 00790966

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

所属（過去の研究課題 情報に基づく）*注記: 2020/4/1 – 2021/4/1 : 香川大学, 医学部, 助教

審査区分/研究分野: 研究代表者

小区分50010:腫瘍生物学関連

キーワード: 研究代表者

2光子励起顕微鏡 / 膵癌 / 血行性肝転移

研究課題研究成果共同研究者

「研究課題をさがす」で表示
テキスト（CSV）で出力

テキスト（CSV）で出力

注目研究はありません。

研究者を探す

成澤 裕子

Ｊグローバル

リサーチマップ

研究代表者

研究代表者

成澤裕子