Tokushima University / Educator and Researcher Directory --- Yoshimoto, Katsuhiko

Personal Web Page

https://researchmap.jp/read0054339 (researchmap)

Field of Study

○	Endocrinology and Metabolism, Molecular Genetics, Pharmacology, Cell Biology, Nutrition
○	Endocrinology and Metabolism, Molecular Genetics, Pharmacology, Cell Biology, Nutrition
○	Metabolism
○	Dental Pharmacology

Subject of Study

○	Molecular mechanisms of endocrine tumorigenesis (endocrine tumors, familial tumors, gene abnormality, expression of hormone genes, Pituitary, Parathyroid) (Endocrine tumors maintain differentiation phenotypes such as hormone secretion and have benign phenotypes. We focus on the molecular mechanisms of development of endocrine tumors including hereditary tumors.)
○	Molecular biology of pancreatic islets (pancreatic islets, insulin gene, glucagon gene, diabetic complications, transgenic mice, transcription factor, beta-cell specific genes, incretin) (Pancreatic beta cells are one of the highly differentiated cells in which a variety of cell-specific genes operate their functions and contribute to the physiological homeostasis. To better understand the development and function of beta cells, we analyze the role of novel transcription factors on insulin gene expression. Further, we try to discover novel beta cell-specific genes.)
○	obesity, adipokine (adipocyte, bioactive substance)
○	Biomarkers in saliva (nucleic acid)

Book / Paper

Book:

1.	Katsuhiko Yoshimoto : 28章ビオチン (訳), 西村書店, Nov. 2018.
2.	Katsuhiko Yoshimoto : 27章コバラミン(ビタミンB12)(訳), 西村書店, Nov. 2018.
3.	Katsuhiko Yoshimoto : 14章セレン(訳), 西村書店, Nov. 2018.
4.	Katsuhiko Yoshimoto and Takeo Iwata : ホルモンの分泌調節:ネガティブフィードバック機構など, 株式会社診断と治療社, May 2018.
5.	Katsuhiko Yoshimoto, Takeo Iwata and Noriko Mizusawa : 遺伝性・家族性下垂体腫瘍, 株式会社診断と治療社, Tokyo, Nov. 2016.
6.	Katsuhiko Yoshimoto : 序文, Ishiyaku Publishers,Inc., May 2014.
7.	Katsuhiko Yoshimoto, Masashi Akaike, Minoru Irahara and Keiko Aota : 歯科医師のための医学ハンドブック, 医歯薬出版株式会社, Tokyo, May 2014.
8.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa, Zhi-Rong Qian, Shima Wan Nazatul Shahidan, Shinji Ono and Kyoko Ishimoto : Pituitary adenomas: role of cyclin-dependent kinase inhibitors, Springer, Oct. 2013.
9.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa and 小野信二 : アクロメガリーの病態生理, Medical Review Co.,Ltd, Jul. 2013.
10.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa and Shinji Ono : アクロメガリーの発症にかかわる遺伝子異常, Medical Review Co.,Ltd, Jul. 2013.
11.	Katsuhiko Yoshimoto, Takeo Iwata and Noriko Mizusawa : 遺伝性・家族性下垂体腫瘍, 株式会社診断と治療社, Apr. 2012.
12.	Katsuhiko Yoshimoto, 加藤悦子 and 小林亜由美 : 第5章疾患別栄養療法血液疾患 47.貧血, IGAKU-SHOIN Ltd.Tokyo,Japan, Tokyo, Nov. 2009.
13.	Katsuhiko Yoshimoto : VI. 特異な疾患概念 6. 多発性内分泌腫瘍症1型など, IGAKU-SHOIN Ltd.Tokyo,Japan, Tokyo, Oct. 2009.
14.	Toshiaki Sano and Katsuhiko Yoshimoto : II. 下垂体腫瘍の基礎研究 2.下垂体腺腫の分子病理学, IGAKU-SHOIN Ltd.Tokyo,Japan, Tokyo, Oct. 2009.
15.	Katsuhiko Yoshimoto : アプドーマ，異所性ホルモン産生腫瘍，異所性ホルモン症候群，遺伝性内分泌腺症，APUD系細胞，家族性甲状腺髄様癌，家族性副甲状腺機能亢進症，胸腺ホルモン，シップル症候群，神経内分泌腫瘍，多発性内分泌腺腫症1型，多発性内分泌腺腫症2A型，多発性内分泌腺腫症2B型，パラニューローマ，プレホルモン，プロホルモン，プロホルモン変換酵素, 副甲状腺機能亢進症ー顎腫瘍症候群, 家族性成長ホルモン産生腺腫, IGAKU-SHOIN Ltd.Tokyo,Japan, Tokyo, Feb. 2009.
16.	Katsuhiko Yoshimoto and 橋本理恵 : 貧血に対する栄養管理, Medical Review Co.,Ltd, Osaka, May 2008.
17.	Katsuhiko Yoshimoto, Noriko Mizusawa, Takeo Iwata, Daisuke Nagao, Hossain Md.Golam, 露口勝, Toshiaki Sano and 内野眞也 : 【内分泌クリニカル・カンファランス】副甲状腺家族性副甲状腺機能亢進症2家系におけるHRPT2遺伝子変異の解析, Sep. 2006.
18.	Eiji Takeda, Toshiya Okahisa, Yasuko Takahashi, 国清紀子, Akiko Matsumura, Yutaka Nakaya, Masaharu Nishi, Yutaka Taketani, Katsuhiko Yoshimoto, Junji Terao, 美馬福恵, Masami Yoshioka, 山田静恵, Keisuke Ishizawa, 鈴木麗子, chiyo Fujita, Hidekazu Arai, Masashi Kuwahata and Kazuko Okada : 栄養管理のチーム医療, 文光堂, Tokyo, Apr. 2006.
19.	Yutaka Nakaya, Masashi Kuwahata, Akira Tangoku, Toshio Doi, Yutaka Taketani, Yoshihiko Noma, Eiji Takeda, Hiroyuki Azuma, Mitsuo Shimada, Nobuhiro Kurita, Tetsuro Ohmori, Masaharu Nishi, Yoshinori Aono, Yasuhiko Nishioka, Katsuhiko Yoshimoto and ほか 65名 : NST用語ハンドブック, Medical Review Co.,Ltd, Tokyo, Feb. 2006.
20.	Katsuhiko Yoshimoto, Xu Bing, Noriko Mizusawa, Takeo Iwata, Daisuke Nagao, Golam Md. Hossain, Akira Miyauchi, Seiji Kuma, Mitsuyoshi Hirokawa and Toshiaki Sano : Somatic mutations of the CTNNB1 gene in cribriform-morular variant of papillary thyroid carcinoma., Transworld Research Network, Kerala, India, 2006.
21.	Katsuhiko Yoshimoto : 貧血に対する栄養管理, Medical Review Co.,Ltd, Osaka, Sep. 2004.
22.	Katsuhiko Yoshimoto and Shiro Saito : 多発性内分泌腫瘍症, 文光堂, Tokyo, Nov. 2003.
23.	Katsuhiko Yoshimoto : アプドーマ，異所性ホルモン産生腫瘍，異所性ホルモン症候群，遺伝性内分泌腺症，APUD系細胞，家族性甲状腺髄様癌，家族性副甲状腺機能亢進症，胸腺ホルモン，シップル症候群，神経内分泌腫瘍，多発性内分泌腺腫症1型，多発性内分泌腺腫症2A型，多発性内分泌腺腫症2B型，パラニューローマ，プレホルモン，プロホルモン，プロホルモン変換酵素, IGAKU-SHOIN Ltd.Tokyo,Japan, Tokyo, Mar. 2003.
24.	John P Blezikian, Katsuhiko Yoshimoto, Martin R Pollak, Ernestina Schipani, Harold Jupner, Edward M Brown, Andrew Arnold and Rajesh V Thakker : Genetic Disorders of Parathyroid Hormone Action., Lippincott Williams & Wilkins, Philadelphia, May 2002.
25.	Katsuhiko Yoshimoto and Andrew Arnold : Disorders Affecting Parathyroid Hormone., Lippincott Williams & Wilkins, Philadelphia, May 2002.
26.	Hiroyuki Iwahana, Miwa Fujimura, Yoko Takahashi, Takeshi Iwabuchi, Katsuhiko Yoshimoto and Mitsuo Itakura : Multiple Fluorescence-Based PCR-SSCP Analysis Using Internal Fluorescent Labeling of PCR Products, Eaton Publishing, Natick, Jan. 2000.
27.	Katsuhiko Yoshimoto, 板東浩 and 木村建彦 : 多発性内分泌腺腫瘍 (MEN), 株式会社中外医学社, Tokyo, Jan. 1999.
28.	Katsuhiko Yoshimoto and Shiro Saito : 多発性内分泌腫瘍症, 文光堂, Tokyo, Jan. 1999.
29.	Katsuhiko Yoshimoto : 多発性内分泌腫瘍症, KINPODO, INC., Kyoto, Jan. 1997.
30.	Katsuhiko Yoshimoto : 異所性PT H産生により高カルシウム血症をきたした肺小細胞癌の一例 p.115-118, 齋藤史郎教授退官記念事業会, 徳島大学医学部内科学第一講座, Mar. 1996.
31.	Katsuhiko Yoshimoto : MEN1, MEN2遺伝子, YODOSHA CO., LTD., Tokyo, Jan. 1996.
32.	Mitsuo Itakura, Maki Moritani, Katsuhiko Yoshimoto, Chikara Hashimoto, Satoshi Otsuka, Toshiaki Sano and Jun-ichi Miyazaki : Immuno-stimulatory versus Immunosuppressive Roles of IL-10 in Type I Diabetes: Analysis with IL-10-Producing Transgenic Non-Obese Diabetic Mice., Birkhauser Boston, Boston, Jan. 1996.
33.	Katsuhiko Yoshimoto and Mitsuo Itakura : differential display, Shujunsha Co.Ltd., Tokyo, Jan. 1995.
34.	Mitsuo Itakura, Maki Moritani, Fumi Tashiro, Chikara Hashimoto, Jun-ichi Miyazaki, Setsuko Ii, Eiji Kudo, Hiroyuki Iwahana, Yoshio Hayashi, Toshiaki Sano and Katsuhiko Yoshimoto : Paracrine IL-10 Accelerates Autoimmune Insulitis and Diabetes in Transgenic NOD mice, Elsevier Science Publishers, Amsterdam, Jan. 1995.
35.	Mitsuo Itakura and Katsuhiko Yoshimoto : 糖尿病治療-将来の展望遺伝子治療, 株式会社診断と治療社, Tokyo, Jan. 1994.
36.	Shiro Saito, 横越浩, Katsuhiko Yoshimoto and 齋藤晴比古 : 多発性内分泌腫瘍症とその遺伝子異常, トプコ出版部, Tokyo, Jan. 1990.
37.	Ryuichi Yamasaki, Haruhiko Saito, Toshiaki Sano, Katsuhiko Yoshimoto and Shiro Saito : Secretion of Growth Hormone (GH)-Releasing Hormone and GH in Normal and Diseased States., Elsevier Science Publishers, Amsterdam, Jan. 1989.
38.	Shiro Saito, Haruhiko Saito, Katsuhiko Yoshimoto, Yutaka Yokogoshi and Toshiaki Sano : Production and Secretion of Neuropeptides in Pheochromocytoma., Elsevier Science Publishers, Amsterdam, Jan. 1988.

Academic Paper (Judged Full Paper):

1.	Tomoyo Hara, Ryoko Uemoto, Akiko Sekine, Yukari Mitsui, Shiho Masuda, Hiroki Yamagami, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Yasumasa Ikeda, Itsuro Endo, Soichi Honda, Katsuhiko Yoshimoto, Akira Kondo, Toshiaki Tamaki, Toshio Matsumoto, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Plasma Heparin Cofactor II Activity Is Inversely Associated with Hepatic Fibrosis of Non-Alcoholic Fatty Liver Disease in Patients with Type 2 Diabetes Mellitus., Journal of Atherosclerosis and Thrombosis, 2022. (Summary) Plasma HCII activity was inversely associated with clinical hepatic fibrosis indices including FIB-4 index, NFS and APRI and with the prevalence of advanced hepatic fibrosis in patients with T2DM. The results suggest that HCII can serve as a novel biomarker for assessment of hepatic fibrosis of NAFLD in patients with T2DM. (Tokushima University Institutional Repository) ● Metadata: 118258 (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.63752 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36244745 ● Search Scopus @ Elsevier (PMID): 36244745 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.63752 (Tokushima University Institutional Repository: 118258, DOI: 10.5551/jat.63752, PubMed: 36244745)
2.	Noriko Mizusawa, Nagakatsu Harada, Takeo Iwata, Izumi Ohigashi, Mitsuo Itakura and Katsuhiko Yoshimoto : Identification of protease serine S1 family member 53 as a mitochondrial protein in murine islet beta cells, Islets, Vol.14, No.1, 1-13, 2021. (Keyword) Prss53 / pancreatic β-cell / mitochondria (Tokushima University Institutional Repository) ● Metadata: 117033 (Link to Publication Site) ● Publication site (DOI): 10.1080/19382014.2021.1982325 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34636707 ● Summary page in Scopus @ Elsevier: 2-s2.0-85116882945 (Tokushima University Institutional Repository: 117033, DOI: 10.1080/19382014.2021.1982325, PubMed: 34636707, Elsevier: Scopus)
3.	Tomoyo Hara, Ryoko Uemoto, Akiko Sekine, Yukari Mitsui, Shiho Masuda, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Yasumasa Ikeda, Itsuro Endo, Soichi Honda, Katsuhiko Yoshimoto, Akira Kondo, Toshiaki Tamaki, Toshio Matsumoto, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Plasma Heparin Cofactor II Activity Is Inversely Associated with Albuminuria and Its Annual Deterioration in Patients with Diabetes., Journal of Diabetes Investigation, 2021. (Summary) The plasma HCII activity was inversely and specifically associated with glomerular injury in patients with diabetes. The results suggest that HCII can serve as a novel predictive factor for early-stage DKD development, as represented by albuminuria. (Tokushima University Institutional Repository) ● Metadata: 116545 (Link to Publication Site) ● Publication site (DOI): 10.1111/jdi.13602 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34043882 ● Search Scopus @ Elsevier (PMID): 34043882 ● Search Scopus @ Elsevier (DOI): 10.1111/jdi.13602 (Tokushima University Institutional Repository: 116545, DOI: 10.1111/jdi.13602, PubMed: 34043882)
4.	Noriaki Fukuhara, Takeo Iwata, Naoko Inoshita, Katsuhiko Yoshimoto, Masanobu Kitagawa, Hirokazu Fukuhara, Keita Tatsushima, Mitsuo Yamaguchi-Okada, Akira Takeshita, Junko Ito, Yasuhiro Takeuchi, Shozo Yamada and Hiroshi Nishioka : Immunohistochemistry or Molecular Analysis: Which Method Is Better for Subtyping Craniopharyngioma?, Endocrine Pathology, 2020. (Summary) Craniopharyngioma (CP) is mainly classified into two pathological subtypes: adamantinomatous (ACP) and papillary (PCP). CTNNB1 (β-catenin) mutations are detected in ACPs, and the BRAF V600E mutation is detected in PCPs. However, genetic analysis is not always possible in general medical practice. In this study, we investigated whether immunohistochemistry could replace genetic analysis as an aid in subtype diagnosis. Here, 38 CP patients who had undergone their first tumor resection were included. Among the 38 cases, 22 were morphologically diagnosed as ACP, 10 cases were diagnosed as PCP, and six cases were diagnosed as undetermined CP that were morphologically difficult to classify as either ACP or PCP. Results of immunohistochemistry and genetic analysis and clinical features were compared. Based on the immunohistochemistry, 26 (22 ACPs and four undetermined CPs) showed nuclear β-catenin expression, 11 (nine PCPs and two undetermined CPs) exhibited positive BRAF V600E immunostaining, and one PCP showed membranous β-catenin expression and negative BRAF V600E immunostaining. Among the 26 nuclear β-catenin expression cases, 11 had CTNNB1 mutations; however, 15 cases had mutations of neither CTNNB1 nor BRAF V600E. All 11 BRAF V600E immunopositive cases had BRAF V600E mutations. When comparing clinical features, pediatric patients and those with tumor calcification and less solid components on MRI more commonly had nuclear β-catenin expression tumors than BRAF V600E immunopositive tumors, reflecting the differences in clinical features between ACP and PCP. Accordingly, immunohistochemistry can replace genetic analysis as an aid to determine the subtype diagnosis of CP in general medical practice. (Tokushima University Institutional Repository) ● Metadata: 115294 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12022-020-09644-z (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32965631 ● Search Scopus @ Elsevier (PMID): 32965631 ● Search Scopus @ Elsevier (DOI): 10.1007/s12022-020-09644-z (Tokushima University Institutional Repository: 115294, DOI: 10.1007/s12022-020-09644-z, PubMed: 32965631)
5.	P Marques, F Caimari, LC Hernández-Ramírez, D Collier, D Iacovazzo, A Ronaldson, K Magid, CT Lim, K Stals, S Ellard, AB Grossman, M Korbonits, Takeo Iwata, Katsuhiko Yoshimoto and Consortium International FIPA The : Significant benefits of AIP testing and clinical screening in familial isolated and young-onset pituitary tumors, The Journal of Clinical Endocrinology and Metabolism, Vol.105, No.6, 1-14, 2020. (Summary) Germline mutations in the aryl hydrocarbon receptor-interacting protein (AIP) gene are responsible for a subset of familial isolated pituitary adenoma (FIPA) cases and sporadic pituitary neuroendocrine tumors (PitNETs). To compare prospectively diagnosed AIP mutation-positive (AIPmut) PitNET patients with clinically presenting patients and to compare the clinical characteristics of AIPmut and AIPneg PitNET patients. 12-year prospective, observational study. We studied probands and family members of FIPA kindreds and sporadic patients with disease onset ≤18 years or macroadenomas with onset ≤30 years (n = 1477). This was a collaborative study conducted at referral centers for pituitary diseases. AIP testing and clinical screening for pituitary disease. Comparison of characteristics of prospectively diagnosed (n = 22) vs clinically presenting AIPmut PitNET patients (n = 145), and AIPmut (n = 167) vs AIPneg PitNET patients (n = 1310). Prospectively diagnosed AIPmut PitNET patients had smaller lesions with less suprasellar extension or cavernous sinus invasion and required fewer treatments with fewer operations and no radiotherapy compared with clinically presenting cases; there were fewer cases with active disease and hypopituitarism at last follow-up. When comparing AIPmut and AIPneg cases, AIPmut patients were more often males, younger, more often had GH excess, pituitary apoplexy, suprasellar extension, and more patients required multimodal therapy, including radiotherapy. AIPmut patients (n = 136) with GH excess were taller than AIPneg counterparts (n = 650). Prospectively diagnosed AIPmut patients show better outcomes than clinically presenting cases, demonstrating the benefits of genetic and clinical screening. AIP-related pituitary disease has a wide spectrum ranging from aggressively growing lesions to stable or indolent disease course. (Tokushima University Institutional Repository) ● Metadata: 114398 (Link to Publication Site) ● Publication site (DOI): 10.1210/clinem/dgaa040 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31996917 ● Search Scopus @ Elsevier (PMID): 31996917 ● Search Scopus @ Elsevier (DOI): 10.1210/clinem/dgaa040 (Tokushima University Institutional Repository: 114398, DOI: 10.1210/clinem/dgaa040, PubMed: 31996917)
6.	Hou-Shi Ma, Lu Elaine Wang, Wen-Fei Xu, Shozo Yamada, Katsuhiko Yoshimoto, Zhi-Rong Qian, Long Shi, Li-Li Liu and Xu-Hui Li : Overexpression of DNA (Cytosine-5)-Methyltransferase 1 (DNMT1) And DNA (Cytosine-5)-Methyltransferase 3A (DNMT3A) Is Associated with Aggressive Behavior and Hypermethylation of Tumor Suppressor Genes in Human Pituitary Adenomas., Medical Science Monitor, Vol.24, 4841-4850, 2018. (Summary) BACKGROUND Alteration of DNA methylation of tumor suppressor genes (TSGs) is one of the most consistent epigenetic changes in human cancers. DNMTs play several important roles in DNA methylation and development of cancers. Regarding DNMTs protein expressions, little is known about the clinical significance and correlation with promoter methylation status of TSGs in human pituitary adenomas. MATERIAL AND METHODS We analyzed the protein expression of 3 DNMTs using immunohistochemistry and assessed DNA hypermethylation of RASSF1A, CDH13, CDH1, and CDKN2A (p16) in 63 pituitary adenomas. We examined associations between DNMTs expression and clinicopathological features or promoter methylation status of TSGs. RESULTS Overexpression of DNMTs was detected in pituitary adenomas. Frequencies of DNMT1 overexpression were significantly higher in macroadenomas, invasive tumors, and grade III and IV tumors. DNMT3A was frequently detected in invasive tumors and grade IV tumors. In addition, DNMT1 and DNMT3A were frequently detected in high-methylation tumors. Furthermore, in multivariate logistic regression, the significant association between DNMT1 or DNMT3A and high-methylation status persisted after adjusting for clinicopathological features. CONCLUSIONS Our findings suggested that tumor overexpression of DNMT1 and DNMT3A is associated with tumor aggressive behavior and high-methylation status in pituitary adenomas. Our data support a possible role of DNMT1 and DNMT3A in TSG promoter methylation leading to pituitary adenoma invasion and suggest that inhibition of DNMTs has the potential to become a new therapeutic approach for invasive pituitary adenoma. (Tokushima University Institutional Repository) ● Metadata: 111966 (Link to Publication Site) ● Publication site (DOI): 10.12659/MSM.910608 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30002361 ● Summary page in Scopus @ Elsevier: 2-s2.0-85050105384 (Tokushima University Institutional Repository: 111966, DOI: 10.12659/MSM.910608, PubMed: 30002361, Elsevier: Scopus)
7.	Caimari Francisca, Hernández-Ramírez Cristina Laura, Dang N Mary, Gabrovska Plamena, Iacovazzo Donato, Stals Karen, Ellard Sian, Korbonits Márta, Takeo Iwata, Katsuhiko Yoshimoto and consortium FIPA International : Risk category system to identify pituitary adenoma patients with AIP mutations., Journal of Medical Genetics, Vol.55, No.4, 254-260, 2018. (Summary) Predictive tools to identify patients at risk for gene mutations related to pituitary adenomas are very helpful in clinical practice. We therefore aimed to develop and validate a reliable risk category system for aryl hydrocarbon receptor-interacting protein () mutations in patients with pituitary adenomas. An international cohort of 2227 subjects were consecutively recruited between 2007 and 2016, including patients with pituitary adenomas (familial and sporadic) and their relatives. All probands (n=1429) were screened for mutations, and those diagnosed with a pituitary adenoma prospectively, as part of their clinical screening (n=24), were excluded from the analysis. Univariate analysis was performed comparing patients with and without mutations. Based on a multivariate logistic regression model, six potential factors were identified for the development of a risk category system, classifying the individual risk into low-risk, moderate-risk and high-risk categories. An internal cross-validation test was used to validate the system. 1405 patients had a pituitary tumour, of which 43% had a positive family history, 55.5% had somatotrophinomas and 81.5% presented with macroadenoma. Overall, 134 patients had an mutation (9.5%). We identified four independent predictors for the presence of an mutation: age of onset providing an odds ratio (OR) of 14.34 for age 0-18 years, family history (OR 10.85), growth hormone excess (OR 9.74) and large tumour size (OR 4.49). In our cohort, 71% of patients were identified as low risk (<5% risk of mutation), 9.2% as moderate risk and 20% as high risk (≥20% risk). Excellent discrimination (c-statistic=0.87) and internal validation were achieved. We propose a user-friendly risk categorisation system that can reliably group patients into high-risk, moderate-risk and low-risk groups for the presence of mutations, thus providing guidance in identifying patients at high risk of carrying an mutation. This risk score is based on a cohort with high prevalence of mutations and should be applied cautiously in other populations. (Tokushima University Institutional Repository) ● Metadata: 113266 (Link to Publication Site) ● Publication site (DOI): 10.1136/jmedgenet-2017-104957 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29440248 ● Summary page in Scopus @ Elsevier: 2-s2.0-85044819768 (Tokushima University Institutional Repository: 113266, DOI: 10.1136/jmedgenet-2017-104957, PubMed: 29440248, Elsevier: Scopus)
8.	Y Nagata, N Inoshita, N Fukuhara, M Yamaguchi-Okada, H Nishioka, Takeo Iwata, Katsuhiko Yoshimoto and Shozo Yamada : Growth hormone-producing pituitary adenomas in childhood and young adulthood: clinical features and outcomes., Pituitary, Vol.21, No.1, 1-9, 2018. (Summary) Growth hormone (GH)-producing pituitary adenomas (PAs) in childhood or young adulthood are rare, and the details surrounding these tumors remain enigmatic. We present the clinical, pathological and genetic features of this disease. We identified 25 patients aged 20 years or younger with GH-producing PAs who underwent surgery between 2003 and 2016 at Toranomon Hospital in Tokyo. We retrospectively reviewed the clinical data, treatment outcomes and pathological features of these patients to shed light on childhood acromegaly. The cohort comprised 14 male and 11 female patients whose average age at the time of surgery was 17.3 years. Germline AIP mutations were present in 5 of 13 patients examined, and Carney complex was identified in 2 of 25 patients. The mean maximum tumor diameter was 26.7 mm, and total resection assessed during surgery was achieved in 17 patients. Based on their respective pathological findings, patients were divided into the following 4 groups: sparsely granulated adenomas (5), densely granulated (DG) adenomas (6), plurihormonal adenomas (9), and silent subtype 3 (SS3) adenomas (5). During the mean follow-up period of 50.3 months, complete endocrinological remission was achieved in 14 of 25 patients (56%) by surgery alone and in 19 patients (76%) after postoperative adjuvant therapy. GH-producing PAs in young patients are intriguing and difficult to treat due to their distinct tumor characteristics, including a lower incidence of the DG subtype and a higher incidence of SS3 adenomas and genetic abnormalities. Therefore, multi-modal therapies are essential to achieve optimal clinical outcomes. (Tokushima University Institutional Repository) ● Metadata: 112137 (Link to Publication Site) ● Publication site (DOI): 10.1007/s11102-017-0836-4 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28849339 ● Summary page in Scopus @ Elsevier: 2-s2.0-85028548176 (Tokushima University Institutional Repository: 112137, DOI: 10.1007/s11102-017-0836-4, PubMed: 28849339, Elsevier: Scopus)
9.	Takeo Iwata, Kyoko Kuribayashi, Masahiko Nakasono, Noriko Saito-Tarashima, Noriaki Minakawa, Noriko Mizusawa, Rie Kido and Katsuhiko Yoshimoto : The AMPK/mTOR pathway is involved in D-dopachrome tautomerase gene transcription in adipocytes differentiated from SGBS cells, a human preadipocyte cell line, Cytokine, Vol.96, 195-202, 2017. (Summary) In adipose tissue, D-dopachrome tautomerase (DDT), a cytokine with structural similarity to macrophage migration inhibitory factor, is mainly expressed in adipocytes rather than preadipocytes and acts as an anti-obesity adipokine in an autocrine manner. However, its transcriptional regulation is largely unknown. In order to explore molecules affecting DDT transcription, a chemical library screening using HEK293 cells stably expressing a DDT promoter-reporter construct was performed. Several derivatives of 5-aminoimidazole-4-carboxamide-1--d-ribofuranoside (AICAR), an AMP-activated protein kinase (AMPK) activator, were identified as transcriptional activators of the DDT gene. Furthermore, DDT mRNA levels were reduced in SGBS adipocytes treated with compound C, an AMPK inhibitor, suggesting involvement of AMPK in DDT transcription. Overexpression of the FOXO1 constitutive active form reduced transcriptional activity of the DDT gene in SGBS cells, but increased it in HEK293 cells. Cell-type specific effects were also observed in the DDT gene expression of cells treated with AS1842856, a FOXO1 inhibitor. Finally, involvement of the mammalian target of rapamycin (mTOR) signaling in DDT transcription in SGBS adipocytes was investigated. Rapamycin, an inhibitor of mTOR, increased DDT mRNA levels and attenuated the inhibitory effects of compound C on DDT mRNA levels in SGBS adipocytes. In conclusion, DDT transcription may be regulated in a cell-dependent manner, and were enhanced by AMPK activation in SGBS adipocytes through inhibiting the mTOR signaling. (Tokushima University Institutional Repository) ● Metadata: 111466 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.cyto.2017.04.017 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28445821 ● Summary page in Scopus @ Elsevier: 2-s2.0-85018474373 (Tokushima University Institutional Repository: 111466, DOI: 10.1016/j.cyto.2017.04.017, PubMed: 28445821, Elsevier: Scopus)
10.	Otsuka Ryo, Nagakatsu Harada, Aoki Shouhei, Shirai Kanna, Kazuchika Nishitsuji, Nozaki Ayane, Hatakeyama Adzumi, Masayuki Shono, Noriko Mizusawa, Katsuhiko Yoshimoto, Yutaka Nakaya, Hiroshi Kitahata and Hiroshi Sakaue : C-terminal region of GADD34 regulates eIF2alpha dephosphorylation and cell proliferation in CHO-K1 cells., Cell Stress & Chaperones, Vol.21, No.1, 29-40, 2016. (Summary) GADD34 is a member of a growth arrest and DNA damage (GADD)-inducible gene family. Here, we established a novel Chinese hamster ovary (CHO)-K1-derived cell line, CHO-K1-G34M, which carries a nonsense mutation (termed the Q525X mutation) in the GADD34 gene. The Q525X mutant protein lacks the C-terminal 66 amino acids required for GADD34 to bind to and activate protein phosphatase 1 (PP1). We investigated the effects of GADD34 with or without the Q525X mutation on the phosphorylation status of PP1 target proteins, including the subunit of eukaryotic initiation factor 2 (eIF2) and glycogen synthase kinase 3 (GSK3). CHO-K1-G34M cells had higher levels of eIF2 phosphorylation compared to the control CHO-K1-normal cells both in the presence and absence of endoplasmic reticulum stress. Overexpression of the wild-type GADD34 protein in CHO-K1-normal cells largely reduced eIF2 phosphorylation, while overexpression of the Q525X mutant did not produce similar reductions. Meanwhile, neither wild type nor Q525X mutation of GADD34 affected the GSK3 phosphorylation status. GADD34 also did not affect the canonical Wnt signaling pathway downstream of GSK3. Cell proliferation rates were higher, while expression levels of the cyclin-dependent kinase inhibitor p21 were lower in CHO-K1-G34M cells compared to the CHO-K1-normal cells. The GADD34 Q525X mutant had a reduced ability to inhibit cell proliferation and enhance p21 expression of the CHO-K1-normal cells compared to the wild-type GADD34 protein. These results suggest that the GADD34 protein C-terminal plays important roles in regulating not only eIF2 dephosphorylation but also cell proliferation in CHO-K1 cells. (Tokushima University Institutional Repository) ● Metadata: 110106 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12192-015-0633-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26318739 ● Summary page in Scopus @ Elsevier: 2-s2.0-84951905379 (Tokushima University Institutional Repository: 110106, DOI: 10.1007/s12192-015-0633-9, PubMed: 26318739, Elsevier: Scopus)
11.	Yuki Iwawaki, Noriko Mizusawa, Takeo Iwata, Nobuaki Higaki, Takaharu Goto, Megumi Watanabe, Yoritoki Tomotake, Tetsuo Ichikawa and Katsuhiko Yoshimoto : MiR-494-3p induced by compressive force inhibits cell proliferation in MC3T3-E1 cells., Journal of Bioscience and Bioengineering, Vol.120, No.4, 456-462, 2015. (Summary) Mechanical stimuli regulate fundamental cell processes such as proliferation, differentiation, and morphogenesis. We attempted to identify microRNA (miRNA) whose expression is changed during compressive treatment in MC3T3-E1, a pre-osteoblastic cell line. Microarray analysis followed by reverse transcription-quantitative polymerase chain reaction revealed that compressive force at 294 Pa for 24 h in MC3T3-E1 cells increased levels of miR-494-3p, miR-146a-5p, miR-210-3p, and miR-1247-3p. Among these miRNAs, miR-494-3p was found to inhibit cell proliferation in MC3T3-E1 cells. Furthermore, cells subjected to compressive force showed slower cell growth compared with control cells. Levels of mRNA for fibroblast growth factor receptor 2 (FGFR2) and Rho-associated coiled-coil kinase 1 (ROCK1), which were predicted to be targets of miR-494-3p, were decreased by compressive force or overexpression of miR-494-3p mimics in MC3T3-E1 cells. Furthermore, binding sites of miR-494-3p within 3'-untranslated regions of Fgfr2 and Rock1 were determined using luciferase reporter assay. In conclusion, compressive force affected expressions of several miRNAs including miR-494-3p in MC3T3-E1 cells. Compressive force might inhibit cell proliferation in osteoblasts by up-regulating miR-494-3p followed by FGFR2 and ROCK1 gene repressions. (Keyword) 3' Untranslated Regions / Cell Line / Cell Proliferation / Down-Regulation / Gene Expression Regulation / Humans / Luciferases / MicroRNAs / Oligonucleotide Array Sequence Analysis / Osteoblasts / RNA, Messenger / Receptor, Fibroblast Growth Factor, Type 2 / Reverse Transcriptase Polymerase Chain Reaction / Stress, Mechanical / Up-Regulation / rho-Associated Kinases (Tokushima University Institutional Repository) ● Metadata: 109479 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jbiosc.2015.02.006 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25795570 ● Summary page in Scopus @ Elsevier: 2-s2.0-84938332268 (Tokushima University Institutional Repository: 109479, DOI: 10.1016/j.jbiosc.2015.02.006, PubMed: 25795570, Elsevier: Scopus)
12.	C Laura Hernández-Ramírez, Plamena Gabrovska, Judit Dénes, Karen Stals, Giampaolo Trivellin, Daniel Tilley, Francesco Ferraù, Jane Evanson, Sian Ellard, B Ashley Grossman, Federico Roncaroli, R Mônica Gadelha, Márta Korbonits, Takeo Iwata, Katsuhiko Yoshimoto and Consortium FIPA International : Landscape of familial isolated and young-onset pituitary adenomas: prospective diagnosis in AIP mutation carriers., The Journal of Clinical Endocrinology and Metabolism, Vol.100, No.9, E1242-E1254, 2015. (Summary) A quarter of the AIPmut carriers screened were diagnosed with pituitary disease, justifying this screening and suggesting a variable clinical course for AIPmut positive pituitary adenomas. (Tokushima University Institutional Repository) ● Metadata: 109656 (Link to Publication Site) ● Publication site (DOI): 10.1210/jc.2015-1869 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26186299 ● Summary page in Scopus @ Elsevier: 2-s2.0-84940115216 (Tokushima University Institutional Repository: 109656, DOI: 10.1210/jc.2015-1869, PubMed: 26186299, Elsevier: Scopus)
13.	Takeo Iwata, T Tamanaha, R Koezuka, M Tochiya, H Makino, I Kishimoto, Noriko Mizusawa, S Ono, N Inoshita, Shozo Yamada, A Shimatsu and Katsuhiko Yoshimoto : Germline deletion and a somatic mutation of the PRKAR1A gene in a Carney complex-related pituitary adenoma., European Journal of Endocrinology, Vol.172, No.1, K5-K10, 2015. (Summary) The objective was to assess involvement of loss of the PRKAR1A gene encoding a type 1α regulatory subunit of cAMP-dependent protein kinase A located on 17q24 in a Carney complex (CNC)-related pituitary adenoma. We investigated aberrations of the PRKAR1A gene in a CNC patient with a GH-producing pituitary adenoma, whose family has three other members with probable CNC. A gene mutation was identified by a standard DNA sequencing method based on PCR. DNA copy number was measured to evaluate allelic loss on 17q24 by quantitative PCR. The breakpoints of deletion were determined by cloning a rearranged region in the deleted allele. A PRKAR1A mutation of c.751_758del8 (p.S251LfsX16) was found in genomic DNA obtained from a pituitary adenoma, but not leukocytes from the patient. Reduced DNA copy number at loci including the PRKAR1A gene on 17q24 was detected in both the tumor and leukocytes, suggesting a deletion at the loci at the germline level. The deletion size was determined to be ∼ 0.5 Mb and this large deletion was also found in two other family members. This is the first case showing a CNC-related pituitary adenoma with the combination of somatic mutation and a large inherited deletion of the PRKAR1A gene. Biallelic inactivation of PRKAR1A appears to be necessary for the development of CNC-related pituitary adenoma. (Keyword) Adenoma / Aged / Carney Complex / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / Female / Gene Deletion / Germ-Line Mutation / Humans / Middle Aged / Pedigree / Pituitary Neoplasms / Young Adult (Tokushima University Institutional Repository) ● Metadata: 109643 (Link to Publication Site) ● Publication site (DOI): 10.1530/EJE-14-0685 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25336503 ● Summary page in Scopus @ Elsevier: 2-s2.0-84920365005 (Tokushima University Institutional Repository: 109643, DOI: 10.1530/EJE-14-0685, PubMed: 25336503, Elsevier: Scopus)
14.	Li Xu-Hui, Wang Lu Elaine, Zhou Hai-Meng, Katsuhiko Yoshimoto and Zhi-Rong Qian : MicroRNAs in Human Pituitary Adenomas., International Journal of Endocrinology, Vol.2014, 435171, 2014. (Summary) MicroRNAs (miRNAs) are a class of recently identified noncoding RNAs that regulate gene expression at posttranscriptional level. Due to the large number of genes regulated by miRNAs, miRNAs play important roles in many cellular processes. Emerging evidence indicates that miRNAs are dysregulated in pituitary adenomas, a class of intracranial neoplasms which account for 10-15% of diagnosed brain tumors. Deregulated miRNAs and their targets contribute to pituitary adenomas progression and are associated with cell cycle control, apoptosis, invasion, and pharmacological treatment of pituitary adenomas. To provide an overview of miRNAs dysregulation and functions of these miRNAs in pituitary adenoma progression, we summarize the deregulated miRNAs and their targets to shed more light on their potential as therapeutic targets and novel biomarkers. (Tokushima University Institutional Repository) ● Metadata: 109635 (Link to Publication Site) ● Publication site (DOI): 10.1155/2014/435171 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25548562 ● Search Scopus @ Elsevier (PMID): 25548562 ● Search Scopus @ Elsevier (DOI): 10.1155/2014/435171 (Tokushima University Institutional Repository: 109635, DOI: 10.1155/2014/435171, PubMed: 25548562)
15.	Omar Maningo Rodis, Edward Barroga, J Patrick Barron, James Hobbs, Jayanetti A. Jayawardena, Ikuo Kageyama, Bukasa Kalubi, Clive Langham, Yoshizo Matsuka, Yoichiro Miyake, Naoko Seki, Hiroko Oka, Martin Peters, Yo Shibata, Roxana Stegaroiu, Kazuyoshi Suzuki, Shigeru Takahashi, Hironori Tsuchiya, Toshiko Yoshida and Katsuhiko Yoshimoto : A proposed core curriculum for dental English education in Japan., BMC Medical Education, Vol.14, 239, 2014. (Summary) Globalization of the professions has become a necessity among schools and universities across the world. It has affected the medical and dental professions in terms of curriculum design and student and patient needs. In Japan, where medicine and dentistry are taught mainly in the Japanese language, profession-based courses in English, known as Medical English and Dental English, have been integrated into the existing curriculum among its 83 medical and 29 dental schools. Unfortunately, there is neither a core curriculum nor a model syllabus for these courses. This report is based on a survey, two discussion forums, a workshop, and finally, the drafting of a proposed core curriculum for dental English approved by consensus of the participants from each university. The core curriculum covers the theoretical aspects, including dental English terms and oral pathologies; and practical aspects, including blended learning and dentist-patient communication. It is divided into modules and is recommended to be offered for at least two semesters. The core curriculum is expected to guide curriculum developers in schools where dental English courses are yet to be offered or are still in their early development. It may also serve as a model curriculum to medical and dental schools in countries in Asia, Europe, Africa, and Central and South America, where English is not the medium of instruction. (Tokushima University Institutional Repository) ● Metadata: 114762 (Link to Publication Site) ● Publication site (DOI): 10.1186/s12909-014-0239-4 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25404383 ● Search Scopus @ Elsevier (PMID): 25404383 ● Search Scopus @ Elsevier (DOI): 10.1186/s12909-014-0239-4 (Tokushima University Institutional Repository: 114762, DOI: 10.1186/s12909-014-0239-4, PubMed: 25404383)
16.	Takeo Iwata, Shozo Yamada, Junko Ito, Naoko Inoshita, Noriko Mizusawa, Shinji Ono and Katsuhiko Yoshimoto : A Novel C-terminal Nonsense Mutation, Q315X, of the Aryl Hydrocarbon Receptor-Interacting Protein Gene in a Japanese Familial Isolated Pituitary Adenoma Family., Endocrine Pathology, Vol.25, No.3, 273-281, 2014. (Summary) Although the cause of familial isolated pituitary adenoma (FIPA) remains unknown in many cases, germline mutations in the aryl hydrocarbon receptor-interacting protein (AIP) gene were identified in approximately 20 % of families with FIPA. We investigated the AIP gene mutation by a standard sequencing method in 12 members of a Japanese two-generation FIPA family, which includes 3 patients with early-onset acromegaly. Multiplex ligation-dependent probe amplification analysis in a tumor sample was attempted to examine the loss of heterozygosity (LOH) in the locus. The effect of the detected mutation on cell proliferation was investigated. A germline mutation of c.943C > T (p.Q315X) generating an AIP protein with the C-terminal end deleted was found in the FIPA family. Biallelic inactivation of AIP by a combination of the germline mutation and LOH at 11q13 was confirmed in the tumor. The nonsense mutation disrupted the ability to inhibit cell proliferation. We conclude that p.Q315X mutation in the AIP gene is a pathogenic variant and the C-terminal region of AIP plays an important role in the predisposition to pituitary adenomas. (Tokushima University Institutional Repository) ● Metadata: 109644 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12022-014-9318-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24789813 ● Search Scopus @ Elsevier (PMID): 24789813 ● Search Scopus @ Elsevier (DOI): 10.1007/s12022-014-9318-7 (Tokushima University Institutional Repository: 109644, DOI: 10.1007/s12022-014-9318-7, PubMed: 24789813)
17.	Tae Nakano-Tateno, Toru Tateno, Maw Maw Hlaing, Lei Zheng, Katsuhiko Yoshimoto, Shozo Yamada, L Sylvia Asa and Shereen Ezzat : FGFR4 polymorphic variants modulate phenotypic features of Cushing disease., Molecular Endocrinology, Vol.28, No.4, 525-533, 2014. (Summary) Cushing disease is a potentially lethal condition resulting from hormone excess, usually due to a small pituitary tumor that fails to respond to negative feedback inhibition. A minority of patients develop larger, more aggressive tumors of the same lineage but with modest hormone excess. Here we show that a common polymorphism in the fibroblast growth factor receptor 4 (FGFR4) transmembrane domain yields receptor isoforms with distinct properties that mediate these biological differences. Forced expression of the major FGFR4-G388 variant allele supports pY-signal transducer and activator of transcription (STAT3) responses. In contrast, expression of the minor FGFR4-R388 allele enhances STAT3 serine phosphorylation, driving cellular growth. In addition, FGFR4-R388 enhances glucocorticoid receptor phosphorylation and nuclear translocation. Consistent with these findings, glucocorticoid administration resulted in enhanced hormone negative feedback in mice with knock-in of the FGFR4 variant allele. Moreover, clinical data from patients with pituitary tumors revealed that those homozygous for the R388 allele have a higher frequency of silent corticotroph macroadenomas than FGFR4-G388 carriers, who were more likely to have small but hormonally active microadenomas. These findings demonstrate that the FGFR4 transmembrane polymorphic variants can modulate cellular growth and sensitivity to glucocorticoid hormone negative feedback through distinct STAT3 modifications of relevance to the human forms of Cushing disease. (Link to Publication Site) ● Publication site (DOI): 10.1210/me.2013-1412 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24625004 ● Search Scopus @ Elsevier (PMID): 24625004 ● Search Scopus @ Elsevier (DOI): 10.1210/me.2013-1412 (DOI: 10.1210/me.2013-1412, PubMed: 24625004)
18.	Guangfei Xu, Jiao Liu, Katsuhiko Yoshimoto, Gang Chen, Takeo Iwata, Noriko Mizusawa, Zhiqing Duan, Chunhua Wan and Junkang Jiang : 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induces expression of p27(kip¹) and FoxO3a in female rat cerebral cortex and PC12 cells., Toxicology Letters, Vol.226, No.3, 294-302, 2014. (Summary) 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a potent toxin that alters normal brain development, producing cognitive disability and motor dysfunction. Previous studies in rats have proved that female rats are more sensitive to TCDD lethality than male ones. Recent studies have shown that TCDD induces cell cycle arrest and apoptosis, but the regulatory proteins involved in these processes have yet to be elucidated. In this study, we constructed an acute TCDD injury female rat model, and investigated the effects of TCDD on apoptosis and expression of cell cycle regulators, forkhead box class O 3a (FoxO3a) and p27(kip1), in the central nervous system (CNS). Increased levels of active caspase-3 were observed in the cerebral cortex of female rats treated with TCDD, suggesting that TCDD-induced apoptosis occurs in the CNS. The terminal deoxynucleotidyl transferase-mediated biotinylated-dUTP nick-end labeling assay showed that apoptosis primarily occurred in neurons. Furthermore, Western blot analysis, reverse transcription-polymerase chain reaction, and immunohistochemistry showed a significant up-regulation of FoxO3a and p27(kip1) in the cerebral cortex. Immunofluorescent labeling indicated that FoxO3a and p27(kip1) were predominantly localized in apoptotic neurons, but not in astrocytes. In vitro experiments using PC12, a rat neuron-like pheochromocytoma cell line, also revealed that TCDD induced apoptosis and an increase in FoxO3a and p27(kip1) expression. Furthermore, knockdown of FoxO3a expression inhibited p27(kip1) transcription and TCDD-induced apoptosis. Based on our data, induction of FoxO3a may play an important role in TCDD-induced neurotoxicity. (Keyword) Animals / Apoptosis / Cerebral Cortex / Cyclin-Dependent Kinase Inhibitor p27 / Female / Forkhead Transcription Factors / PC12 Cells / Rats / Rats, Sprague-Dawley / Receptors, Aryl Hydrocarbon / Tetrachlorodibenzodioxin (Link to Publication Site) ● Publication site (DOI): 10.1016/j.toxlet.2014.02.019 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24594276 ● Search Scopus @ Elsevier (PMID): 24594276 ● Search Scopus @ Elsevier (DOI): 10.1016/j.toxlet.2014.02.019 (DOI: 10.1016/j.toxlet.2014.02.019, PubMed: 24594276)
19.	Guangfei Xu, Yuanye Li, Katsuhiko Yoshimoto, Qiyun Wu, Gang Chen, Takeo Iwata, Noriko Mizusawa, Chunhua Wan and Xiaoke Nie : 2,3,7,8-Tetrachlorodibenzo-p-dioxin stimulates proliferation of HAPI microglia by affecting the Akt/GSK-3/cyclin D1 signaling pathway., Toxicology Letters, Vol.224, No.3, 362-370, 2013. (Summary) 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is an environmental toxin that induces apoptosis of neurons and a pro-inflammatory response in microglial cells. First, we found that TCDD induced proliferation of HAPI microglial cells in a dose- and time-dependent manner. Flow cytometry analysis showed that this proliferation by TCDD was due to mainly enhancing the G1 to S phase transition. Next, it was found that TCDD treatment led to up-regulation of cyclin D1, which induces cell cycle progression from G1 to S phase, in a time-dependent manner. As for molecular mechanism, we revealed that TCDD was capable of inducing Akt phosphorylation and activation, resulting in phosphorylation and inactivation of glycogen synthase kinase-3 (GSK-3). Inactivated GSK-3 attenuated proteasomal degradation of cyclin D1 by reducing Thr(286)-phosphorylated cyclin D1 levels. Moreover, inactivated GSK-3 increased cyclin D1 gene transcription by increasing its transcription factor -catenin in the nucleus. Further, blockage of phosphoinositide 3-kinase/Akt kinase with their specific inhibitors, LY294002 and Akt 1/2 kinase inhibitor, significantly reduced TCDD-enhanced proliferation of HAPI microglial cells. In conclusion, TCDD stimulates proliferation of HAPI microglial cells by affecting the Akt/GSK-3/cyclin D1 signaling pathway. (Keyword) Cell Adhesion / Cell Count / Cell Cycle / Cell Line / Cell Proliferation / Cyclin D1 / Deoxyuridine / Environmental Pollutants / Enzyme-Linked Immunosorbent Assay / Glycogen Synthase Kinase 3 / Humans / Microglia / Oncogene Protein v-akt / Phosphorylation / RNA / RNA, Small Interfering / Real-Time Polymerase Chain Reaction / Signal Transduction / Tetrachlorodibenzodioxin / beta Catenin (Link to Publication Site) ● Publication site (DOI): 10.1016/j.toxlet.2013.11.003 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24231000 ● Search Scopus @ Elsevier (PMID): 24231000 ● Search Scopus @ Elsevier (DOI): 10.1016/j.toxlet.2013.11.003 (DOI: 10.1016/j.toxlet.2013.11.003, PubMed: 24231000)
20.	Guangfei Xu, Yuanye Li, Katsuhiko Yoshimoto, Gang Chen, Chunhua Wan, Takeo Iwata, Noriko Mizusawa, Zhiqing Duan, Jiao Liu and Junkang Jiang : 2,3,7,8-Tetrachlorodibenzo-p-dioxin-induced inflammatory activation is mediated by intracellular free calcium in microglial cells, Toxicology, Vol.308, 158-167, 2013. (Summary) 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has been known to induce inflammatory signaling in a number of cell types and tissues. However, the adverse effects of TCDD on the central nervous system (CNS) have not been entirely elucidated. In this study, using reverse transcriptase PCR (RT-PCR) and ELISA, we showed that TCDD up-regulated the expression and secretion of tumor necrosis factor-alpha (TNF-α) in a time-dependent manner in cultured HAPI microglial cells. TCDD also caused a fast (within 30min as judged by the increase in its mRNA level) activation of cytosolic phospholipase A2 (cPLA2). This initial action was accompanied by up-regulation of cyclooxygenase-2 (COX-2), an important inflammation marker within 1h after TCDD treatment. These pro-inflammatory responses were inhibited by two types of Ca(2+) blockers, bis-(o-aminophenoxy) ethane-N,N,N',N'-tetra-acetic acid acetoxymethyl ester (BAPTA-AM) and nifedipine, thus, indicating that the effects are triggered by initial increase in the intracellular concentration of free Ca(2+) ([Ca(2+)]i). Further, TCDD exposure could induce phosphorylation- and ubiquitination-dependent degradation of I Bα, and the translocation of NF-κB p65 from the cytosol to the nucleus in this microglial cell line. Thus, the NF-κB signaling pathway can be activated after TCDD treatment. However, Ca(2+) blockers also obviously attenuated NF-κB activation and transnuclear transport induced by TCDD. In concert with these results, we highlighted that the secretion of pro-inflammatory cytokine and NF-κB activation induced by TCDD can be mediated by elevation of [Ca(2+)]i in HAPI microglial cells. (Keyword) Animals / Calcium / Inflammation / Intracellular Fluid / Microglia / Rats / Rats, Sprague-Dawley / Tetrachlorodibenzodioxin (Link to Publication Site) ● Publication site (DOI): 10.1016/j.tox.2013.04.002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23583884 ● Summary page in Scopus @ Elsevier: 2-s2.0-84877349038 (DOI: 10.1016/j.tox.2013.04.002, PubMed: 23583884, Elsevier: Scopus)
21.	Hiromi Nakae, Daisuke Hinode, 薮内さつき, Masami Yoshioka, Hiroki Iga, Fumiaki Kawano and Katsuhiko Yoshimoto : The usefulness of the educational management network system for promoting "dental education program with community-rearing", The Journal of Japan Society of Dental Hygiene Education, Vol.4, No.1, 49-54, 2013. (Keyword) 地域育成型歯学教育 / 教育管理ネットワークシステム / 学外体験学習 / dental education program with community-rearing / the educational management network system / practice in off-campus experiential learning (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1522262181041421824 (CiNii: 1522262181041421824)
22.	Kyoko Ishimoto, Takeo Iwata, Hisaaki Taniguchi, Noriko Mizusawa, Eiji Tanaka and Katsuhiko Yoshimoto : d-Dopachrome tautomerase promotes IL-6 expression and inhibits adipogenesis in preadipocytes., Cytokine, Vol.60, 772-777, 2012. (Summary) We previously identified d-dopachrome tautomerase (DDT) as a novel adipokine whose mRNA levels in adipocytes are negatively correlated with obesity-related clinical parameters, and which acts on adipocytes to regulate lipid metabolism. Here we investigated functions of DDT on preadipocytes. Recombinant DDT (rDDT) enhanced both the expression and secretion of interleukin-6 (IL-6) in SGBS cells, a human preadipocyte cell line. Treatment with rDDT increased levels of phosphorylated ERK1/2, but not p38, in SGBS cells, and rDDT-induced IL-6 mRNA expression was attenuated by pretreatment with an ERK inhibitor, U0126. Knockdown of CD74, but not CD44, inhibited rDDT-induced IL-6 mRNA expression in SGBS cells. These results suggested that the rDDT-induced IL-6 expression in preadipocytes occurred through the CD74-ERK pathway. Furthermore, in SGBS cells subjected to adipogenic induction, rDDT decreased the amount of triacylglycerol, number of cells with oil droplets, and levels of mRNA encoding adipocyte marker proteins. Increased expression of CCAAT/enhancer binding protein families and peroxisome proliferator-activated receptor 2 during adipogenesis was inhibited in the cells treated with rDDT. These results suggested DDT to inhibit adipogenesis by suppressing the expression of genes encoding adipogenic regulators in preadipocytes. (Tokushima University Institutional Repository) ● Metadata: 109657 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.cyto.2012.07.037 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22951300 ● Search Scopus @ Elsevier (PMID): 22951300 ● Search Scopus @ Elsevier (DOI): 10.1016/j.cyto.2012.07.037 (Tokushima University Institutional Repository: 109657, DOI: 10.1016/j.cyto.2012.07.037, PubMed: 22951300)
23.	Takeo Iwata, Hisaaki Taniguchi, Masamichi Kuwajima, Takako Taniguchi, Okuda Yuko, Akiko Sukeno, Kyoko Ishimoto, Noriko Mizusawa and Katsuhiko Yoshimoto : The action of D-dopachrome tautomerase as an adipokine in adipocyte lipid metabolism, PLoS ONE, Vol.7, No.3, e33402, 2012. (Summary) Adipose tissue is a critical exchange center for complex energy transactions involving triacylglycerol storage and release. It also has an active endocrine role, releasing various adipose-derived cytokines (adipokines) that participate in complex pathways to maintain metabolic and vascular health. Here, we found D-dopachrome tautomerase (DDT) as an adipokine secreted from human adipocytes by a proteomic approach. DDT mRNA levels in human adipocytes were negatively correlated with obesity-related clinical parameters such as BMI, and visceral and subcutaneous fat areas. Experiments using SGBS cells, a human preadipocyte cell line, revealed that DDT mRNA levels were increased in an adipocyte differentiation-dependent manner and DDT was secreted from adipocytes. In DDT knockdown adipocytes differentiated from SGBS cells that were infected with the adenovirus expressing shRNA against the DDT gene, mRNA levels of genes involved in both lipolysis and lipogenesis were slightly but significantly increased. Furthermore, we investigated AMP-activated protein kinase (AMPK) signaling, which phosphorylates and inactivates enzymes involved in lipid metabolism, including hormone-sensitive lipase (HSL) and acetyl-CoA carboxylase (ACC), in DDT knockdown adipocytes. The AMPK phosphorylation of HSL Ser-565 and ACC Ser-79 was inhibited in DDT knockdown cells and recovered in the cells treated with recombinant DDT (rDDT), suggesting that down-regulated DDT in adipocytes brings about a state of active lipid metabolism. Furthermore, administration of rDDT in db/db mice improved glucose intolerance and decreased serum free fatty acids levels. In the adipose tissue from rDDT-treated db/db mice, not only increased levels of HSL phosphorylated by AMPK, but also decreased levels of HSL phosphorylated by protein kinase A (PKA), which phosphorylates HSL to promote its activity, were observed. These results suggested that DDT acts on adipocytes to regulate lipid metabolism through AMPK and/or PKA pathway(s) and improves glucose intolerance caused by obesity. (Keyword) AMP-Activated Protein Kinases / Adipocytes / Adipokines / Animals / Blotting, Western / Body Mass Index / Cell Differentiation / DNA Primers / Gene Knockdown Techniques / Humans / Intramolecular Oxidoreductases / Lipid Metabolism / Mice / Microscopy, Fluorescence / Phosphorylation / Proteomics / Reverse Transcriptase Polymerase Chain Reaction / Signal Transduction (Tokushima University Institutional Repository) ● Metadata: 109634 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0033402 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22428043 ● Search Scopus @ Elsevier (PMID): 22428043 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0033402 (Tokushima University Institutional Repository: 109634, DOI: 10.1371/journal.pone.0033402, PubMed: 22428043)
24.	中江弘美, Daisuke Hinode, 薮内さつき, Yuko Takeuchi, Masami Yoshioka, Hiroki Iga, Masanori Nakano, Hideo Yoshida, Kazumi Ozaki, Masaru Hada, Fumiaki Kawano and Katsuhiko Yoshimoto : 地域高齢者との福祉体験学習の教育効果と地域貢献事業としての評価, Journal of University Education Research, Vol.8, 17-24, 2011. (Summary) The purose of this study is to evaluate the educational effect by the welfare-experience learning program with aged people in community，and to evaluate this program as the regional contribution. This program is to aim at having a consciousness of becoming the dental professional in the University of Tokushima，Faculty of Dentistry，and they were carried out with 16 institutions (a total of 28 times).This program makes students accompany the oral health guidance"long-life oral healthy classroom"，and they carried out the experience study as on auxiliary person of the variaus functional oral-training for elderly people.By the investigation of the student's report, there are students who recognized the achievement objectives which are roles of the way concerning regional contribution as dental professionals in community. On the other hand，the questionnaire to the participating persoonnel was conducted in order to evalaote this program as the regional contrtbution. As a result，this program is useful to elderly people and the understanding of institution personnel is also deepened this practice. As mentioned above，the result of having is suitable for the educational goal "to have a consciousness of becoming the dental professional". Furthermore，this program was considered that future continuation is also expected by deepening of an understanding to the personnel's functional oral-training program.本研究の目的は，地域高齢者との福祉体験学習における学生への教育効果と，地域貢献事業としての評価をすることである．徳島大学歯学部では，医療人を志すものとしての自覚を持つことを目的とした取り組みを県内16カ所の施設で合計28回実施した．これは，学生が口腔保健指導「お口の健康長寿教室」において，高齢者を対象とした口腔機能訓練の補助者として体験学習するものである．学習後のレポートから，到達目標とした地域貢献の在り方や歯科専門職としての役割を認識する学生が多くを占めた．一方，地域貢献事業として評価するため，参加職員への調査を行った結果，利用者への役立ちに加え，多くの施設職員の理解も深まったとのアンケート結果が得られた．以上から，本取り組みは学生への教育目標「医療人としての自覚を持つ」に沿った成果が得られており，また，施設職員の口腔機能向上プ口グラムへの盤解の深まりから，今後の継続が期待される． (Keyword) experience learning / educational effects / regional contribution (Tokushima University Institutional Repository) ● Metadata: 82982 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050302172854724224 (Tokushima University Institutional Repository: 82982, CiNii: 1050302172854724224)
25.	Yohko Hirata, Toshio Hosaka, Takeo Iwata, Le Thi Kim Chung, Bayasgalan Jambaldorj, Kiyoshi Teshigawara, Nagakatsu Harada, Hiroshi Sakaue, Tohru Sakai, Katsuhiko Yoshimoto and Yutaka Nakaya : Vimentin binds IRAP and is involved in GLUT4 vesicle trafficking., Biochemical and Biophysical Research Communications, Vol.405, No.1, 96-101, 2011. (Summary) Insulin-responsive aminopeptidase (IRAP) and GLUT4 are two major cargo proteins of GLUT4 storage vesicles (GSVs) that are translocated from a postendosomal storage compartment to the plasma membrane (PM) in response to insulin. The cytoplasmic region of IRAP is reportedly involved in retention of GSVs. In this study, vimentin was identified using the cytoplasmic domain of IRAP as bait. The validity of this interaction was confirmed by pull-down assays and immunoprecipitation in 3T3-L1 adipocytes. In addition, it was shown that GLUT4 translocation to the PM by insulin was decreased in vimentin-depleted adipocytes, presumably due to dispersing GSVs away from the cytoskeleton. These findings suggest that the IRAP binding protein, vimentin, plays an important role in retention of GSVs. (Keyword) 3T3-L1 Cells / Animals / Cystinyl Aminopeptidase / Cytoplasmic Vesicles / Gene Knockdown Techniques / Glucose Transporter Type 4 / Mice / Protein Transport / Vimentin (Tokushima University Institutional Repository) ● Metadata: 113298 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2010.12.134 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21216232 ● Search Scopus @ Elsevier (PMID): 21216232 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2010.12.134 (Tokushima University Institutional Repository: 113298, DOI: 10.1016/j.bbrc.2010.12.134, PubMed: 21216232)
26.	Setsuko Hatakeyama, Noriko Mizusawa, Reiko Tsutsumi, Katsuhiko Yoshimoto, Harumi Mizuki, Shigeru Yasumoto, Shigehiro Sato and Yasunori Takeda : Establishment of human dental epithelial cell lines expressing ameloblastin and enamelin by transfection of hTERT and cdk4 cDNAs., Journal of Oral Pathology & Medicine, Vol.40, No.3, 227-234, 2010. (Summary) We established three cell lines by transfection of hTERT and cdk4 cDNAs, which were characterized as dental epithelial progenitor cells containing ameloblast-lineage cell phenotype. (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1600-0714.2010.00950.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20923449 ● Search Scopus @ Elsevier (PMID): 20923449 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1600-0714.2010.00950.x (DOI: 10.1111/j.1600-0714.2010.00950.x, PubMed: 20923449)
27.	Mustafizur Md Rahman, Zhi-Rong Qian, Elaine Wang Lu, Katsuhiko Yoshimoto, Masahiko Nakasono, Razia Sultana, Tomoyuki Yoshida, Toshitetsu Hayashi, Reiji Haba, Mitsuaki Ishida, Hidetoshi Okabe and Toshiaki Sano : DNA methyltransferases 1, 3a, and 3b overexpression and clinical significance in gastroenteropancreatic neuroendocrine tumors., Human Pathology, Vol.41, No.8, 1069-1078, 2010. (Summary) The alteration of DNA methylation is one of the most common epigenetic changes in human cancers. Three genes, namely, DNA methyltransferase 1, 3a, and 3b, which code for DNA methyltransferases that affect promoter methylation status, are thought to play an important role in the development of cancers and may be good anticancer therapy targets. The methylation of tumor suppressor genes has been reported in gastroenteropancreatic neuroendocrine tumors; however, there have been no studies about DNA methyltransferase protein expression and its clinical significance in gastroenteropancreatic neuroendocrine tumors. In this study, the expression of DNA methyltransferase 1, 3a, and 3b was studied in 63 gastroenteropancreatic neuroendocrine tumors by immunohistochemistry. The expression of DNA methyltransferase 1, 3a, and 3b was frequently detected in gastroenteropancreatic neuroendocrine tumors (87%, 81%, and 75%, respectively). The DNA methyltransferase 3a expression level was significantly higher in poorly differentiated neuroendocrine carcinomas than in well-differentiated neuroendocrine tumors or well-differentiated neuroendocrine carcinomas (P < .01 and P < .05, respectively). The expression of DNA methyltransferase 1, 3a, and 3b showed significantly higher levels in stage IV tumors than in stage I or II tumors. In addition, the expression levels of DNA methyltransferase 1, 3a, and 3b were positively correlated with the MIB-1 labeling index in gastroenteropancreatic neuroendocrine tumors (R = 0.293, P = .019; R = 0.457, P = .001; and R = 0.249, P = .049; respectively). In addition, the expression levels and positive immunostaining frequencies of DNA methyltransferase 3a and 3b were significantly lower in midgut neuroendocrine tumors than in foregut or hindgut neuroendocrine tumors. Our findings suggest that the overexpression of DNA methyltransferase 1, 3a, and 3b is related to tumorigenesis and the progression of gastroenteropancreatic neuroendocrine tumors. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.humpath.2010.01.011 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20381114 ● Search Scopus @ Elsevier (PMID): 20381114 ● Search Scopus @ Elsevier (DOI): 10.1016/j.humpath.2010.01.011 (DOI: 10.1016/j.humpath.2010.01.011, PubMed: 20381114)
28.	Lu Elaine Wang, Zhi-Rong Qian, Mustafizur Md Rahman, Katsuhiko Yoshimoto, Shozo Yamada, Eiji Kudo and Toshiaki Sano : Increased expression of HMGA1 correlates with tumour invasiveness and proliferation in human pituitary adenomas., Histopathology, Vol.56, No.4, 501-509, 2010. (Summary) AIMS: High-mobility group A1 (HMGA1) is highly expressed in various benign and malignant tumours. The development of pituitary adenoma in Hmga1 transgenic mice has been reported. However, no studies have investigated HMGA1 expression and its clinical significance in human pituitary adenomas. METHODS AND RESULTS: Immunohistochemical expression of HMGA1 was analysed with respect to various clinicopathological factors in 95 pituitary adenomas. Nuclear expression of HMGA1 was observed in 62% of pituitary adenomas, whereas normal adenohypophysial tissues were negative. Although HMGA1 expression was frequently detected in clinically non-functioning adenomas - 90% of silent adrenocorticotropic hormone (ACTH), 76.2% of follicle-stimulating hormone/luteinizing hormone and 100% of null cell adenomas - it was also detected in 48.1% of growth hormone (GH), 60% of mixed GH/prolactin (PRL), 62.5% of PRL, 66.6% of thyroid-stimulating hormone and 37.5% of ACTH adenomas. HMGA1 expression was significantly higher in invasive adenomas or macroadenomas than in non-invasive adenomas or microadenomas (invasive versus non-invasive, P < 0.05; macroadenoma versus microadenoma, P < 0.05). In addition, HMGA1 showed the highest level in grade IV, more aggressive pituitary adenomas, than in grades I, II and III (IV versus I, P = 0.01; IV versus II, P = 0.01; IV versus III, P = 0.07). Furthermore, a significant correlation between HMGA1 expression and MIB-1 labelling index was observed (R = 0.368, P < 0.0002). CONCLUSIONS: These findings suggest that HMGA1 up-regulation has an important oncogenic role in pituitary tumorigenesis, as well as being a novel molecular marker of tumour proliferation and invasiveness. (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1365-2559.2010.03495.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20459557 ● Search Scopus @ Elsevier (PMID): 20459557 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2559.2010.03495.x (DOI: 10.1111/j.1365-2559.2010.03495.x, PubMed: 20459557)
29.	Lu Elaine Wang, Zhi-Rong Qian, Masahiko Nakasono, Toshihito Tanahashi, Katsuhiko Yoshimoto, Yoshimi Bando, Eiji Kudo, Mitsuo Shimada and Toshiaki Sano : High expression of Toll-like receptor 4/myeloid differentiation factor 88 signals correlates with poor prognosis in colorectal cancer., British Journal of Cancer, Vol.102, No.5, 908-915, 2010. (Summary) BACKGROUND: The Toll-like receptor (TLR) 4 signalling pathway has been shown to have oncogenic effects in vitro and in vivo. To demonstrate the role of TLR4 signalling in colon tumourigenesis, we examined the expression of TLR4 and myeloid differentiation factor 88 (MyD88) in colorectal cancer (CRC). METHODS: The expression of TLR4 and MyD88 in 108 CRC samples, 15 adenomas, and 15 normal mucosae was evaluated by immunohistochemistry, and the correlations between their immunoscores and clinicopathological variables, including disease-free survival (DFS) and overall survival (OS), were analysed. RESULTS: Compared with normal mucosae and adenomas, 20% cancers displayed high expression of TLR4, and 23% cancers showed high expression of MyD88. The high expression of TLR4 and MyD88 was significantly correlated with liver metastasis (P=0.0001, P=0.0054). In univariate analysis, the high expression of TLR4 was significantly associated with shorter OS (hazard ratio (HR): 2.17; 95% confidence interval (95% CI): 1.15-4.07; P=0.015). The high expression of MyD88 expression was significantly associated with poor DFS and OS (HR: 2.33; 95% CI: 1.31-4.13; P=0.0038 and HR: 3.03; 95% CI: 1.67-5.48; P=0.0002). The high combined expression of TLR4 and MyD88 was also significantly associated with poor DFS and OS (HR: 2.25; 95% CI: 1.27-3.99; P=0.0053 and HR: 2.97; 95% CI: 1.64-5.38; P=0.0003). Multivariate analysis showed that high expressions of TLR4 (OS: adjusted HR: 1.88; 95% CI: 0.99-3.55; P=0.0298) and MyD88 (DFS: adjusted HR: 1.93; 95% CI: 1.01-3.67; P=0.0441; OS: adjusted HR: 2.25; 95% CI: 1.17-4.33; P=0.0112) were independent prognostic factors of OS. Furthermore, high co-expression of TLR4/MyD88 was strongly associated with both poor DFS and OS. CONCLUSION: Our findings suggest that high expression of TLR4 and MyD88 is associated with liver metastasis and is an independent predictor of poor prognosis in patients with CRC. (Keyword) Adenocarcinoma, Mucinous / Aged / Colon / Colorectal Neoplasms / female / Follow-Up Studies / Humans / Immunoenzyme Techniques / Liver Neoplasms / male / Myeloid Differentiation Factor 88 / Neoplasm Invasiveness / Neoplasm Recurrence, Local / Peritoneal Neoplasms / Prognosis / Rectum / Survival Rate / Toll-Like Receptor 4 / Tumor Markers, Biological (Tokushima University Institutional Repository) ● Metadata: 114377 (Link to Publication Site) ● Publication site (DOI): 10.1038/sj.bjc.6605558 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20145615 ● Summary page in Scopus @ Elsevier: 2-s2.0-77649272127 (Tokushima University Institutional Repository: 114377, DOI: 10.1038/sj.bjc.6605558, PubMed: 20145615, Elsevier: Scopus)
30.	Golam Md Hossain, Takeo Iwata, Noriko Mizusawa, Nazatul Shahidan Wan Shima, Toru Okutsu, Kyoko Ishimoto and Katsuhiko Yoshimoto : Compressive force inhibits adipogenesis through COX-2-mediated down-regulation of PPARgamma2 and C/EBPalpha., Journal of Bioscience and Bioengineering, Vol.109, No.3, 297-303, 2010. (Summary) Various mechanical stimuli affect differentiation of mesoderm-derived cells such as osteoblasts or myoblasts, suggesting that adipogenesis may also be influenced by mechanical stimulation. However, effects of mechanical stimuli on adipogenesis are scarcely known. Compressive force was applied to a human preadipocyte cell line, SGBS. Levels of gene expression were estimated by real-time reverse transcription-polymerase chain reaction. The accumulation of lipids was evaluated by Sudan III or Oil Red O staining. In SGBS cells subjected to a compressive force of 226 Pa for 12 h before adipogenic induction, adipogenesis was inhibited. Compressive force immediately after adipogenic induction did not affect the adipogenesis. The expression of peroxisome proliferator-activated receptor (PPAR) gamma2 and CCAAT/enhancer binding protein (C/EBP) alpha mRNA during adipogenesis was inhibited by compressive force, whereas C/EBPbeta and C/EBPdelta mRNA levels were unaffected. In preadipocytes, compressive force increased mRNA levels of Krüppel-like factor 2, preadipocyte factor 1, WNT10b, and cyclooxygenase-2 (COX-2) which are known as negative regulators for the PPARgamma2 and C/EBPalpha genes. Furthermore, a COX-2 inhibitor completely reversed the inhibition of adipogenesis by compressive force. In conclusion, compressive force inhibited adipogenesis by suppressing expression of PPARgamma2 and C/EBPalpha in a COX-2-dependent manner. (Keyword) Adipocytes / Adipogenesis / CCAAT-Enhancer-Binding Protein-alpha / Cells, Cultured / Compressive Strength / Cyclooxygenase 2 / Down-Regulation / Humans / Mechanotransduction, Cellular / PPAR gamma / Physical Stimulation / Stress, Mechanical (Tokushima University Institutional Repository) ● Metadata: 109655 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jbiosc.2009.09.003 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20159581 ● Search Scopus @ Elsevier (PMID): 20159581 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jbiosc.2009.09.003 (Tokushima University Institutional Repository: 109655, DOI: 10.1016/j.jbiosc.2009.09.003, PubMed: 20159581)
31.	Susana Igreja, S Harvinder Chahal, Peter King, B Graeme Bolger, Umasuthan Srirangalingam, Leonardo Guasti, Paul J Chapple, Giampaolo Trivellin, Maria Gueorguiev, Katie Guegan, Karen Stals, Bernard Khoo, V Ajith Kumar, Sian Ellard, B Ashley Grossman, Márta Korbonits, Takeo Iwata, Katsuhiko Yoshimoto and 他54名 : Characterization of aryl hydrocarbon receptor interacting protein (AIP) mutations in familial isolated pituitary adenoma families., Human Mutation, Vol.31, No.8, 950-960, 2010. (Summary) Familial isolated pituitary adenoma (FIPA) is an autosomal dominant condition with variable genetic background and incomplete penetrance. Germline mutations of the aryl hydrocarbon receptor interacting protein (AIP) gene have been reported in 15-40% of FIPA patients. Limited data are available on the functional consequences of the mutations or regarding the regulation of the AIP gene. We describe a large cohort of FIPA families and characterize missense and silent mutations using minigene constructs, luciferase and beta-galactosidase assays, as well as in silico predictions. Patients with AIP mutations had a lower mean age at diagnosis (23.6+/-11.2 years) than AIP mutation-negative patients (40.4+/-14.5 years). A promoter mutation showed reduced in vitro activity corresponding to lower mRNA expression in patient samples. Stimulation of the protein kinase A-pathway positively regulates the AIP promoter. Silent mutations led to abnormal splicing resulting in truncated protein or reduced AIP expression. A two-hybrid assay of protein-protein interaction of all missense variants showed variable disruption of AIP-phosphodiesterase-4A5 binding. In summary, exonic, promoter, splice-site, and large deletion mutations in AIP are implicated in 31% of families in our FIPA cohort. Functional characterization of AIP changes is important to identify the functional impact of gene sequence variants. (Keyword) Adult / Alternative Splicing / Amino Acid Sequence / Animals / Cell Line / Cyclic AMP / Cyclic AMP-Dependent Protein Kinases / family / Female / Gene Expression Regulation, Neoplastic / Humans / Intracellular Signaling Peptides and Proteins / Male / Middle Aged / Molecular Sequence Data / Mutant Proteins / Mutation / Mutation, Missense / Pedigree / Pituitary Neoplasms / Promoter Regions, Genetic / RNA Splice Sites / RNA, Messenger / Rats / signal transduction (Link to Publication Site) ● Publication site (DOI): 10.1002/humu.21292 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20506337 ● Search Scopus @ Elsevier (PMID): 20506337 ● Search Scopus @ Elsevier (DOI): 10.1002/humu.21292 (DOI: 10.1002/humu.21292, PubMed: 20506337)
32.	Golam M Hossain, Takeo Iwata, Noriko Mizusawa, Zhi-Rong Qian, Nazatul Shahidan Wan Shima, Toru Okutsu, Shozo Yamada, Toshiaki Sano and Katsuhiko Yoshimoto : Expression of p18(INK4C) is down-regulated in human pituitary adenomas., Endocrine Pathology, Vol.20, No.2, 114-121, 2009. (Summary) Cyclin-dependent kinase inhibitors represented by the INK4 family comprising p16(INK4A), p15(INK4B), p18(INK4C), and p19(INK4D) are regulators of the cell cycle shown to be aberrant in many types of cancer. Mice lacking p18(Ink4c) exhibit a series of phenotypes including the development of widespread organomegaly and pituitary adenomas. The objective of our study is to examine the role of p18(INK4C) in the pathogenesis of human pituitary tumors. The protein and mRNA levels of p18(INK4C) were examined by immunohistochemistry and real-time reverse transcription-polymerase chain reaction, respectively. The methylation status of the p18(INK4C) gene promoter and somatic mutations of the p18(INK4C) gene were also investigated. p18(INK4C) protein expression was lost or significantly reduced in 64% of pituitary adenomas compared with levels in normal pituitary glands. p18(INK4C) mRNA levels were low in all ACTH adenomas and non-functioning (NF)-FSH and in 42%, 70% and 66% of GH, PRL, and subtype 3 adenomas, respectively. p18(INK4C) mRNA levels were significantly associated with p18(INK4C) protein levels. Neither methylated promoters in pituitary adenomas, except in one NF-FSH adenoma, nor somatic mutations of the p18(INK4C) gene in any pituitary adenomas were detected. The down-regulation of p18(INK4C) expression may contribute to the tumorigenesis of pituitary adenomas. (Keyword) Adenoma / Adult / Aged / Aged, 80 and over / Cyclin-Dependent Kinase Inhibitor p18 / DNA Methylation / Down-Regulation / Female / Gene Expression Regulation, Neoplastic / Humans / Male / Middle Aged / Mutation / Pituitary Neoplasms / RNA, Messenger (Tokushima University Institutional Repository) ● Metadata: 109645 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12022-009-9076-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19401813 ● Search Scopus @ Elsevier (PMID): 19401813 ● Search Scopus @ Elsevier (DOI): 10.1007/s12022-009-9076-0 (Tokushima University Institutional Repository: 109645, DOI: 10.1007/s12022-009-9076-0, PubMed: 19401813)
33.	Takeo Iwata, Masamichi Kuwajima, Akiko Sukeno, Naozumi Ishimaru, Yoshio Hayashi, Martin Wabitsch, Noriko Mizusawa, Mitsuo Itakura and Katsuhiko Yoshimoto : YKL-40 secreted from adipose tissue inhibits degradation of type I collagen., Biochemical and Biophysical Research Communications, Vol.388, No.3, 511-516, 2009. (Summary) Obesity is considered a chronic low-grade inflammatory status and the stromal vascular fraction (SVF) cells of adipose tissue (AT) are considered a source of inflammation-related molecules. We identified YKL-40 as a major protein secreted from SVF cells in human visceral AT. YKL-40 expression levels in SVF cells from visceral AT were higher than in those from subcutaneous AT. Immunofluorescence staining revealed that YKL-40 was exclusively expressed in macrophages among SVF cells. YKL-40 purified from SVF cells inhibited the degradation of type I collagen, a major extracellular matrix of AT, by matrix metalloproteinase (MMP)-1 and increased rate of fibril formation of type I collagen. The expression of MMP-1 in preadipocytes and macrophages was enhanced by interaction between these cells. These results suggest that macrophage/preadipocyte interaction enhances degradation of type I collagen in AT, meanwhile, YKL-40 secreted from macrophages infiltrating into AT inhibits the type I collagen degradation. (Keyword) Adipocytes / Adipose Tissue / Adult / Aged / Cells, Cultured / Coculture Techniques / Collagen Type I / Female / Glycoproteins / Humans / Inflammation / Lectins / Macrophages / Male / Matrix Metalloproteinase 1 / Middle Aged / Obesity / Stromal Cells (Tokushima University Institutional Repository) ● Metadata: 109641 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2009.08.024 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19666003 ● Search Scopus @ Elsevier (PMID): 19666003 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2009.08.024 (Tokushima University Institutional Repository: 109641, DOI: 10.1016/j.bbrc.2009.08.024, PubMed: 19666003)
34.	Zhi-Rong Qian, Sylvia L Asa, Haruhiko Siomi, Mikiko Siomi, Katsuhiko Yoshimoto, Shozo Yamada, Elaine Lu Wang, Md Mustafizur Rahman, Hiroshi Inoue, Mitsuo Itakura, Eiji Kudo and Toshiaki Sano : Overexpression of HMGA2 relates to reduction of the let-7 and its relationship to clinicopathological features in pituitary adenomas., Modern Pathology, Vol.22, No.3, 431-441, 2009. (Summary) High-mobility group A2 is highly expressed during embryogenesis and in various benign and malignant tumors. Recent studies report that high-mobility group A2 is negatively regulated by the let-7 microRNAs (miRNAs) family in vitro. The development of pituitary adenomas in high-mobility group A2 transgenic mice showed that high-mobility group A2 may be involved in pituitary tumorigenesis. However, no studies have investigated the clinical significance of high-mobility group A2 and its relationship to the let-7 miRNA family in human pituitary adenomas. Using immunohistochemistry, we analyzed high-mobility group A2 expression with respect to various clinicopathologic factors in 98 pituitary adenomas. Overexpression of high-mobility group A2 was observed in 39% (38/98) of pituitary adenomas compared with normal adenohypophysial tissue and was frequently found in adenomas including prolactin (PRL), adrenocorticotrophic hormone, or follicle-stimulating hormone/luteinizing hormone and in null cell adenomas, but relatively rare in growth hormone (GH) and mixed GH/PRL adenomas. High-mobility group A2 expression was significantly associated with tumor invasion (P<0.05) and was significantly higher in grade IV than in grades I, II, and III adenomas (P<0.05). High levels of high-mobility group A2 expression were more frequently observed in macroadenomas than in microadenomas (P<0.05). High levels of high-mobility group A2 expression also significantly correlated with the proliferation marker Ki-67 (P<0.0001). Real-time quantitative RT-PCR analysis was carried out to evaluate the expression of let-7 in 55 pituitary adenomas. Subsequently, decreased expression of let-7 was confirmed in 23 of 55 (42%) adenomas and was correlated with high-grade tumors (P<0.05). An inverse correlation between let-7 and high-mobility group A2 expression was evident (R=-0.33, P<0.05). These findings support a causal link between let-7 and high-mobility group A2 whereby loss of let-7 expression induces high-mobility group A2 upregulation that represents an important mechanism in pituitary tumorigenesis and progression. (Keyword) Adenoma / Disease Progression / Female / Gene Expression / HMGA2 Protein / Humans / Immunohistochemistry / Male / MicroRNAs / Pituitary Neoplasms / Reverse Transcriptase Polymerase Chain Reaction / Tumor Markers, Biological / Up-Regulation (Link to Publication Site) ● Publication site (DOI): 10.1038/modpathol.2008.202 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19136928 ● Search Scopus @ Elsevier (PMID): 19136928 ● Search Scopus @ Elsevier (DOI): 10.1038/modpathol.2008.202 (DOI: 10.1038/modpathol.2008.202, PubMed: 19136928)
35.	Masaki Yoshida, Nagakatsu Harada, Hironori Yamamoto, Yutaka Taketani, Nagakatsu Harada, Yunjie Yin, Atsushi Hattori, Tomoe Zenitani, Sayuri Hara, Haruka Yonemoto, Aki Nakamura, Masayuki Nakano, Kazuaki Mawatari, Kiyoshi Teshigawara, Hidekazu Arai, Toshio Hosaka, Akira Takahashi, Katsuhiko Yoshimoto and Yutaka Nakaya : Identification of cis-acting promoter sequences required for expression of the glycerol-3-phosphate acyltransferase 1 gene in mice., Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids, Vol.1791, No.1, 39-52, 2009. (Summary) Glycerol-3-phosphate acyltransferase 1 (GPAT1) is a rate limiting enzyme in de novo glycerophospholipid synthesis. The murine GPAT1 promoter sequence (the "classical" sequence) was reported previously. However, the organization of this DNA sequence does not fully match the mouse genome sequences on NCBI/GenBank. Here we have identified net cis-acting promoter sequences for the mouse GPAT1 gene: promoter 1a which includes part of the classical sequence and the downstream promoter 1b. Promoter 1a facilitates transcription of two alternative GPAT1 transcript variants, GPAT1-V1 and V2, while promoter 1b produces a third transcript variant, GPAT1-V3. Upstream stimulating factor-1 (USF-1) controlled both promoters whereas sterol regulatory element-binding protein-1 (SREBP-1) exclusively regulated promoter 1a activity in vitro. Feeding increased GPAT1-V1 and V2, but not V3 mRNA levels in mouse liver. The obese condition of db/db mice did not alter the hepatic expression levels of any of the three GPAT1 variants. Feeding enhanced hepatic mRNA levels, intranuclear protein levels and promoter 1a-binding levels of SREBP-1, but not of USF-1. Thus, promoter 1a was exclusively activated by routine feeding in vivo. Our results indicate differential roles of the two promoters in the regulation of hepatic GPAT1 gene expression in mice. (Keyword) Animals / Base Sequence / Cell Line, Tumor / Gene Expression Regulation, Enzymologic / Glycerol-3-Phosphate O-Acyltransferase / Hepatocytes / Humans / Male / Mice / Mice, Obese / Promoter Regions, Genetic / RNA Interference / Sterol Regulatory Element Binding Protein 1 / Upstream Stimulatory Factors (Tokushima University Institutional Repository) ● Metadata: 113301 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbalip.2008.09.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18983939 ● Search Scopus @ Elsevier (PMID): 18983939 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbalip.2008.09.005 (Tokushima University Institutional Repository: 113301, DOI: 10.1016/j.bbalip.2008.09.005, PubMed: 18983939)
36.	Daisuke Hinode, Hiroki Iga, Masanori Nakano, Fumiaki Kawano and Katsuhiko Yoshimoto : 教育GP「高齢社会を担う地域育成型歯学教育」(第1報) 高齢者交流学習による教育効果, Shikoku Dental Research, Vol.22, No.1, 129-131, 2009. (Summary) 歯学部1年生22名(口腔保健学科16名，歯学科6名)を対象に，平成20年度に実施した高齢者交流学習の教育効果について考察した．交流前には同施設長より生と死，老いについて特別講義を受け，4回目の交流後及び最終回の交流後にふり返り授業を実施した．交流学習の教育効果については毎回の学習記録と共に自己評価を10点満点で記載させた．養護老人ホームにおいて高齢者との1対1の交流からコミュニケーションを養う交流学習を実施した結果，交流後の学習記録に認められる心に深く感じた内容や自己評価点数の上昇，更に四つの到達目標に沿った表現の記載が参加学生から認められたことから，1年次に実施した取り組みは人間力の向上という一般目標に適した有効な教育カリキュラムであると思われた． (Keyword) 歯科学生カリキュラム教育測定コミュニケーション医療従事者-患者関係地域社会歯科学特別養護老人ホーム高齢者歯科医療歯学大学教育高齢化社会ヒト成人(19~44) 歯学 (Tokushima University Institutional Repository) ● Metadata: 109789 (Tokushima University Institutional Repository: 109789)
37.	Chrysanthia A. Leontiou, Maria Gueorguiev, Jacqueline der Spuy van, Richard Quinton, Francesca Lolli, Sevda Hassan, Harvinder S. Chahal, Susana C. Igreja, Suzanne Jordan, Janice Rowe, Marie Stolbrink, Helen C. Christian, Jessica Wray, David Bishop-Bailey, Dan M. Berney, John A. H. Wass, Vera Popovic, Antônio Ribeiro-Oliveira, Monica R. Gadelha, John P. Monson, Scott A. Akker, Julian R. E. Davis, Richard N. Clayton, Katsuhiko Yoshimoto, Takeo Iwata, Akira Matsuno, Kuniki Eguchi, Mâdâlina Musat, Daniel Flanagan, Gordon Peters, Graeme B. Bolger, J Paul Chapple, Lawrence A. Frohman, Ashley B. Grossman and Márta Korbonits : The role of the aryl hydrocarbon receptor-interacting protein gene in familial and sporadic pituitary adenomas., The Journal of Clinical Endocrinology and Metabolism, Vol.93, No.6, 2390-2401, 2008. (Summary) Mutations have been identified in the aryl hydrocarbon receptor-interacting protein (AIP) gene in familial isolated pituitary adenomas (FIPA). It is not clear, however, how this molecular chaperone is involved in tumorigenesis. AIP sequence changes and expression were studied in FIPA and sporadic adenomas. The function of normal and mutated AIP molecules was studied on cell proliferation and protein-protein interaction. Cellular and ultrastructural AIP localization was determined in pituitary cells. Twenty-six FIPA kindreds and 85 sporadic pituitary adenoma patients were included in the study. Nine families harbored AIP mutations. Overexpression of wild-type AIP in TIG3 and HEK293 human fibroblast and GH3 pituitary cell lines dramatically reduced cell proliferation, whereas mutant AIP lost this ability. All the mutations led to a disruption of the protein-protein interaction between AIP and phosphodiesterase-4A5. In normal pituitary, AIP colocalizes exclusively with GH and prolactin, and it is found in association with the secretory vesicle, as shown by double-immunofluorescence and electron microscopy staining. In sporadic pituitary adenomas, however, AIP is expressed in all tumor types. In addition, whereas AIP is expressed in the secretory vesicle in GH-secreting tumors, similar to normal GH-secreting cells, in lactotroph, corticotroph, and nonfunctioning adenomas, it is localized to the cytoplasm and not in the secretory vesicles. Our functional evaluation of AIP mutations is consistent with a tumor-suppressor role for AIP and its involvement in familial acromegaly. The abnormal expression and subcellular localization of AIP in sporadic pituitary adenomas indicate deranged regulation of this protein during tumorigenesis. (Keyword) Acromegaly / Adenoma / Adolescent / Adult / Aged / Cell Proliferation / Child / Cyclic Nucleotide Phosphodiesterases, Type 4 / female / Gene Expression Regulation, Neoplastic / Genetic Testing / Human Growth Hormone / Humans / Intracellular Signaling Peptides and Proteins / male / Middle Aged / Pituitary Neoplasms / Protein Binding / Proteins / Transfection / Tumor Cells, Cultured (Link to Publication Site) ● Publication site (DOI): 10.1210/jc.2007-2611 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18381572 ● Summary page in Scopus @ Elsevier: 2-s2.0-45149085453 (DOI: 10.1210/jc.2007-2611, PubMed: 18381572, Elsevier: Scopus)
38.	Zhi-Rong Qian, Toshiaki Sano, Katsuhiko Yoshimoto, Asa L Sylvia, Shozo Yamada, Noriko Mizusawa and Eiji Kudo : Tumor-specific down-regulation and methylation of the CDH13 (H-cadherin) and CDH1 (E-cadherin) genes correlate with aggressiveness of human pituitary adenomas, Modern Pathology, Vol.20, No.12, 1269-1277, 2007. (Summary) The gene products of CDH13 and CDH1, H-cadherin and E-cadherin, respectively, play a key role in cell-cell adhesion. Inactivation of the cadherin-mediated cell adhesion system caused by aberrant methylation is a common finding in human cancers, indicating that the CDH13 and CDH1 function as tumor suppressor and invasion suppressor genes. In this study, we analyzed the expression of H-cadherin mRNA and E-cadherin protein in 5 normal pituitary tissues and 69 primary pituitary adenomas including all major types by quantitative real-time RT-PCR (qRT-PCR) and immunohistochemistry, respectively. Reduced expression of H-cadherin was detected in 54% (28/52) of pituitary tumors and was significantly associated with tumor aggressiveness (P<0.05). E-cadherin expression was lost in 30% (21 of 69) and significantly reduced in 32% (22 of 69) of tumors. E-cadherin expression was significantly lower in grade II, III, and IV than in grade I adenomas (P=0.015, P=0.029, and P=0.01, respectively). Using methylation-specific PCR (MSP), promoter hypermethylation of CDH13 and CDH1 was detected in 30 and 36% of 69 adenomas, respectively, but not in 5 normal pituitary tissues. Methylation of CDH13 was observed more frequently in invasive adenomas (42%) than in non-invasive adenomas (19%) (P<0.05) and methylation of CDH1 was more frequent in grade IV adenomas compared with grade I adenomas (P<0.05). Methylation of either CDH13 or CDH1 was identified in 35 cases (51%) and was more frequent in grade IV invasive adenomas than in grade I non-invasive adenomas (P<0.05 and P<0.05, respectively). Downregulation of expression was correlated with promoter hypermethylation in CDH13 and CDH1. In conclusion, the tumor-specific downregulation of expression and methylation of CDH13 and CDH1, alone or in combination, may be involved in the development and invasive growth of pituitary adenomas. (Keyword) Adenoma / Adult / Cadherins / DNA Methylation / Down-Regulation / Female / Gene Expression / Humans / Immunohistochemistry / Male / Middle Aged / Pituitary Neoplasms / Promoter Regions, Genetic / Reverse Transcriptase Polymerase Chain Reaction / Tumor Markers, Biological (Link to Publication Site) ● Publication site (DOI): 10.1038/modpathol.3800965 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17873891 ● Search Scopus @ Elsevier (PMID): 17873891 ● Search Scopus @ Elsevier (DOI): 10.1038/modpathol.3800965 (DOI: 10.1038/modpathol.3800965, PubMed: 17873891)
39.	Asa L Sylvia, DiGiovanni Rebecca, Jiang Jing, Ward L Megan, Loesch Kimberly, Shozo Yamada, Toshiaki Sano and Katsuhiko Yoshimoto : A Growth Hormone Receptor Mutation Impairs Growth Hormone Autofeedback Signaling in Pituitary Tumors., Cancer Research, Vol.67, No.15, 7505-7511, 2007. (Summary) Pituitary tumors are a diverse group of neoplasms that are classified based on clinical manifestations, hormone excess, and histomorphologic features. Those that cause growth hormone (GH) excess and acromegaly are subdivided into morphologic variants that have not yet been shown to have pathogenetic significance or predictive value for therapy and outcome. Here, we identify a selective somatic histidine-to-leucine substitution in codon 49 of the extracellular domain of the GH receptor (GHR) in a morphologic subtype of human GH-producing pituitary tumors that is characterized by the presence of cytoskeletal aggresomes. This GHR mutation significantly impairs glycosylation-mediated receptor processing, maturation, ligand binding, and signaling. Pharmacologic GH antagonism recapitulates the morphologic phenotype of pituitary tumors from which this mutation was identified, inducing the formation of cytoskeletal keratin aggresomes. This novel GHR mutation provides evidence for impaired hormone autofeedback in the pathogenesis of these pituitary tumors. It explains the lack of responsiveness to somatostatin analogue therapy of this tumor type, in contrast to the exquisite sensitivity of tumors that lack aggresomes, and has therapeutic implications for the safety of GH antagonism as a therapeutic modality in acromegaly. (Keyword) Adenoma / Carrier Proteins / Cell Proliferation / Feedback, Physiological / Humans / Immunoenzyme Techniques / Mutagenesis, Site-Directed / Mutation / Peptide Fragments / Pituitary Neoplasms / Signal Transduction (Link to Publication Site) ● Publication site (DOI): 10.1158/0008-5472.CAN-07-0219 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17671221 ● Search Scopus @ Elsevier (PMID): 17671221 ● Search Scopus @ Elsevier (DOI): 10.1158/0008-5472.CAN-07-0219 (DOI: 10.1158/0008-5472.CAN-07-0219, PubMed: 17671221)
40.	Takeo Iwata, Noriko Mizusawa, Yutaka Taketani, Mitsuo Itakura and Katsuhiko Yoshimoto : Parafibromin tumor suppressor enhances cell growth in the cells expressing SV40 large T antigen., Oncogene, Vol.26, No.42, 6176-6183, 2007. (Summary) Parafibromin (PF) is a 531-amino acid protein encoded by HRPT2, a putative tumor suppressor gene recently implicated in the autosomal-dominant hyperparathyroidism-jaw tumor familial cancer syndrome and sporadic parathyroid carcinoma. To investigate effects of PF's overexpression on cell proliferation, we performed assays in four different cell lines. The transient overexpression of PF inhibited cell growth in HEK293 and NIH3T3 cells, but enhanced cell growth in the SV40 large T antigen-expressing cell lines such as 293FT and COS7 cells. In 293FT cells, PF was found to interact with SV40 large T antigen and its overexpression promoted entry into the S phase, implying that the interaction enhanced progression through the cell cycle. The tumor suppressor protein PF acts as a positive regulator of cell growth similar to an oncoprotein in the presence of SV40 large T antigen. (Keyword) Animals / Antigens, Polyomavirus Transforming / COS Cells / Cell Line / Cell Proliferation / Cercopithecus aethiops / Fibroblasts / Humans / Mice / NIH 3T3 Cells / Simian virus 40 / Tumor Suppressor Proteins (Tokushima University Institutional Repository) ● Metadata: 109649 (Link to Publication Site) ● Publication site (DOI): 10.1038/sj.onc.1210445 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17404568 ● Search Scopus @ Elsevier (PMID): 17404568 ● Search Scopus @ Elsevier (DOI): 10.1038/sj.onc.1210445 (Tokushima University Institutional Repository: 109649, DOI: 10.1038/sj.onc.1210445, PubMed: 17404568)
41.	Takeo Iwata, Shozo Yamada, Noriko Mizusawa, HM Golam, Toshiaki Sano and Katsuhiko Yoshimoto : The aryl hydrocarbon receptor-interacting protein gene is rarely mutated in sporadic GH-secreting adenomas, Clinical Endocrinology, Vol.66, No.4, 499-502, 2007. (Summary) Recently, germline mutations of aryl hydrocarbon receptor-interacting protein (AIP) gene located on 11q13 were identified in patients with pituitary adenoma predisposition. AIM/PATIENTS AND METHODS: We investigated the involvement of the AIP gene in one family with isolated familial somatotropinomas (IFS). To investigate the role of AIP in sporadic GH-secreting adenomas, we first analysed somatic mutations in 40 tumours. Second, DNA from corresponding leucocytes was analysed in tumours showing genetic changes of the AIP gene. Germline mutation of AIP was found in an IFS family. Bi-allelic inactivation of AIP by a combination of germline mutation and loss of heterozygosity were confirmed in two pituitary adenomas. Mutation analysis of the AIP gene in the 40 sporadic GH-secreting adenomas showed no mutations except for a missense mutation, suggesting that germline mutations in patients diagnosed with sporadic acromegaly or gigantism were rare. In a patient with gigantism, a missense mutation of V49M was identified at the germline level. Based on these results, we conclude that the loss of function of AIP contributes to IFS, but not for most Japanese sporadic GH-secreting adenomas. (Keyword) Adult / Aged / Female / Growth Hormone-Secreting Pituitary Adenoma / Humans / Intracellular Signaling Peptides and Proteins / Loss of Heterozygosity / Male / Middle Aged / Mutation / Pedigree / Pituitary Neoplasms / Proteins / Sequence Analysis, DNA (Tokushima University Institutional Repository) ● Metadata: 109642 (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1365-2265.2007.02758.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17371465 ● Search Scopus @ Elsevier (PMID): 17371465 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2265.2007.02758.x (Tokushima University Institutional Repository: 109642, DOI: 10.1111/j.1365-2265.2007.02758.x, PubMed: 17371465)
42.	Y Yamashia, T Akiyama, Noriko Mizusawa, Katsuhiko Yoshimoto and M Goto : A case of hyperparathyroidism-jaw tumour syndrome found in the treatment of an ossifying fibroma in the maxillary bone, International Journal of Oral and Maxillofacial Surgery, Vol.36, No.4, 365-369, 2007. (Summary) Hyperparathyroidism-jaw tumour (HPT-JT) syndrome is characterized by parathyroid tumours as well as by ossifying fibromas of the mandible and maxilla, renal cysts, or Wilms' tumours. Recently, the gene responsible for HPT-JT syndrome has been identified as the HRPT2 tumour suppressor gene. In an 18-year-old male, a tumour in the maxilla was first diagnosed as an ossifying fibroma. During biochemical screening before surgery, the patient received a diagnosis of primary hyperparathyroidism. Neck computed tomography scanning showed a parathyroid tumour. Surgical excisions to remove the jaw tumour and parathyroid adenoma were performed. The postoperative course has been uneventful and a follow up at 2 years revealed no evidence of recurrence. The HRPT2 germline mutation of 39delC was detected in the proband, but not in his unaffected parents. These results suggested that the germline mutation occurred de novo. (Keyword) Adenoma / Adolescent / Diagnosis, Differential / Fibroma, Ossifying / Follow-Up Studies / Gene Deletion / Germ-Line Mutation / Humans / Hyperparathyroidism, Primary / Male / Maxillary Neoplasms / Parathyroid Neoplasms / Syndrome / Tomography, X-Ray Computed / Tumor Suppressor Proteins (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ijom.2006.08.007 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17052894 ● Search Scopus @ Elsevier (PMID): 17052894 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ijom.2006.08.007 (DOI: 10.1016/j.ijom.2006.08.007, PubMed: 17052894)
43.	Nagakatsu Harada, S Hara, M Yoshida, T Zenitani, Kazuaki Mawatari, M Nakano, Akira Takahashi, Toshio Hosaka, Katsuhiko Yoshimoto and Yutaka Nakaya : Molecular cloning of a murine glycerol-3-phosphate acyltransferase-like protein 1 (xGPAT1)., Molecular and Cellular Biochemistry, Vol.297, No.1-2, 41-51, 2007. (Summary) A novel murine glycerol-3-phosphate acyltransferase-like protein 1 (named xGPAT1) has been cloned. The mouse xGPAT1 gene is located on mouse Chromosome 2, spans >19 kb, and consists of at least 23 exons. The protein is 32% identical and 72% similar to mouse mitochondrial GPAT (mtGPAT) on the amino acid level. Sequencing analysis confirmed that xGPAT1 has a 2403-bp open reading frame (ORF) that encodes an 801-amino acid protein with an estimated molecular mass of 89.1 kDa. A hydropathy plot of the deduced xGPAT1 protein showed a high degree of similarity with that of the mtGPAT protein. Using 5'-rapid amplification of cDNA ends, two alternate, untranslated exon 1 (1a and b) isoforms were obtained, generating variants xGPAT1-v1 and xGPAT1-v2. xGPAT1-v1 is expressed in mouse heart, liver, spleen, kidney and murine inner medullary collecting duct 3 (mIMCD3) cells, while xGPAT1-v2 is expressed in mouse liver, spleen, kidney, white and brown adipose tissues and 3T3-L1 pre- and post-adipocytes. xGPAT1 was distributed in the membrane fraction and showed GPAT activity when epitope-tagged xGPAT1 was expressed in Chinese hamster ovary (CHO)-K1 cells. (Keyword) Amino Acid Sequence / Animals / Base Sequence / CHO Cells / Cell Line / Chromosomes, Mammalian / Cloning, Molecular / Cricetinae / Cricetulus / Epitopes / Exons / Gene Expression Profiling / Gene Expression Regulation, Enzymologic / Glycerol-3-Phosphate O-Acyltransferase / Introns / Mice / Mice, Inbred C57BL / Mitochondria / Molecular Sequence Data / RNA, Messenger / Sequence Homology, Amino Acid (Link to Publication Site) ● Publication site (DOI): 10.1007/s11010-006-9321-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17013544 ● Search Scopus @ Elsevier (PMID): 17013544 ● Search Scopus @ Elsevier (DOI): 10.1007/s11010-006-9321-5 (DOI: 10.1007/s11010-006-9321-5, PubMed: 17013544)
44.	Noriko Mizusawa, Shinya Uchino, Takeo Iwata, Masaru Tsuyuguchi, Yasuyo Suzuki, Tsunenori Mizukoshi, Yoshio Yamashita, Akihiro Sakurai, Shinichi Suzuki, Mutsuo Beniko, Hideki Tahara, Masato Fujisawa, Nobuyuki Kamata, Kenji Fujisawa, Tohru Yashiro, Daisuke Nagao, Golam Md. Hossain, Toshiaki Sano, Shiro Noguchi and Katsuhiko Yoshimoto : Genetic analyses in patients with familial isolated hyperparathyroidism and hyperparathyroidism-jaw tumour syndrome., Clinical Endocrinology, Vol.65, No.1, 9-16, 2006. (Summary) A subset of familial isolated primary hyperparathyroidism (FIHP) is a variant of hyperparathyroidism-jaw tumour syndrome (HPT-JT). AIM/PATIENTS AND METHODS: We investigated the involvement of the HRPT2, MEN1 and CASR genes in 11 provisional FIHP families and two HPT-JT families. Germline mutations of HRPT2 were found in two of the 11 FIHP families and one of the two HPT-JT families. One FIHP family with parathyroid carcinoma and atypical adenomas and another FIHP family with cystic parathyroid adenoma had novel frameshift mutations of 518-521del and 62-66del, respectively. In a patient with HPT-JT, a de novo germline mutation of 39delC was detected. Novel somatic HRPT2 mutations of 70-73del and 95-102del were found in two of five parathyroid tumours in a family with a 518-521del mutation. Biallelic inactivation of HRPT2 by a combination of germline and somatic mutation was confirmed in the parathyroid tumours. The finding that two families diagnosed with FIHP carried HRPT2 mutations suggests that they have occult HPT-JT. In the remaining 10 families, one family had a missense MEN1 mutation. No mutations of CASR were detected. Our results confirm the need to test for HRPT2 in FIHP families, especially those with parathyroid carcinomas, atypical adenomas or adenomas with cystic change. (Keyword) Adenoma / Adult / Aged / DNA Mutational Analysis / Female / Frameshift Mutation / Gene Deletion / Genes, Tumor Suppressor / Genotype / Germ-Line Mutation / Humans / Hyperparathyroidism, Primary / Jaw Neoplasms / Loss of Heterozygosity / Male / Methylation / Microsatellite Repeats / Middle Aged / Multiple Endocrine Neoplasia Type 1 / Mutation / Parathyroid Neoplasms / Pedigree / Promoter Regions, Genetic / Receptors, Calcium-Sensing / Sequence Analysis, DNA / Tumor Suppressor Proteins (Tokushima University Institutional Repository) ● Metadata: 113299 (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1365-2265.2006.02534.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16817812 ● Summary page in Scopus @ Elsevier: 2-s2.0-33745207986 (Tokushima University Institutional Repository: 113299, DOI: 10.1111/j.1365-2265.2006.02534.x, PubMed: 16817812, Elsevier: Scopus)
45.	Zhi-Rong Qian, Toshiaki Sano, Katsuhiko Yoshimoto, Shozo Yamada, Akira Ishizuka, Noriko Mizusawa, Hidehisa Horiguchi, Mitsuyoshi Hirokawa and L Sylvia Asa : Inactivation of RASSF1A tumor suppressor gene by aberrant promoter hypermethylation in human pituitary adenomas., Laboratory Investigation; a Journal of Technical Methods and Pathology, Vol.85, No.4, 464-473, 2005. (Summary) Aberrant promoter methylation and resultant silencing of several tumor suppressor genes play an important role in the pathogenesis of many tumor types. The human Ras association domain family 1A gene (RASSF1A), recently cloned from the lung tumor locus at 3p21.3, was shown to be frequently inactivated by hypermethylation of its promoter region in a number of malignancies. We have investigated the expression and epigenetic changes of this novel universal tumor suppressor gene in pituitary adenomas and correlated the data with clinicopathologic findings. Fresh frozen normal pituitary tissues and 52 primary pituitary adenomas including all major types were examined. Methylation-specific polymerase chain reaction (MSP), combined bisulfite restriction analysis (COBRA), bisulfite sequencing and semiquantitative reverse transcription-polymerase chain reaction were used to analyze DNA promoter methylation status and the mRNA expression of RASSF1A, respectively. High levels of RASSF1A transcript and no methylation of the RASSF1A promoter were found in normal pituitary tissues. RASSF1A promoter methylation was detected in 20 of 52 (38%) adenomas including all major types of pituitary adenomas. However, a lower frequency of methylation of the RASSF1A promoter was found in gonadotroph cell adenomas (15%) compared with growth hormone cell, prolactin cell, or adrenocorticotropic hormone cell adenomas (54, 46 and 50%, respectively). Methylation frequency was higher in the most aggressive adenomas (87% in grade IV tumors, P=0.0163). In addition, methylation of the RASSF1A promoter potentially correlated with higher labeling index of the proliferation marker Ki-67 (P=0.1475). Loss or significant reduction of RASSF1A messenger RNA transcripts was identified in 18 of 20 (90%) adenomas with hypermethylation of RASSF1A (P<0.0001). Our data suggest that promoter hypermethylation of RASSF1A and resultant alterations of RASSF1A expression may play a critical role in pituitary tumorigenesis and may be involved in tumor progression. (Keyword) Adenoma / Base Sequence / DNA Methylation / Female / Humans / immunohistochemistry / Male / Molecular Sequence Data / Pituitary Neoplasms / Promoter Regions, Genetic / Reverse Transcriptase Polymerase Chain Reaction / Tumor Suppressor Proteins (Link to Publication Site) ● Publication site (DOI): 10.1038/labinvest.3700248 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15711568 ● Search Scopus @ Elsevier (PMID): 15711568 ● Search Scopus @ Elsevier (DOI): 10.1038/labinvest.3700248 (DOI: 10.1038/labinvest.3700248, PubMed: 15711568)
46.	Setsuko Hatakeyama, Syuichiro Hayashi, Y Yoshida, Akiko Otsubo, Katsuhiko Yoshimoto, Yuko Oikawa and Masanobu Sato : Retinoic acid disintegrated desmosomes and hemidesmosomes in stratified oral keratinocytes, Journal of Oral Pathology & Medicine, Vol.33, No.10, 622-628, 2004. (Summary) Although it is known that retinoic acid (RA) regulates the cellular differentiation of skin keratinocytes, the effects of RA on the anchoring junction have not been clarified. The effects of all-trans RA on cell-cell and cell-matrix connections of gingival epithelial (GE)1 cells in a multilayered culture were investigated. Ultrastructures of GE1 cells were observed and immunohistochemistry was used to detect keratin 4, keratin 13, and desmoglein expression. Reverse transcription-polymerase chain reaction was performed to detect expression of desmosome and hemidesmosome-associating adhesion molecules, keratin 13, and keratin14. Retinoic acid caused immunohistochemical diminution of keratin 4, keratin 13, and desmoglein. Ultrastructurally, RA induced drastic loss of typical desmosomes and complete loss of hemidesmosomes. RA significantly decreased the transcript levels of keratin 13, keratin 14, desmoglein 1, and desmocollin 1 in a dose-dependent manner. The 230-kD bullous pemphigoid antigen (BPAG1) gene expression was also reduced by RA, whereas transcript levels of integrin alpha6, integrin beta4, the 180-kD bullous pemphigoid antigen (BPAG2), and laminin 5 were not affected. These results indicated that RA disintegrated not only desmosomes by depriving the cells of desmoglein 1, desmocollin 1, keratin 13, and keratin 4, but also hemidesmosomes by reducing the expression of BPAG1 and keratin 14 in basal keratinocytes. (Keyword) oral keratinocytes / retinoic acid / desmosome / hemidesmosome / bullous pemphigoid antigen / keratin / polymerase chain reaction / EPIDERMOLYSIS-BULLOSA / PEMPHIGUS FOLIACEUS / SKIN FRAGILITY / DIFFERENTIATION / GENE / DESMOGLEIN-3 / VULGARIS / DISEASE (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1600-0714.2004.00245.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15482329 ● Search Scopus @ Elsevier (PMID): 15482329 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1600-0714.2004.00245.x (DOI: 10.1111/j.1600-0714.2004.00245.x, PubMed: 15482329)
47.	松尾英男, Shozo Yamada, 野村明, 黄舜範, 高畠一郎, 陳祐仁, 土屋克巳, 阪井哲男, 吉江利香, 村田厚夫, Katsuhiko Yoshimoto and 脇坂晟 : Differential Gene Expressions in Two Histologically Different Types of a Growth Hormone-Releasing Pituitary Adenoma, Journal of the Kyorin Medical Society, Vol.35, No.2, 167-175, 2004. (Keyword) pituitary adenoma / growth hormone / cell adhesion / cadherin / catenin / junctional plakoglobin / gene expression / cDNA array (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282679876578304 (CiNii: 1390282679876578304)
48.	Noriko Mizusawa, Tomoko Hasegawa, Izumi Ohigashi, Chisato Kosugi, Nagakatsu Harada, Mitsuo Itakura and Katsuhiko Yoshimoto : Differentiation Penotypes of Pancreatic Islet β- and α-cells are Closely Related with Homeotic Genes and a Group of Differentially Expressed Genes., Gene, Vol.331, No.28, 53-63, 2004. (Summary) To identify the genes that determine differentiation phenotypes, we compared gene expression of pancreatic islet beta- and alpha-cells, which are derived from the common precursor and secrete insulin and glucagon, respectively. The expression levels of homeotic genes including Hox genes known to determine region specificity in the antero-posterior (AP) body axis, tissue-specific homeobox genes, and other 8,734 genes were compared in a beta- and alpha-cell line of MIN6 and alpha TC1.6. The expression of homeotic genes were surveyed with reverse transcription-polymerase chain reaction (RT-PCR) using degenerate primers corresponding to invariant amino acid sequences within the homeodomain and subsequently with specific primers. Expression of Hoxc6, Hoxc9, Hoxc10, Pdx1, Cdx2, Gbx2, Pax4, and Hlxb9 genes in MIN6 was higher than those in alpha TC1.6, while expression of Hoxa2, Hoxa3, Hoxa5, Hoxa6, Hoxa7, Hoxa9, Hoxa10, Hoxa13, Hoxb3, Hoxb5, Hoxb6, Hoxb13, Hoxb8, and Brain4 genes in alpha TC1.6 was higher than those in MIN6. Out of 8,734 mouse genes screened with high-density mouse cDNA microarrays for MIN6- and alpha TC1.6-derived cDNA, 58 and 25 genes were differentially over- and under-expressed in MIN6, respectively. GLUTag, which is derived from a large bowel tumor and expresses the proglucagon gene, showed a comparatively similar expression profile to that of alpha TC1.6 in both homeotic and other genes analyzed in cDNA microarray. Our results are consistent with the interpretation that not only the tissue-specific homeotic genes, but also Hox genes are related to differentiation phenotypes of pancreatic beta- and alpha-cells rather than their regional specification of the body in vertebrates. (Keyword) Animals / Blotting, Northern / cell differentiation / Cell Line, Transformed / Cell Line, Tumor / DNA, Complementary / Gene Expression Profiling / Genes, Homeobox / Islets of Langerhans / Mice / NIH 3T3 Cells / Oligonucleotide Array Sequence Analysis / Phenotype / RNA, Messenger / Reverse Transcriptase Polymerase Chain Reaction (Tokushima University Institutional Repository) ● Metadata: 112035 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.gene.2004.01.016 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15094191 ● Search Scopus @ Elsevier (PMID): 15094191 ● Search Scopus @ Elsevier (DOI): 10.1016/j.gene.2004.01.016 (Tokushima University Institutional Repository: 112035, DOI: 10.1016/j.gene.2004.01.016, PubMed: 15094191)
49.	Setsuko Ii, Mika Ohta, Eiji Kudo, Takashi Yamaoka, Tomokazu Tachikawa, Maki Moritani, Mitsuo Itakura and Katsuhiko Yoshimoto : Redox State-Dependent and Sorbitol Accumulation-Independent Diabetic Albuminuria in Mice with Transgene-Derived Human Aldose Reductase and Sorbitol Dehydrogenase Deficiency., Diabetologia, Vol.47, No.3, 541-548, 2004. (Summary) We investigated the role played by sorbitol accumulation in the kidney in the development of diabetic albuminuria. We created mice ( hAR-Tg:SDH null) with transgene-derived human aldose reductase and sorbitol dehydrogenase (SDH) deficiency, and analysed (i). the contribution of accumulated sorbitol to urinary albumin excretion rate, and (ii). the effect of the aldose reductase inhibitor, epalrestat, on the diabetic redox state, including decreased renal reduced glutathione concentrations or increased lactate to pyruvate ratios in the diabetic kidney. Compared to littermates, non-diabetic transgenic mice had a 2.6-fold increase in aldose reductase mRNA. In a diabetic group, aldose reductase mRNA in hAR-Tg mice was 2.7-fold higher than in littermates. In the diabetic and non-diabetic groups, hAR-Tg:SDH null mice had the highest sorbitol content among all four genetic types including hAR-Tg:SDH null, SDH null, hAR-Tg and littermates. The urinary albumin excretion rate in non-diabetic groups was similar in the four genetic types of mouse. In diabetic groups it was greater than in non-diabetic groups, but did not correlate with the sorbitol content among the four genetic types of mouse. When aldose reductase inhibitor and streptozotocin were given simultaneously at 6 weeks of age, epalrestat prevented diabetic increases in urinary albumin excretion rate and completely prevented diabetic decreases in reduced glutathione concentrations and diabetic increases in lactate to pyruvate ratios, even in the presence of transgenic aldose reductase. The degree of diabetic albuminuria in genetically modified mice is dependent on the redox state and independent of polyol accumulation; aldose reductase inhibitor can prevent diabetic albuminuria by normalising diabetic redox changes. (Keyword) Albuminuria / Aldehyde Reductase / Animals / Diabetic Nephropathies / Humans / L-Iditol 2-Dehydrogenase / Mice / Mice, Knockout / Mice, Transgenic / Oxidation-Reduction / Sorbitol (Link to Publication Site) ● Publication site (DOI): 10.1007/s00125-004-1325-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14968292 ● Search Scopus @ Elsevier (PMID): 14968292 ● Search Scopus @ Elsevier (DOI): 10.1007/s00125-004-1325-7 (DOI: 10.1007/s00125-004-1325-7, PubMed: 14968292)
50.	Masayuki Shimamura, Roy C Brown, Betty E Lemmon, Tomohiro Akashi, Koichi Mizuno, Naohisa Nishihara, Ken-Ichi Tomizawa, Katsuhiko Yoshimoto, Hironori Deguchi, Hiroshi Hosoya, Tetsuya Horio and Yoshinobu Mineyuki : gamma-Tubulin in Basal Land Plants: Characterization, Localization, and Implication in the Evolution of Acentriolar Microtubule Organizing Centers., The Plant Cell, Vol.16, No.1, 45-59, 2004. (Summary) Although seed plants have gamma-tubulin, a ubiquitous component of centrosomes associated with microtubule nucleation in algal and animal cells, they do not have discrete microtubule organizing centers (MTOCs) comparable to animal centrosomes, and the organization of microtubule arrays in plants has remained enigmatic. Spindle development in basal land plants has revealed a surprising variety of MTOCs that may represent milestones in the evolution of the typical diffuse acentrosomal plant spindle. We have isolated and characterized the gamma-tubulin gene from a liverwort, one of the extant basal land plants. Sequence similarity to the gamma-tubulin gene of higher plants suggests that the gamma-tubulin gene is highly conserved in land plants. The G9 antibody to fission yeast gamma-tubulin recognized a single band of 55 kD in immunoblots from bryophytes. Immunohistochemistry with the G9 antibody clearly documented the association of gamma-tubulin with various MTOC sites in basal land plants (e.g., discrete centrosomes with and without centrioles and the plastid surface in monoplastidic meiosis of bryophytes). Changes in the distribution of gamma-tubulin occur in a cell cycle-specific manner during monoplastidic meiosis in the liverwort Dumortiera hirsuta. gamma-Tubulin changes its localization from the plastid surface in prophase I to the spindle, from the spindle to phragmoplasts and the nuclear envelope in telophase I, and back to the plastid surfaces in prophase II. In vitro experiments show that gamma-tubulin is detectable on the surface of isolated plastids and nuclei of D. hirsuta, and microtubules can be repolymerized from the isolated plastids. gamma-Tubulin localization patterns on plastid and nuclear surfaces are not affected by the destruction of microtubules by oryzalin. We conclude that gamma-tubulin is a highly conserved protein associated with microtubule nucleation in basal land plants and that it has a cell cycle-dependent distribution essential for the orderly succession of microtubule arrays. (Keyword) Amino Acid Sequence / Antibodies / Bryophyta / Cell Nucleus / Cloning, Molecular / Cross Reactions / DNA, Plant / Dinitrobenzenes / Evolution, Molecular / Hepatophyta / Immunohistochemistry / Meiosis / Microscopy, Immunoelectron / Microtubule-Organizing Center / Molecular Sequence Data / Phylogeny / Plant Proteins / Plants / Plastids / Sequence Analysis, DNA / Sequence Homology, Amino Acid / Sulfanilamides / Tubulin (Link to Publication Site) ● Publication site (DOI): 10.1105/tpc.016501 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14660802 ● Search Scopus @ Elsevier (PMID): 14660802 ● Search Scopus @ Elsevier (DOI): 10.1105/tpc.016501 (DOI: 10.1105/tpc.016501, PubMed: 14660802)
51.	Soichi Honda, Chisato Kosugi, Shozo Yamada, Toshiaki Sano, Toshio Matsumoto, Mitsuo Itakura and Katsuhiko Yoshimoto : Human Pituitary Adenomas Infrequently Contain Inactivation of Retinoblastoma 1 Gene and Activation of Cyclin Dependent Kinase 4 Gene., Endocrine Journal, Vol.50, No.3, 309-318, 2003. (Summary) Components of cyclinD1/cyclin-dependent kinase 4 (CDK4)/p16INK4a/pRb pathway are the frequent target of many tumor types. We examined the role of retinoblastoma susceptibility gene (RB1) and the CDK4 gene in human pituitary tumorigenesis. For the RB1 gene, pRb expression and loss of heterozygosity (LOH) on 13q in pituitary adenomas were analysed. Immunostaining of pRb revealed lack of expression in 1 of 29 pituitary adenomas. In 4 of 31 pituitary adenomas, allelic imbalances including LOH of RB1 on 13q14 were detected. Three of 4 pituitary adenomas, in which one adenoma lacked pRb expression, had a common LOH region at least from D13S219 on 13q12.3-q13 to D13S265 on 13q31-32. Interphase fluorescence in situ hybridization with a probe of RB1 showed 2 copies of RB1 gene suggesting that mitotic recombination events, not deletion or chromosome loss, led to LOH in the 3 pituitary adenomas analyzed. All 27 exons, intron-exon boundaries, and essential promoter region of RB1 gene were then sequenced in genomic DNA from 4 pituitary adenomas with allelic imbalance on 13q14 including one adenoma without pRb expression and 3 adenomas with pRb expression. Any somatic mutations, insertions, or microdeletions in the RB1 gene were not detected in 4 pituitary adenomas. Methylation sensitive (MS)-polymerase chain reaction (PCR) and bisulfite sequencing analysis revealed hypomethylated status of CpG islands in the promoter region of the RB1 genes of 4 pituitary adenomas. In addition, activating mutations of CDK4 gene, which is a component of cyclinD1/CDK4/p16INK4a/pRb pathway, were not detected in 31 pituitary adenomas. Based on these results, it is concluded that somatic mutations of the RB1 gene or CDK4 gene do not appear to play a major role in pituitary tumorigenesis. This supports the presence of potential tumor suppressor gene(s) on 13q12.3-q13 to 13q31-32 in pituitary adenomas. (Keyword) Adenoma / Adult / Aged / Chromosomes, Human, Pair 13 / Cyclin-Dependent Kinase 4 / Cyclin-Dependent Kinases / DNA Methylation / Female / Gene Expression Regulation, Neoplastic / Genes, Retinoblastoma / Humans / Immunohistochemistry / In Situ Hybridization, Fluorescence / Loss of Heterozygosity / Male / Middle Aged / Mutation / Pituitary Neoplasms / Polymerase Chain Reaction / Promoter Regions, Genetic / Proto-Oncogene Proteins (Tokushima University Institutional Repository) ● Metadata: 111695 (Link to Publication Site) ● Publication site (DOI): 10.1507/endocrj.50.309 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12940460 ● Search Scopus @ Elsevier (PMID): 12940460 ● Search Scopus @ Elsevier (DOI): 10.1507/endocrj.50.309 (Tokushima University Institutional Repository: 111695, DOI: 10.1507/endocrj.50.309, PubMed: 12940460)
52.	Hiroyuki Yamasaki, Noriko Mizusawa, Shinji Nagahiro, Shozo Yamada, Toshiaki Sano, Mitsuo Itakura and Katsuhiko Yoshimoto : GH-Secreting Pituitary Adenomas Infrequently Contain Inactivating Mutations of PRKAR1A and LOH of 17q23-24., Clinical Endocrinology, Vol.58, No.4, 464-470, 2003. (Summary) The molecular events leading to the development of GH-secreting pituitary tumours remain largely unknown. Gsalpha (GNAS1) mutations are found in 27-43% of sporadic GH-secreting adenomas in the Caucasian population, but the frequency of GNAS1 mutations in Japanese and Korean acromegalic patients was reported to be lower, 4-9% and 16%, respectively. Other genes responsible for the tumourigenesis of GH-secreting pituitary adenomas have not been detected yet. PRKAR1A, which codes for the RIalpha regulatory subunit of cyclic AMP-dependent protein kinase A (PKA) on 17q23-24, was recently reported to contain inactivating mutations in some Carney complex families, which involved GH-secreting adenomas in about 10%. We re-evaluated the frequency of GNAS1 mutations and investigated PRKAR1A on the hypothesis that it might play a role in the tumourigenesis of GH-secreting adenomas. We analysed exons 8 and 9 of GNAS1 and all exons and the exon-intron boundaries of PRKAR1A with the PCR and by direct sequencing using genomic DNA extracted from 32 GH-secreting pituitary adenomas (30 GH-secreting adenomas, two GH and PRL-secreting adenomas) and 28 corresponding peripheral blood samples, and performed loss of heterozygosity (LOH) analysis of 17q23-24 with four microsatellite markers and intragenic markers of PRKAR1A. Seventeen of 32 (53.1%) tumours showed somatic-activating mutations of GNAS1: 16 (53.3%) of 30 GH-secreting adenomas and one of two GH and PRL-secreting adenomas. Neither inactivating somatic mutations of PRKAR1A nor LOH of 17q23-24 were detected in any of the tumours examined. We reconfirm the important role of activating mutations of GNAS1 in GH-secreting adenomas, and conclude that PRKAR1A does not play a significant role in the tumourigenesis. (Keyword) Adenoma / Adult / Aged / Chromosomes, Human, Pair 17 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / Cyclic AMP-Dependent Protein Kinases / Female / Gene Silencing / Growth Hormone / Growth Hormone-Releasing Hormone / Humans / Loss of Heterozygosity / Male / Middle Aged / Pituitary Neoplasms / Polymerase Chain Reaction / Statistics, Nonparametric (Link to Publication Site) ● Publication site (DOI): 10.1046/j.1365-2265.2003.01740.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12641630 ● Search Scopus @ Elsevier (PMID): 12641630 ● Search Scopus @ Elsevier (DOI): 10.1046/j.1365-2265.2003.01740.x (DOI: 10.1046/j.1365-2265.2003.01740.x, PubMed: 12641630)
53.	Bing Xu, Akira Miyauchi, Shinya Uchino, Yoshizo Sekihara, Mitsuyoshi Hirokawa, Toshiaki Sano and Katsuhiko Yoshimoto : A Predominant Increase of APC Gene Isoform with Exon 9a in a Case of Attenuated Familial Adenomatous Polyposis., Clinical Genetics, Vol.63, No.1, 71-72, 2003. (Keyword) Adenomatous Polyposis Coli / Adenomatous Polyposis Coli Protein / Adult / DNA, Complementary / Female / Humans / Protein Isoforms / RNA Processing, Post-Transcriptional (Link to Publication Site) ● Publication site (DOI): 10.1034/j.1399-0004.2003.630111.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12519375 ● Search Scopus @ Elsevier (PMID): 12519375 ● Search Scopus @ Elsevier (DOI): 10.1034/j.1399-0004.2003.630111.x (DOI: 10.1034/j.1399-0004.2003.630111.x, PubMed: 12519375)
54.	Bing Xu, Katsuhiko Yoshimoto, Akira Miyauchi, Seiji Kuma, Noriko Mizusawa, Mitsuyoshi Hirokawa and Toshiaki Sano : Cribriform-Morular Variant of Papillary Thyroid Carcinoma: A Pathological and Molecular Genetics Study with Evidence of Frequent Somatic Mutations in exon 3 of the b-catenin Gene., The Journal of Pathology, Vol.199, No.1, 58-67, 2003. (Summary) The cribriform-morular variant (C-MV), an unusual and peculiar subtype of papillary thyroid carcinoma (PTC), has been observed frequently in familial adenomatous polyposis (FAP)-associated thyroid carcinoma and also in sporadic thyroid carcinoma. In this paper, five young women with the C-MV of PTC, aged 22-34 years at cancer diagnosis, are reported; two of them had attenuated FAP. Grossly, one FAP-associated tumour and one sporadic tumour were multicentric and the others were solitary. Histologically, the tumours were encapsulated and exhibited a combination of cribriform, follicular, trabecular, solid, and papillary patterns of growth, with morular areas. Immunohistochemically, the tumour cells showed cytoplasmic expression of thyroglobulin, neuron-specific enolase, epithelial membrane antigen, high- and low-molecular-weight cytokeratins, vimentin, and bcl-2 protein; nuclear expression of oestrogen and progesterone receptors, and retinoblastoma protein; and cytoplasmic and nuclear accumulation of beta-catenin. Germline mutations of the adenomatous polyposis coli (APC) gene were investigated using the protein truncation test in four subjects, including two FAP individuals. Germline APC mutation was identified in only one FAP patient with the multicentric C-MV of PTC, who had a thymidine deletion at codon 512, resulting in a frameshift leading to a premature stop codon. No loss of heterozygosity of loci close to the APC gene was detected in tumour tissues from these four patients. Somatic mutation analysis of exon 3 of the beta-catenin gene (CTNNB1) revealed alterations in seven tumours from all five individuals: one at a serine residue (codon 29), three at amino acids adjacent to serine or threonine residues (codons 22, 39, and 44), and three at other amino acids (codons 49, 54, and 56). Moreover, each of two different tumours examined from two patients with the multicentric C-MV of PTC, had different somatic mutations of the CTNNB1 gene. Taken together, these data suggest that accumulation of mutant beta-catenin contributes to the development of the C-MV of PTC. (Keyword) Adenocarcinoma, Papillary / Adenomatous Polyposis Coli / Adult / Cytoskeletal Proteins / Exons / Female / Genes, APC / Humans / Immunohistochemistry / Loss of Heterozygosity / Mutation / Thyroid Gland / Thyroid Neoplasms / Trans-Activators / beta Catenin (Link to Publication Site) ● Publication site (DOI): 10.1002/path.1225 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12474227 ● Search Scopus @ Elsevier (PMID): 12474227 ● Search Scopus @ Elsevier (DOI): 10.1002/path.1225 (DOI: 10.1002/path.1225, PubMed: 12474227)
55.	Bing Xu, Mitsuyoshi Hirokawa, Katsuhiko Yoshimoto, Hitoshi Miki, Masahiro Takahashi, Seiji Kuma and Toshiaki Sano : Spindle Epithelial Tumor with Thymus-like Differentiation of the Thyroid: A Case Report with Pathological and Molecular Genetics Study., Human Pathology, Vol.34, No.2, 190-193, 2003. (Summary) We report an unusual case of spindle epithelial tumor with thymus-like differentiation (SETTLE) of the thyroid present in a 6-year-old boy. The tumor, located at both the left lobe and isthmus, was a circumscribed mass with slightly gritty whorled appearance. Microscopically, the lobulated, highly cellular, spindle cell neoplasm was arranged in intersecting bundles and fascicles separated by fibrous bands. Benign-appearing glands entrapped within fibrous bands and foci of squamous differentiation within spindle cells were observed. Immunohistochemically, the spindle cells were diffusely positive for cytokeratins, vimentin, and alpha-smooth muscle actin and patchily reactive for muscle-specific actin and epithelial membrane antigen, exhibiting myoepithelial differentiation. The spindle cells were also patchily immunopositive for p53 protein. Molecular genetic analysis revealed Ki-ras gene mutations at codons 13 (GGC(gly) to AGC(ser)) and 15 (GGC(gly) to AGC(ser)) on the same allele. Mutation of the p53 gene was not detected. This is the first report on Ki-ras oncogene mutations in a case of SETTLE. (Keyword) Actins / Alleles / Cell Differentiation / Child / Epithelium / Genes, ras / Humans / Immunohistochemistry / Keratins / Male / Mutation / Thymus Gland / Thyroid Gland / Thyroid Neoplasms / Tumor Suppressor Protein p53 / Vimentin (Link to Publication Site) ● Publication site (DOI): 10.1053/hupa.2003.29 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12612889 ● Search Scopus @ Elsevier (PMID): 12612889 ● Search Scopus @ Elsevier (DOI): 10.1053/hupa.2003.29 (DOI: 10.1053/hupa.2003.29, PubMed: 12612889)
56.	Zhi-Rong Qian, Chei Chiun Li, Hiroyuki Yamasaki, Noriko Mizusawa, Katsuhiko Yoshimoto, Shozo Yamada, Takashi Tashiro, Hidehisa Horiguchi, Shingo Wakatsuki, Mitsuyoshi Hirokawa and Toshiaki Sano : Role of E-cadherin, alpha-, beta-, and gamma-catenins, and p120 (cell adhesion molecules) in prolactinoma behavior., Modern Pathology, Vol.15, No.12, 1357-1365, 2002. (Summary) E-cadherin/catenin complex regulates cellular adhesion and motility and is believed to function as an invasion suppressor system. In a number of cancers, abnormal and reduced expression of E-cadherin/catenin complex is associated with tumor invasion and metastasis. Prolactinomas show frequent invasion on the surrounding structures, despite their histologically benign nature. Furthermore, gender-based differences in endocrine and surgical findings are found in patients with prolactinoma. To understand biological factors governing prolactinoma behavior, this study analyzed the expression of E-cadherin; alpha-, beta-, and gamma-catenins; p120; and cell proliferation marker MIB-1 labeling index in 13 invasive tumors (9 in men, 4 in women), 26 noninvasive tumors (4 in men, 22 in women), and 8 normal anterior pituitaries by immunohistochemistry. Immunostaining of E-cadherin; alpha-, beta-, and gamma-catenins; and p120 showed a membranous pattern of reactivity and generally stronger in normal pituitaries than in prolactinomas. Expression of E-cadherin and beta-catenin was significantly lower in invasive than in noninvasive prolactinomas (P <.002 and P <.005, respectively), and reduced expression of E-cadherin and beta-catenin was more frequent in invasive than in noninvasive prolactinomas (P <.001 and P <.05, respectively); in contrast, gamma-catenin expression showed higher in invasive than in noninvasive prolactinomas (P <.05). Expression of E-cadherin was significantly lower in macroprolactinomas than in microprolactinomas (P <.01), and decreased expression of E-cadherin and beta-catenin predicted high MIB-1 expression (P <.05). Moreover, the expression of E-cadherin and beta-catenin was significantly lower in macroprolactinomas in men than in those in women (P <.01 and P <.02, respectively). No statistical correlations were observed between expression of alpha-catenin, p120, and clinicopathologic features. In conclusion, the reduction of E-cadherin and beta-catenin expression was related to invasiveness and proliferative status of prolactinomas and correlated with the more aggressive behavior of prolactinomas in men compared with in women. (Keyword) Adolescent / Adult / Aged / Cadherins / Cell Adhesion Molecules / Cytoskeletal Proteins / Desmoplakins / Female / Humans / immunohistochemistry / Ki-67 Antigen / Male / Middle Aged / Phosphoproteins / Pituitary Neoplasms / Prolactinoma / Trans-Activators / alpha Catenin / beta Catenin / gamma Catenin (Link to Publication Site) ● Publication site (DOI): 10.1097/01.MP.0000039572.75188.1A (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12481018 ● Search Scopus @ Elsevier (PMID): 12481018 ● Search Scopus @ Elsevier (DOI): 10.1097/01.MP.0000039572.75188.1A (DOI: 10.1097/01.MP.0000039572.75188.1A, PubMed: 12481018)
57.	Chisato Tanaka, Shinya Uchino, Shiro Noguchi, Tetsuya Nishioka, Hiromi Yamasaki and Katsuhiko Yoshimoto : Biallelic inactivation by somatic mutations of the MEN1 gene in sporadic parathyroid tumors, Cancer Letters, Vol.175, No.2, 175-179, 2002. (Summary) We report three sporadic parathyroid tumors with biallelic inactivation of the multiple endocrine neoplasia type 1 (MEN1) gene. Three parathyroid tumors had two somatic mutations (K119del and 864del8, 363insT and 1767delT, and 508del33 and W341X, respectively). The mutations in both alleles detected by long-range polymerase chain reaction and subcloning in three tumors would likely result in a nonfunctional menin protein in parathyroid glands. These results show that the MEN1 gene is inactivated not only by a combination of somatic mutations and loss of heterozygosity, but also by somatic double mutations located on different alleles. The results directly confirmed the participation of MEN1 in the tumorigenesis of sporadic parathyroid tumors. (Keyword) Adult / Aged / Alleles / Amino Acid Sequence / Female / Genes, Tumor Suppressor / Germ-Line Mutation / Humans / Molecular Sequence Data / Mutation / Neoplasm Proteins / Parathyroid Neoplasms / Polymerase Chain Reaction / Polymorphism, Single-Stranded Conformational / Proto-Oncogene Proteins / Sequence Deletion (Link to Publication Site) ● Publication site (DOI): 10.1016/S0304-3835(01)00729-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11741745 ● Search Scopus @ Elsevier (PMID): 11741745 ● Search Scopus @ Elsevier (DOI): 10.1016/S0304-3835(01)00729-7 (DOI: 10.1016/S0304-3835(01)00729-7, PubMed: 11741745)
58.	Bing Xu, Toshiaki Sano, Katsuhiko Yoshimoto and Shozo Yamada : Downregulation of E-cadherin and its Undercoat Proteins in Pituitary Growth Hormone Cell Adenomas with Prominent Fibrous Bodies., Endocrine Pathology, Vol.13, No.4, 341-351, 2002. (Summary) The cadherin-catenin complex regulates cellular adhesion and motility, and genetic alterations in these molecules play a critical role in multistage tumorigenesis. In this study, the expression of three major type I classic cadherins E-, N-, and P-cadherin and their undercoat proteins alpha-, beta-, and gamma-catenin, and pp120 was investigated in 127 pituitary adenomas and 10 normal adenohypophyseal glands using an immunohistochemical technique with highly specific monoclonal antibodies. In normal pituitary glands, E-cadherin, catenins, and pp120 were strongly expressed on almost all hormone-producing cell-cell boundaries, N-cadherin was weakly immunoreactive on a few cell-cell boundaries, and P-cadherin was negative. In pituitary adenomas, a correlation was not identified among expression of E-cadherin, catenins, or pp120 with patient age, sex, hormone level, tumor size, and/or invasiveness, respectively. Expression of E-cadherin, catenins, and pp120 was significantly reduced in 24 growth hormone (GH) cell adenomas with prominent fibrous bodies compared with the other subtypes of pituitary adenomas and normal pituitary glands (p < 0.0001, respectively). Methylation-specific polymerase chain reaction analysis revealed that the E-cadherin gene promoter region was methylated in 6 of 16 (37.5%) GH cell adenomas with prominent fibrous bodies examined, 2 of which displayed total methylation, but not in 10 GH cell adenomas without fibrous bodies. No mutation of exon 3 of the beta-catenin gene was found in 16 GH cell adenomas with prominent fibrous bodies or in 10 other subtypes of pituitary adenomas that showed unremarkable intracellular presence of beta-catenin protein. In conclusion, the decreased expression of the E-cadherin catenin complex and methylation of the E-cadherin gene promoter region only in GH cell adenomas with prominent fibrous bodies may be an event associated with the formation of fibrous bodies. (Keyword) Adenoma / Cadherins / Cytoskeletal Proteins / DNA Methylation / Desmoplakins / Down-Regulation / Exons / Human Growth Hormone / Humans / Immunohistochemistry / Mutation / Pituitary Neoplasms / Promoter Regions, Genetic / Trans-Activators / alpha Catenin / beta Catenin / gamma Catenin (Link to Publication Site) ● Publication site (DOI): 10.1385/EP:13:4:341 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12665652 ● Search Scopus @ Elsevier (PMID): 12665652 ● Search Scopus @ Elsevier (DOI): 10.1385/EP:13:4:341 (DOI: 10.1385/EP:13:4:341, PubMed: 12665652)
59.	Chiun Chei Li, Bing Xu, Mitsuyoshi Hirokawa, Zhi-Rong Qian, Katsuhiko Yoshimoto, Hidehisa Horiguchi, Shingo Wakatsuki, Takashi Tashiro and Toshiaki Sano : Alterations of E-cadherin, a-catenin and b-catenin expression in neuroendocrine tumors of the gastrointestinal tract., Virchows Archiv, Vol.440, No.2, 145-154, 2002. (Summary) Neuroendocrine tumors (NETs) of the gastrointestinal tract comprise a heterogeneous group of neoplasms arising from the diffuse neuroendocrine system. These tumors strongly differ from each other on the basis of different pathogenetic, clinical, functional, histological, and prognostic patterns. Previous studies have shown that abnormal and reduced expression of the E-cadherin/catenin complex in several human cancers is associated with tumor dedifferentiation, advanced clinical stages, and poor survival rate. We assessed correlations between the expression of E-cadherin and catenins, Ki-67, and the following clinicopathological factors: age, embryological site of origin, size, histological growth pattern, the depth of penetration into the intestinal wall, and the presence of metastasis. In this study, reduction of membranous E-cadherin expression to a variable degree was detected in more than two-thirds (42 of 51) of gastrointestinal NETs (19 foregut, 8 midgut, and 24 hindgut) belonging to the complete neuroendocrine neoplastic spectrum [18 well-differentiated NETs, 22 well-differentiated neuroendocrine carcinomas (NECs), and 11 poorly differentiated NECs]. The reduction of E-cadherin expression was concomitant with the reduction of alpha-catenin (44 of 51) and beta-catenin (35 of 51) expression. Our immunohistochemical analysis demonstrated significant differences of percentage of membranous positive cells of E-cadherin, alpha-catenin, or beta-catenin between normal tissues and well-differentiated NETs (P=0.0038, P=0.004, and P=0.0329, respectively), well-differentiated NECs (P<0.001, P<0.001, and P<0.001, respectively) and poorly differentiated NECs (P=0.0002, P<0.0002, and P=0.0002, respectively). Among the gastrointestinal NETs, there were significantly more positive cells of E-cadherin, alpha-catenin, or beta-catenin in well-differentiated NETs than well-differentiated NECs (P=0.0006, P=0.0065, and P=0.0001, respectively) or poorly differentiated NECs (P=0.0053, P=0.0041, and P<0.001, respectively). MIB-1 labeling index generally showed a low proliferative activity in well-differentiated NETs (0.49+/-0.37) and well-differentiated NECs (0.662+/-0.66). A high proliferation rate was observed in poorly differentiated NECs (41.518+/-16.59). MIB-1 labeling index was significantly higher in poorly differentiated NECs than well-differentiated NETs and well-differentiated NECs (P<0.0001 and P<0.0001, respectively). E-cadherin, alpha-catenin, and beta-catenin expression were correlated significantly with transmural tumor invasion (P<0.0001, P=0.0001, and P<0.0001, respectively) and with size (P=0.0013, P=0.0001, and P<0.0001, respectively). These results indicate that the alteration in the E-cadherin/catenin expression may be involved in the growth and progression of gastrointestinal NETs. (Keyword) gastrointestinal neuroendocrine tumors / E-cadherin / alpha-catenin / beta-catenin / Ki-67 / immunohistochemistry / CARCINOID-TUMORS / HUMAN CANCERS / PROGNOSIS / PATHOGENESIS / PROGRESSION / metastasis / protein / LESIONS / KI-67 / APC (Link to Publication Site) ● Publication site (DOI): 10.1007/s004280100529 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11964044 ● Summary page in Scopus @ Elsevier: 2-s2.0-0036182725 (DOI: 10.1007/s004280100529, PubMed: 11964044, Elsevier: Scopus)
60.	Yoshitaka Hosokawa, Alexandros Papanikolau, Robert D Cardiff, Katsuhiko Yoshimoto, Megan Bernstein, Timothy C Wang, Emmet V Schmidt and Andrew Arnold : In Vivo Analysis of Mammary and Non-mammary Tumorigenesis in MMTV-cyclin D1 Transgenic Mice Deficient in p53., Transgenic Research, Vol.10, No.5, 471-478, 2001. (Summary) Overexpression of the cyclin D1 oncogene and inactivation of the p53 tumor suppressor have both been implicated in substantial proportions of sporadic human breast cancers. Transgenic mice with cyclin D1 overexpression targeted to mammary tissue by the MMTV enhancer-promoter have been shown to develop mammary cancers. To investigate the relationship between pathways driven by cyclin D1 overexpression and p53 loss during the development of breast cancers, we crossed MMTV-cyclin D1 mice with p53 heterozygous null (p53+/-) mice. In such crossed mice, cyclin D1-driven mammary neoplasia would need to be substantially accelerated by p53 loss in order for mammary tumors to develop prior to the expected onset of non-mammary tumors characteristic of the p53-deficient background alone. Instead, in mice heterozygous or homozygous for p53 deficiency and simultaneously carrying the MMTV-cyclin D1 transgene, only tumors typically found in p53-deficient mice developed and mammary tumors were not observed. Interestingly, MMTV-cyclin D1/p53+/- mice appeared to develop these non-mammary tumors more rapidly than p53+/- mice, and a majority of the sampled non-mammary tumors from MMTV-cyclin D1/p53+/- mice showed 'ectopic' expression of the MMTV-driven cyclin D1 transgene. Within the constraints of possible genetic background effects and limited sensitivity due to the early emergence of non-mammary tumors, these observations provide no evidence that inactivation of p53 confers a major additional selective advantage to mammary cells overexpressing cyclin D1 in this animal model of human breast cancer. Interestingly, the results do raise the possibility that p53 inactivation might complement or cooperate with cyclin D1 deregulation during the development of some types of non-mammary tumors. (Keyword) Animals / Cyclin D1 / Female / Mammary Glands, Animal / Mammary Neoplasms, Animal / Mammary Tumor Virus, Mouse / Mice / knockout mice / Mice, Transgenic / Neoplasms / Tumor Suppressor Protein p53 (Link to Publication Site) ● Publication site (DOI): 10.1023/A:1012064911751 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11708657 ● Summary page in Scopus @ Elsevier: 2-s2.0-0034777284 (DOI: 10.1023/A:1012064911751, PubMed: 11708657, Elsevier: Scopus)
61.	Yasuo Imanishi, Yoshitaka Hosokawa, Katsuhiko Yoshimoto, Ernestina Schipani, Sanjay Mallya, Alexandros Papanikolaou, Olga Kifor, Takehiko Tokura, Marilyn Sablosky, Felicia Ledgard, Gloria Grnowicz, Timothy C Wang, Emmet V Schmidt, Charles Hall, Edward M Brown, Roderick Bronson and Andrew Arnold : Primary Hyperparathyroidism Caused by Parathyroid-Targeted Overexpression of Cyclin D1 in Transgenic Mice., The Journal of Clinical Investigation, Vol.107, No.9, 1093-1102, 2001. (Summary) The relationship between abnormal cell proliferation and aberrant control of hormonal secretion is a fundamental and poorly understood issue in endocrine cell neoplasia. Transgenic mice with parathyroid-targeted overexpression of the cyclin D1 oncogene, modeling a gene rearrangement found in human tumors, were created to determine whether a primary defect in this cell-cycle regulator can cause an abnormal relationship between serum calcium and parathyroid hormone response, as is typical of human primary hyperparathyroidism. We also sought to develop an animal model of hyperparathyroidism and to examine directly cyclin D1's role in parathyroid tumorigenesis. Parathyroid hormone gene regulatory region--cyclin D1 (PTH--cyclin D1) mice not only developed abnormal parathyroid cell proliferation, but also developed chronic biochemical hyperparathyroidism with characteristic abnormalities in bone and, notably, a shift in the relationship between serum calcium and PTH. Thus, this animal model of human primary hyperparathyroidism provides direct experimental evidence that overexpression of the cyclin D1 oncogene can drive excessive parathyroid cell proliferation and that this proliferative defect need not occur solely as a downstream consequence of a defect in parathyroid hormone secretory control by serum calcium, as had been hypothesized. Instead, primary deregulation of cell-growth pathways can cause both the hypercellularity and abnormal control of hormonal secretion that are almost inevitably linked together in this common disorder. (Keyword) Adenoma / Animals / Bone and Bones / Calcium / Calcium-Binding Proteins / Chromosome Aberrations / Chromosome Disorders / Cyclin D1 / Gene Rearrangement / Humans / Hyperparathyroidism / Mice / Mice, Transgenic / Parathyroid Hormone / Parathyroid Neoplasms (Tokushima University Institutional Repository) ● Metadata: 109648 (Link to Publication Site) ● Publication site (DOI): 10.1172/JCI10523 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11342573 ● Summary page in Scopus @ Elsevier: 2-s2.0-0035014450 (Tokushima University Institutional Repository: 109648, DOI: 10.1172/JCI10523, PubMed: 11342573, Elsevier: Scopus)
62.	Kenji Sasahara, Takashi Yamaoka, Maki Moritani, Katsuhiko Yoshimoto, Yasuhiro Kuroda and Mitsuo Itakura : Molecular Cloning and Tissue-specific Expression of a New Member of the Regenerating Protein Family, Islet Neogenesis-associated Protein-related Protein., Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Vol.1500, No.1, 142-146, 2000. (Summary) Islet neogenesis-associated protein (INGAP) is a protein expressed during islet neogenesis. We have cloned a novel cDNA having a similar sequence to INGAP cDNA. The cDNA encodes 175 amino acids designated INGAP-related protein (INGAPrP). INGAP is expressed in cellophane-wrapped pancreas, but not in normal pancreas, whereas INGAPrP was abundantly expressed in normal pancreas. (Keyword) Acute-Phase Proteins / Animals / Antigens, Neoplasm / Base Sequence / Blotting, Northern / Calcium-Binding Proteins / Cloning, Molecular / Duodenum / Humans / Lectins, C-Type / Lithostathine / Mice / Molecular Sequence Data / Muscle, Skeletal / Nerve Tissue Proteins / Organ Specificity / Pancreas / Protein Biosynthesis / Proteins / Sequence Homology, Amino Acid / Stomach / Tumor Markers, Biological (Link to Publication Site) ● Publication site (DOI): 10.1016/S0925-4439(99)00095-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10564727 ● Search Scopus @ Elsevier (PMID): 10564727 ● Search Scopus @ Elsevier (DOI): 10.1016/S0925-4439(99)00095-2 (DOI: 10.1016/S0925-4439(99)00095-2, PubMed: 10564727)
63.	Takashi Yamaoka, Kenji Yoshino, Taketo Yamada, Chiyoko Idehara, MO Hoque, Maki Moritani, Katsuhiko Yoshimoto, Jun-ichi Hata and Mitsuo Itakura : Diabetes and tumor formation in transgenic mice expressing reg I., Biochemical and Biophysical Research Communications, Vol.278, No.2, 368-376, 2000. (Summary) To examine the effect of overexpressed regenerating gene (Reg) I on pancreatic beta-cells, we generated transgenic mice expressing Reg I in islets (Reg-Tg mice). Three lines of Reg-Tg mice were established. In line-1 Reg-Tg mice, the expression level of Reg I mRNA in islets was 7 times higher than those in lines 2 and 3 of Reg-Tg mice, and line 1 mice developed diabetes by apoptosis of beta-cells, as well as various malignant tumors. In addition to the decrease in beta-cells, compensatory islet regeneration and proliferation of ductal epithelial cells were observed in line-1 Reg-Tg mice. Because Reg I protein was secreted primarily into pancreatic ducts from acinar cells, it may primarily stimulate the proliferation of ductal epithelial cells, and not beta-cells, and their differentiation into islets. Moreover, the tumor-promoting activity of Reg I protein should be considered for its possible clinical applications. (Keyword) Animals / Diabetes Mellitus, Experimental / Female / Insulin / Islets of Langerhans / Mice / Mice, Inbred C57BL / Mice, Inbred DBA / Mice, Transgenic / Neoplasms, Experimental / Phenotype / RNA, Messenger / Regeneration / Transgenes (Link to Publication Site) ● Publication site (DOI): 10.1006/bbrc.2000.3813 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11097844 ● Summary page in Scopus @ Elsevier: 2-s2.0-0034687559 (DOI: 10.1006/bbrc.2000.3813, PubMed: 11097844, Elsevier: Scopus)
64.	Maki Kondo, Takashi Yamaoka, Soichi Honda, Yoshihiro Miwa, Rumi Katashima, Maki Moritani, Katsuhiko Yoshimoto, Yoshio Hayashi and Mitsuo Itakura : The Rate of Cell Growth is Regulated by Purine Biosynthesis via ATP Production and G1 to S Phase Transition., The Journal of Biochemistry, Vol.128, No.1, 57-64, 2000.
65.	Takashi Yamaoka, Makiko Yano, Taketo Yamada, Takashi Matsushita, Maki Moritani, Setsuko Ii, Katsuhiko Yoshimoto, Junichi Hata and Mitsuo Itakura : Diabetes and pancreatic tumours in transgenic mice expressing Pax6., Diabetologia, Vol.43, No.3, 332-339, 2000. (Summary) Both endocrine and exocrine cells of the pancreas differentiate from epithelial cells of primitive pancreatic ducts, and four types of pancreatic islet cells (alpha, beta, delta, and PP cells) are derived from the common pluripotent precursor cells. Although Pa x 6 is expressed in all islet cells, Pa x 4 is detected only in beta cells. In homozygous Pa x 4-null mice, beta cells are absent, whereas the number of alpha cells is increased. Therefore, we hypothesized that the balance of Pa x 4 and 6 is one of the determinants by which the common progenitor cells differentiate into alpha or beta cells. To change this balance, we generated transgenic mice overexpressing Pa x 6 driven by the insulin promoter or the PDX1 promoter. In both types of transgenic mice, normal development of beta cells was disturbed, resulting in apoptosis of beta cells and diabetes. In Insulin/Pa x 6-Tg mice, beta cells were specifically affected, whereas in PDX/Pa x 6-Tg mice, developmental abnormalities involved the whole pancreas including hypoplasia of the exocrine pancreas. Furthermore, PDX/Pa x 6-Tg mice experienced proliferation of both ductal epithelia and islet cells and subsequent cystic adenoma of the pancreas. These findings suggest that Pa x 6 promotes the growth of ductal epithelia and endocrine progenitor cells and that the suppression of Pa x 6 is necessary for the normal development of beta cells and the exocrine pancreas. (Keyword) Animals / Cystadenoma / Cysts / DNA-Binding Proteins / Diabetes Mellitus / Eye Proteins / Gene Expression / Homeodomain Proteins / Islets of Langerhans / Mice / Mice, Transgenic / Organ Size / PAX6 Transcription Factor / Paired Box Transcription Factors / Pancreas / Pancreatic Diseases / Pancreatic Neoplasms / Phenotype / Repressor Proteins (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10768094 ● Search Scopus @ Elsevier (PMID): 10768094 (PubMed: 10768094)
66.	Kenji Sasahara, Takashi Yamaoka, Maki Moritani, Masaki Tanaka, Hiroyuki Iwahana, Katsuhiko Yoshimoto, Jun-ichi Miyagawa, Yasuhiro Kuroda and Mitsuo Itakura : Molecular Cloning and Expression Analysis of a Putative Nuclear Protein, SR-25., Biochemical and Biophysical Research Communications, Vol.269, No.2, 444-450, 2000. (Summary) We cloned a full-length mouse cDNA and its human homologue encoding a novel protein designated as "SR-25." In Northern blot analysis, SR-25 mRNA was expressed in all organs tested, and relatively abundant in testis and thymus. Deduced amino acid sequences of mouse SR-25 and human SR-25 showed 77.7% identity. SR-25 has a serine-arginine repeat (SR repeat) and two types of amino acid clusters: a serine cluster and a highly basic cluster. Based on the presence of many nuclear localizing signals and a similarity to RNA splicing proteins, SR-25 is strongly suggested to be a nuclear protein and may contribute to RNA splicing. (Keyword) Amino Acid Sequence / Animals / Base Sequence / Blotting, Southern / Cloning, Molecular / DNA, Complementary / Humans / Mice / Molecular Sequence Data / Nuclear Proteins / RNA, Messenger / Sequence Homology, Amino Acid / Tumor Cells, Cultured (Tokushima University Institutional Repository) ● Metadata: 113522 (Link to Publication Site) ● Publication site (DOI): 10.1006/bbrc.2000.2301 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10708573 ● Summary page in Scopus @ Elsevier: 2-s2.0-0034673523 (Tokushima University Institutional Repository: 113522, DOI: 10.1006/bbrc.2000.2301, PubMed: 10708573, Elsevier: Scopus)
67.	Takumi Abe, Katsuhiko Yoshimoto, Matsuo Taniyama, Kazuo Hanakawa, Hitoshi Izumiyama, Mitsuo Itakura and Kiyoshi Matsumoto : A Germline Mutation of the Multiple Endocrine Neoplasia Type 1 (MEN1) Gene in Japanese Prolactinoma Variant., The Journal of Clinical Endocrinology and Metabolism, Vol.85, No.3, 1327-1330, 2000.
68.	Akira Tomonari, Katsuhiko Yoshimoto, Noriko Mizusawa, Hiroyuki Iwahana and Mitsuo Itakura : Differential Regulation of the Human Insulin Gene Transcription by GG1 and GG2 Elements with GG- and C1-binding Factors., Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression, Vol.1446, No.3, 233-242, 1999. (Summary) Using a human growth hormone reporter system, the introduced mutations in GG1 alone or both GG elements of GG1 and GG2 in the human insulin promoter abolished 94 or 96% of the beta-cell-specific transcriptional activity in a pancreatic islet beta-cell line of MIN6, while the mutations in GG2 or its total deletion abolished 85 or 86% of the transcriptional activity. When linked to the thymidine kinase promoter, mutations in GG1 or both GG elements abolished 74% of the transcriptional activity in MIN6 cells, while the mutations in GG2 or its total deletion abolished 55 or 54%. In the electrophoretic mobility shift assay (EMSA), one nuclear factor was shown to interact with two GG elements, and another C1-binding factor with GG1 and C1. The differential effects of deletions or selective mutations in the GG2 or GG1 sequence in the oligonucleotide probes on the binding activity of GG- or C1-binding factors in EMSA proved the requirement of both GG1 and GG2 or both GG1 and C1, respectively, for the transaction of these two factors. The molecular size of the GG-binding factor was estimated about 30 kDa. Based on these, we conclude that two GG elements contribute, with GG1 more critically than GG2, to the beta-cell-specific transcription of the human insulin gene through transaction with the GG- and C1-binding factors. (Keyword) Animals / Binding, Competitive / COS Cells / Cell Line / Consensus Sequence / DNA-Binding Proteins / Electrophoresis / Gene Expression Regulation / Human Growth Hormone / Humans / Insulin / Islets of Langerhans / Mutation / Neoplasm Proteins / Oligonucleotide Probes / Promoter Regions, Genetic / Thymidine Kinase / Transcription Factors / Transcriptional Activation (Link to Publication Site) ● Publication site (DOI): 10.1016/S0167-4781(99)00096-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10524198 ● Search Scopus @ Elsevier (PMID): 10524198 ● Search Scopus @ Elsevier (DOI): 10.1016/S0167-4781(99)00096-2 (DOI: 10.1016/S0167-4781(99)00096-2, PubMed: 10524198)
69.	Takashi Yamaoka, Makiko Yano, Chiyoko Idehara, Sachiko Tomonari, Maki Moritani, Setsuko Ii, Katsuhiko Yoshimoto, Junichi Hata and Mitsuo Itakura : Apotosis and Remodelling of Beta Cells by Paracrine Interferon-g without Insulitis in Transgenic Mice., Diabetologia, Vol.42, 566-573, 1999.
70.	Katsuhiko Yoshimoto, Chisato Kosugi, Miki Moritani, Eiji Shimizu, Takashi Yamaoka, Shozo Yamada, Toshiaki Sano and Mitsuo Itakura : Infrequent Detectable Somatic Mutations of the RET and Glial Cell Line-Derived Neurotrophic Factor (GDNF) Genes in Human Pituitary Adenomas., Endocrine Journal, Vol.46, No.1, 199-207, 1999. (Summary) RET is a receptor tyrosine kinase expressed in neuroendocrine cells and tumors. RET is activated by a ligand complex comprising glial cell line-derived neurotrophic factor (GDNF) and GDNF receptor-alpha (GDNFR-alpha). Activating mutations of the RET proto-oncogene were found in multiple endocrine neoplasia (MEN) 2 and in sporadic medullary thyroid carcinoma and pheochromocytoma of neuroendocrine origin. Mutations of the RET proto-oncogene and the glial cell line-derived neurotrophic factor (GDNF) gene were examined in human pituitary tumors. No mutations of the RET proto-oncogene including the cysteine-rich region or codon 768 and 918 in the tyrosine kinase domain were detected in 172 human pituitary adenomas either by polymerase chain reaction (PCR)-single strand conformation polymorphism (SSCP) or by PCR-restriction fragment length polymorphism (RFLP). Further, somatic mutations of the GDNF gene in 33 human pituitary adenomas were not detected by PCR-SSCP. One polymorphism of the GDNF gene at codon 145 of TGC or TGT was observed in a prolactinoma. The RET proto-oncogene message was detected in a normal human pituitary gland or 4 of 4 human pituitary adenomas with reverse transcription (RT)-PCR, and in rodent pituitary tumor cell lines with Western blotting. The expression of GDNF gene was detected in 1 of 4 human somatotroph adenomas, 1 of 2 corticotroph adenomas, and 2 of 6 rodent pituitary tumor cell lines with RT-PCR. Based on these, it is concluded that somatic mutations of the RET proto-oncogene or the GDNF gene do not appear to play a major role in the pituitary tumorigenesis in examined tumors. (Keyword) Adenoma / Animals / DNA Mutational Analysis / Drosophila Proteins / Gene Expression / Glial Cell Line-Derived Neurotrophic Factor / Glial Cell Line-Derived Neurotrophic Factor Receptors / Humans / Mice / Mutation / Nerve Growth Factors / Nerve Tissue Proteins / Pituitary Neoplasms / Proto-Oncogene Proteins / Proto-Oncogene Proteins c-ret / RNA, Neoplasm / Rats / Receptor Protein-Tyrosine Kinases / Reverse Transcriptase Polymerase Chain Reaction (Tokushima University Institutional Repository) ● Metadata: 111694 (Link to Publication Site) ● Publication site (DOI): 10.1507/endocrj.46.199 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10426588 ● Search Scopus @ Elsevier (PMID): 10426588 ● Search Scopus @ Elsevier (DOI): 10.1507/endocrj.46.199 (Tokushima University Institutional Repository: 111694, DOI: 10.1507/endocrj.46.199, PubMed: 10426588)
71.	Chisato Kosugi, Takehiko Kimura, Peng Yang, Maki Moritani, Takashi Yamaoka, Shozo Yamada, Toshiaki Sano, Katsuhiko Yoshimoto and Mitsuo Itakura : Analysis of loss of heterozygosity on chromosome 11 and infrequent inactivation of the MEN1 gene in sporadic pituitary adenomas, The Journal of Clinical Endocrinology and Metabolism, Vol.83, No.8, 2631-2634, 1998. (Summary) To investigate the role of tumor suppressor genes in sporadic pituitary adenomas, we first analyzed loss of heterozygosity on 11q13 with microsatellite analysis in 31 tumors. Loss of heterozygosity on 11q13 was detected in 1 mixed GH/PRL adenoma, and the somatic 22-bp deletion of the multiple endocrine neoplasia type 1 (MEN1) gene encoding menin was detected in this tumor. Trisomy 11 suggested by the decreased mean allelic ratios of 66% or 65% for 16 or 13 microsatellite markers, respectively, in 2 of 31 pituitary adenomas was confirmed by interphase fluorescence in situ hybridization. Screening for mutations of the MEN1 gene did not find mutations with PCR-single strand conformation polymorphism analysis in other pituitary adenomas retaining heterozygosity on 11q13. Based on these, it is concluded that inactivation of the MEN1 gene comprises a rare etiology for tumorigenesis of the pituitary gland, and that trisomy 11 or another gene(s) may contribute to the pathogenesis of sporadic pituitary adenomas. (Keyword) Adenoma / Alleles / Chromosomes, Human, Pair 11 / Genes, Tumor Suppressor / Humans / In Situ Hybridization, Fluorescence / Loss of Heterozygosity / Microsatellite Repeats / Multiple Endocrine Neoplasia Type 1 / Pituitary Neoplasms / Polymerase Chain Reaction / Polymorphism, Single-Stranded Conformational / Trisomy (Link to Publication Site) ● Publication site (DOI): 10.1210/jcem.83.8.4888 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9709923 ● Search Scopus @ Elsevier (PMID): 9709923 ● Search Scopus @ Elsevier (DOI): 10.1210/jcem.83.8.4888 (DOI: 10.1210/jcem.83.8.4888, PubMed: 9709923)
72.	Maki Moritani, Katsuhiko Yoshimoto, Suzan F Wong, Chisato Kosugi, Takashi Yamaoka, Toshiaki Sano, Junichi Miyazaki, Hitoshi Kikutani and Mitsuo Itakura : Abrogation of Autoimmune Diabetes in Nonobese Diabetic Mice and Preotection against Effector Lymphocytes by Transgenic Paracrine TGFb-1., The Journal of Clinical Investigation, Vol.102, No.3, 499-506, 1998. (Tokushima University Institutional Repository) ● Metadata: 109647 (Tokushima University Institutional Repository: 109647)
73.	Chisato Kosugi, Katsuhiko Yoshimoto and Mitsuo Itakura : Germ-Line Mutations in MEN1 Patients-Authors' Response., The Journal of Clinical Endocrinology and Metabolism, Vol.83, No.8, 3005, 1998.
74.	Chisato Kosugi, Takehiko Kimura, Peng Yang, Maki Moritani, Takashi Yamaoka, Shozo Yamada, Toshiaki Sano, Katsuhiko Yoshimoto and Mitsuo Itakura : Analysis of Loss of Heterozygosity on Chromosome 11 and Infrequent Inactivation of MEN1 Gene in Sporadic Pituitary Adenomas., The Journal of Clinical Endocrinology and Metabolism, Vol.83, No.8, 2631-2634, 1998.
75.	Chisato Kosugi, Katsuhiko Yoshimoto, Shozo Yamada, Hiroshi Nishioka, Setsuko Ii, Maki Moritani, Takashi Yamaoka and Mitsuo Itakura : Absence of Germline Mutations of the MEN1 Gene in Familial Pituitary Adenoma in Contrast to Multiple Endocrine Neoplasia Type 1 in Japanese., The Journal of Clinical Endocrinology and Metabolism, Vol.83, No.3, 960-965, 1998.
76.	Tetsunari Oyama, Kenji Kashiwabara, Katsuhiko Yoshimoto, Andrew Arnold and Frederick Koerner : Frequent overexpression of the cyclin D1 oncogene in invasive lobular carcinoma of the breast., Cancer Research, Vol.58, No.13, 2876-2880, 1998.
77.	Katsuhiko Yoshimoto, Hideko Endo, Masaru Tsuyuguchi, Chisato Kosugi, Takehiko Kimura, Hiroyuki Iwahana, Genichi Kato, Toshiaki Sano and Mitsuo Itakura : Familial Isolated Primary Hyperparathyroidism with Parathyroid Carcinomas: Clinical and Molecular Features., Clinical Endocrinology, Vol.48, No.1, 67-72, 1998. (Summary) Familial isolated primary hyperparathyroidism (FIHP) is a rare hereditary disorder. We present four patients from a single family with FIHP, and genetic analysis of their parathyroid adenomas and parathyroid carcinoma. DNA was extracted from tumours resected at surgery. Tumours were examined for loss of heterozygosity (LOH) with microsatellite polymorphic markers. The 27-year-old proband (Patient 1) died of parathyroid carcinoma with metastases to the lungs and chest wall. Sixteen years later, his 34-year-old sister (Patient 2) presented with a neck tumour and primary hyperparathyroidism. Family screening revealed parathyroid tumours in his 36-year-old sister (Patient 3) and 29-year-old cousin (Patient 4). Histological examination of resected tumours showed parathyroid carcinoma and adenoma in Patient 2, a parathyroid adenoma in Patient 3, and an atypical parathyroid adenoma in Patient 4. Autopsy of the proband ruled out multiple endocrine neoplasia (MEN) type 1, and the three patients who underwent parathyroidectomy did not exhibit any abnormalities in the pancreas or the pituitary gland. Analysis of tumour DNA from one parathyroid carcinoma (Patient 2), the atypical parathyroid adenoma (Patient 4), and two parathyroid adenomas (Patients 2 and 3) showed limited LOH on chromosomes 13q12.3-q32 in an adenoma of Patient 2 and 9p21-p22 and 13q12.3-q32 in an adenoma of Patient 3. These results suggest the possible contribution of tumour suppressor genes including the retinoblastoma gene and the hereditary breast cancer susceptibility gene (BRCA2) on 13q to parathyroid tumours in this family. (Keyword) Adenoma / Adult / Carcinoma / Chromosomes, Human, Pair 13 / Chromosomes, Human, Pair 9 / Female / Genetic Markers / Humans / Hyperparathyroidism / Loss of Heterozygosity / Male / Parathyroid Neoplasms / Pedigree (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9509070 ● Search Scopus @ Elsevier (PMID): 9509070 (PubMed: 9509070)
78.	Akira Aoki, Toshihiko Tsukada, Hiroko Yasuda, Shinsuke Kayashima, Terumasa Nagase, Teizo Ito, Takashi Suzuki, Susumu Matsukuma, Noriyuki Kuwabara, Katsuhiko Yoshimoto and Ken Yamaguchi : Multiple Endocrine Neoplasia Type 1 Presented with Manic-Depressive Disorder: A Case Report with an Identified MEN 1 Gene Mutation., Japanese Journal of Clinical Oncology, Vol.27, No.6, 419-422, 1997. (Summary) We report a case of multiple endocrine neoplasia type 1 who had repeated hypoglycemic episodes and had previously been diagnosed with bipolar manic-depressive disorder. The patient had a positive family history of multiple endocrine neoplasia type 1 and had multiple pancreatic endocrine tumors, hyperparathyroidism and possibly a pituitary tumor. The pancreatic tumors were resected by subtotal pancreatectomy and examined by histochemical staining and gene analysis. The tumor cells were positive for immunoreactive insulin and glucagon. A microsatellite polymorphism analysis revealed loss of heterozygosity on 11q13 in the tumors. By polymerase chain reaction-based nucleotide sequencing, we identified a germline mutation 483del2 of the MEN1 gene in the normal pancreatic tissue of the patient. This mutation causes a shift of the reading frame of menin mRNA at codon 125. It seems that the wild type allele of the MEN1 gene had been lost in the tumor cells whereas the mutant allele remained intact. This is the first identified MEN1 gene mutation in Japanese families and is different from all MEN1 gene mutations reported previously. (Keyword) Adult / Bipolar Disorder / Codon / Humans / Hyperparathyroidism / Hypoglycemia / Male / Microsatellite Repeats / Multiple Endocrine Neoplasia Type 1 / Mutation / Pancreatectomy / Pancreatic Neoplasms / Pedigree / Pituitary Neoplasms / Polymerase Chain Reaction / RNA, Messenger (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9438006 ● Search Scopus @ Elsevier (PMID): 9438006 (PubMed: 9438006)
79.	Chisato Kosugi, Katsuhiko Yoshimoto, Peng Yang, Takehiko Kimura, Shozo Yamada, Maki Moritani, Toshiaki Sano and Mitsuo Itakura : Infrequent Mutations of p27Kip1 Gene and Trisomy 12 in a Subset of Human Pituitary Adenomas., The Journal of Clinical Endocrinology and Metabolism, Vol.82, No.9, 3141-3147, 1997.
80.	Takashi Yamaoka, Maki Kondo, Soichi Honda, Hiroyuki Iwahana, Maki Moritani, Setsuko Ii, Katsuhiko Yoshimoto and Mitsuo Itakura : Amidophosphoribosyltransferase Limits the Rate of Cell Growth-linked de Novo Purine Biosynthesis in the Presence of Constant Capacity of Salvage Purine Biosynthesis., The Journal of Biological Chemistry, Vol.272, No.28, 17719-17725, 1997.
81.	Hongzhong Min, Eiji Kudo, Akiko Hino, Katsuhiko Yoshimoto, Hiroshi Iwahana, Mitsuo Itakura and Keisuke Izumi : p53 Gene Mutation in N-(4-hydroxybutyl) nitrosamine-induced Urinary Bladder Tumors and N-methyl-N-nitrosourea-induced Colon Tumors of Rats., Cancer Letters, Vol.117, No.1, 81-86, 1997. (Tokushima University Institutional Repository) ● Metadata: 113516 (Tokushima University Institutional Repository: 113516)
82.	Hiroshi Sarui, Katsuhiko Yoshimoto, Shoji Okumura, Masanori Kamura, Hiroshi Takuno, Tatsuo Ishizuka, Hiroshi Takao, Kuniyasu Shimokawa, Mitsuo Itakura, Shigetoyo Saji and Keigo Yasuda : Cystic Glucagonoma with Loss of Heterozygosity on chromosome 11 in Multiple Endocrine Neoplasia Type 1., Clinical Endocrinology, Vol.46, No.4, 511-516, 1997. (Summary) A 52-year-old man with a past history of a pituitary adenoma and hyperparathyroidism due to a parathyroid adenoma was admitted because of a solitary tumour of the pancreas revealed by ultrasonography. His family history was unremarkable. Plasma glucagon levels were slightly elevated (280 ng/l, normal range, 40-180 ng/l) with decreased plasma amino acid levels. Plasma glucagon levels disclosed an exaggerated response during an arginine infusion test and paradoxical elevation during a 75 g oral glucose tolerance test. Endoscopic ultrasonography revealed a monolocular cystic mass of about 3 cm in diameter in the body of the pancreas. A pancreatic tumour was diagnosed before surgery as a cystic glucagonoma. Intra-operative ultrasonography showed one cystic mass in the body of pancreas and two other solid tumours, about 1 cm and 0.5 cm in diameter, in the tail of the pancreas. Histologically, all three tumours showed neoplastic epithelial cells with round nuclei forming cords and/or a ribbon-like arrangement. They showed positive staining for Grimelius' silver stain and immunopositive cells for glucagon. Genetic analysis of the main cystic tumour revealed loss of heterozygosity (LOH) on chromosome 11. After the operation, the responses of plasma glucagon to arginine infusion and oral glucose became normal. Here we describe the usefulness of these provocation tests for early diagnosis and post-operative follow-up in a rare cystic glucagonoma associated with multiple endocrine neoplasia type 1 (MEN 1) which had LOH on chromosome 11. (Keyword) Arginine / Chromosomes, Human, Pair 11 / Glucagon / Glucagonoma / Glucose Tolerance Test / Homozygote / Humans / Male / Middle Aged / Multiple Endocrine Neoplasia Type 1 / Pancreatic Neoplasms / Ultrasonography (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9196616 ● Search Scopus @ Elsevier (PMID): 9196616 (PubMed: 9196616)
83.	Yoshihiro Ninomiya, Yoshio Urano, Katsuhiko Yoshimoto, Hiroyuki Iwahana, Shiro Sasaki, Seiji Arase and Mitsuo Itakura : p53 Gene Mutation Analysis in Porokeratosis and Porokeratosis-associated Squamous Cell Carcinoma., Journal of Dermatological Science, Vol.14, No.3, 173-178, 1997. (Summary) In this and previous studies, we have shown p53 overexpression immunohistochemically in 14 of 17 porokeratotic specimens obtained from 14 lesions of nine cases, and in all six specimens of squamous cell carcinoma (SCC) arising on porokeratotic lesions of two cases. We screened mutations in exons 5 to 10 of the p53 gene in all these specimens by polymerase chain reaction-single strand conformation polymorphism analysis. Mutations of the p53 gene were detected in two of the six SCCs but not in any of the 17 porokeratotic specimens. These two mutations were C to T transitions at codons 146 and 175 in exon 5, which were a nonsense mutation at a dipyrimidine site and a missense mutation at a CG site, respectively. To our knowledge, neither of these mutations has been identified in skin cancers before. Our observations indicate that mutations of the p53 gene are not the major molecular etiology for porokeratosis, but are related to its skin carcinogenesis, and that p53 overexpression in porokeratosis is not due to p53 gene mutations. (Keyword) Adult / Aged / Carcinoma, Squamous Cell / DNA, Neoplasm / Exons / Female / Gene Expression Regulation, Neoplastic / Genes, p53 / Humans / immunohistochemistry / Male / Middle Aged / Mutation / Polymerase Chain Reaction / Polymorphism, Single-Stranded Conformational / Porokeratosis / skin / Skin Neoplasms / Tumor Suppressor Protein p53 (Tokushima University Institutional Repository) ● Metadata: 113521 (Link to Publication Site) ● Publication site (DOI): 10.1016/S0923-1811(96)00569-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9138474 ● Summary page in Scopus @ Elsevier: 2-s2.0-0031106755 (Tokushima University Institutional Repository: 113521, DOI: 10.1016/S0923-1811(96)00569-5, PubMed: 9138474, Elsevier: Scopus)
84.	Katsuhiko Yoshimoto, Chisato Kosugi, Shozo Yamaza, Takehiko Kimura, Hiroyuki Iwahana, Toshiaki Sano and Mitsuo Itakura : Infrequent Mutations of p16INK4A and p15INK4B Genes in Human Pituitary Adenomas., European Journal of Endocrinology, Vol.136, No.1, 74-80, 1997.
85.	Shozo Yamada, Katsuhiko Yoshimoto, Toshiaki Sano, Kouji Tanaka, Mitsuo Itakura, Mitsuo Usui and Akira Teramoto : Inactivation of the Tumor Suppressor Gene on 11q13 in Brothers with Familial Acrogigantism without Multiple Endocrine Neoplasia Type 1., The Journal of Clinical Investigation, Vol.82, 239-242, 1997.
86.	Maki Moritani, Katsuhiko Yoshimoto, Setsuko Ii, Maki Kondo, Hiroyuki Iwahana, Takashi Yamaoka, Toshiaki Sano, Naoko Nakano, Hitoshi Kikutani and Mitsuo Itakura : Prevention of Adoptively Transferred Diabetes in Non-Obese Diabetic Mice with IL-10-Transduced Islet-Specific Th1 Lymphocytes: A Gene Therapy Model for Autoimmune Diabetes., The Journal of Clinical Investigation, Vol.98, No.8, 1851-1859, 1996. (Tokushima University Institutional Repository) ● Metadata: 109646 (Tokushima University Institutional Repository: 109646)
87.	Satoshi Otsuka, Masaki Tanaka, Shiro Saito, Katsuhiko Yoshimoto and Mitsuo Itakura : Molecular Cloning of a cDNA Encoding Human Ribosomal Protein L39., Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression, Vol.1308, No.2, 119-121, 1996. (Summary) A cDNA clone encoding a human ribosomal protein L39 (hRPL39) was isolated through a random cDNA sequencing approach to a cDNA library constructed from a human colon carcinoma cell line of COLO 205. Although levels of hRPL39 mRNA were different in several cell lines including carcinoma cell lines from different tissues, they were shown not to be cell cycle-dependent in a human fibroblast cell line of TIG-1. (Keyword) Amino Acid Sequence / Animals / Base Sequence / Carcinoma / Colonic Neoplasms / DNA, Complementary / Humans / Lung Neoplasms / Mice / Molecular Sequence Data / Ribosomal Proteins / Sequence Homology, Amino Acid / Sequence Homology, Nucleic Acid / Tissue Distribution / Tumor Cells, Cultured (Tokushima University Institutional Repository) ● Metadata: 113514 (Link to Publication Site) ● Publication site (DOI): 10.1016/0167-4781(96)00106-6 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 8764829 ● Search Scopus @ Elsevier (PMID): 8764829 ● Search Scopus @ Elsevier (DOI): 10.1016/0167-4781(96)00106-6 (Tokushima University Institutional Repository: 113514, DOI: 10.1016/0167-4781(96)00106-6, PubMed: 8764829)
88.	Hiroyuki Iwahana, Miwa Fujimura, Setsuko Ii, Maki Kondo, Maki Moritani, Yoko Takahashi, Takashi Yamaoka, Katsuhiko Yoshimoto and Mitsuo Itakura : Molecular Cloning of a Human cDNA Encoding a Trifunctional Enzyme of Carbamoyl- Phosphate Synthetase-Aspartate Transcarbamoylase-Dihydroorotase in de Novo Pyrimidine Synthesis., Biochemical and Biophysical Research Communications, Vol.219, No.1, 249-255, 1996.
89.	Chiyo Horie, Hiroyuki Iwahana, Takahiro Horie, Ichiro Shimizu, Katsuhiko Yoshimoto, Shiro Yogita, Seiki Tashiro, Susumu Ito and Mitsuo Itakura : Detection of Different Quasispecies of Hepatitis C Virus Core Region in Cancerous and Non-cancerous Regions., Biochemical and Biophysical Research Communications, Vol.218, No.3, 674-681, 1996.
90.	Akira Tomonari, Katsuhiko Yoshimoto, Masaki Tanaka, Hiroyuki Iwahana, Jun-ichi Miyazaki and Mitsuo Itakura : GGAAT Motifs Play a Major Role in Transcriptional Activity of the Human Insulin Gene in a Pancreatic Islet Beta Cell Line of MIN6., Diabetologia, Vol.39, 1462-1468, 1996.
91.	Hiroyuki Iwahana, Miwa Fujimura, Yoko Takahashi, Katsuhiko Yoshimoto and Mitsuo Itakura : Multiple Fluorescence-Based PCR-SSCP Analysis Using Internal Fluorescent Labeling of PCR Products., BioTechniques, Vol.21, No.3, 510-519, 1996.
92.	Katsuhiko Yoshimoto, Takehiko Kimura, Chisato Kosugi, Maki Moritani, Hiroyuki Iwahana and Mitsuo Itakura : Absence of Mutations at Codon 768 of the RET Proto-Oncogene in Sporadic and Hereditary Pheochromocytomas., Endocrine Journal, Vol.43, No.1, 109-114, 1996. (Summary) Sixteen sporadic pheochromocytomas, 3 pheochromocytomas in neurofibromatosis 1, and 4 pheochromocytomas in multiple endocrine neoplasia (MEN) 2A or 2B were screened for mutations at codon 768 of the RET proto-oncogene by AluI digestion of polymerase chain reaction PCR products and mutations in exon 13 by PCR-single strand conformation polymorphism (SSCP) analysis. Although mutations at codon 768 (GAG --> GAC; Glu --> Asp) of the RET proto-oncogene were recently reported to be found in 40% of sporadic medullary thyroid carcinomas (MTCs), the absence of missense mutations at codon 768 was confirmed both with PCR-restriction fragment length polymorphism (RFLP) and PCR-SSCP analysis in all examined cases of pheochromocytomas. These results suggest that mutations at codon 768 of the RET proto-oncogene do not represent a frequent mechanism of tumorigenesis for both sporadic and hereditary pheochromocytomas. (Keyword) Adrenal Gland Neoplasms / Adult / Aged / Base Sequence / Codon / Drosophila Proteins / Female / Humans / Male / Middle Aged / Molecular Sequence Data / Multiple Endocrine Neoplasia Type 2a / Multiple Endocrine Neoplasia Type 2b / Mutation / Pheochromocytoma / Polymerase Chain Reaction / Polymorphism, Restriction Fragment Length / Polymorphism, Single-Stranded Conformational / Proto-Oncogene Proteins / Proto-Oncogene Proteins c-ret / Receptor Protein-Tyrosine Kinases (Tokushima University Institutional Repository) ● Metadata: 111693 (Link to Publication Site) ● Publication site (DOI): 10.1507/endocrj.43.109 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 8732460 ● Search Scopus @ Elsevier (PMID): 8732460 ● Search Scopus @ Elsevier (DOI): 10.1507/endocrj.43.109 (Tokushima University Institutional Repository: 111693, DOI: 10.1507/endocrj.43.109, PubMed: 8732460)
93.	Takehiko Kimura, Katsuhiko Yoshimoto, Chisato Kosugi, Yoshihiro Ohkura, Hiroyuki Iwahana, Akira Miyauchi, Toshiaki Sano and Mitsuo Itakura : Obvious mRNA and Protein Expression but Absence of Mutations of the RET Proto-Oncogene in Parathyroid Tumors., European Journal of Endocrinology, Vol.134, No.3, 314-319, 1996.
94.	Katsuhiko Yoshimoto, Rie Marukami, Maki Moritani, Mika Ohta, Hiroyuki Iwahana, Hiromitsu Nakauchi and Katsuhiko Yoshimoto : Loss of Ganciclovir Sensitivity by Exclusion of Thymidine Kinase Gene from Transplanted Proinsulin-Producing Fibroblasts as a Gene Therapy Model for Diabetes., Gene Therapy, Vol.3, No.3, 230-234, 1996. (Summary) To establish a practical method of somatic gene therapy, we aimed to develop a regulatory system at the cellular level using a suicide vector. We introduced the herpes simplex virus type 1 thymidine kinase (HSV-tk) gene into the human proinsulin-producing Ltk-cells and examined whether ganciclovir (GCV) administration could control proinsulin production in vivo. The cells transfected with the HSV-tk gene showed more than 100-fold increase in sensitivity to GCV compared with the parent cells. Analysis of blood glucose in diabetic nude mice with transplanted cells showed that proinsulin production by these cells was strongly suppressed by GCV treatment in vivo as reflected by the reversal to hyperglycemia. However, in the in vivo experiment, the plasmid containing the HSV-tk gene was spontaneously lost from the transplanted cells in one of six cases resulting in the resistance to GCV as reflected by the persistent hypoglycemia and increased tumor size. This system of HSV-tk and administration of GCV may be applicable to gene therapy as a suicide vector, but the system of stable expression of the HSV-tk gene must be established. (Keyword) Animals / Cell Line / Diabetes Mellitus, Experimental / Disease Models, Animal / Fibroblasts / Ganciclovir / Gene Therapy / Herpesviridae / Humans / Mice / Mice, Inbred BALB C / Mice, Inbred C3H / Mice, Nude / Proinsulin / Streptozocin / Thymidine Kinase (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 8646554 ● Search Scopus @ Elsevier (PMID): 8646554 (PubMed: 8646554)
95.	Yoshio Urano, Takashi Asano, Katsuhiko Yoshimoto, Hiroyuki Iwahana, Yoshiaki Kubo, Shoji Kato, Shiro Sasaki, Norifumi Takeuchi, Naoyuki Uchida, Hideki Nakanishi, Seiji Arase and Mitsuo Itakura : Frequent p53 Accumulation in the Chronically Sun-Exposed Epidermis and Clonal Expansion of p53 Mutant Cells in the Epidermis Adjacent to Basal Cell Carcinoma., The Journal of Investigative Dermatology, Vol.104, No.6, 928-932, 1995.
96.	Hiroyuki Iwanaha, Soichi Honda, Toshiyuki Tsujisawa, Yoko Takahashi, Kyo Adzuma, Rumi Katashima, Takashi Yamaoka, Maki Moritani, Katsuhiko Yoshimoto and Mitsuo Itakura : Rat Genomic Structure of Amidophosphoribosyltransferase, cDNA Sequence of Aminoimidazole Ribonucleotide Carboxylase, and Cell Cycle-Dependent Expression of These Two Physically Linked Genes., Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression, Vol.1261, No.3, 369-380, 1995. (Summary) Genomic structure of rat amidophosphoribosyltransferase (ATase; EC 2.4.2.14), which catalyzes the first committed step in de novo purine nucleotide synthesis, was determined by polymerase chain reaction (PCR)-based methods. There are 11 exons and all exon-intron boundaries were conserved among rat, human, and chicken ATase genes. A rat aminoimidazole ribonucleotide carboxylase (AIRC) cDNA encoding a bifunctional enzyme of AIRC (EC 4.1.1.21) at step 6 and SAICAR synthetase (EC 6.3.2.6) at step 7 in de novo purine nucleotide synthesis was cloned and sequenced. The size of the cloned rat AIRC cDNA was 1329 bp, and amino acid identity with human and chicken AIRC was 96 and 85%, respectively. The intergenic sequence using a phage clone and the PCR product disclosed that ATase and AIRC genes are physically linked with the 736 bp sequence between the translation start sites, and the determination of the transcriptional start sites by the primer extension assay for these genes disclosed that distance between the two major transcriptional start sites is 585 bp. The amount of mRNAs of both genes showed approx. 5-6-fold increase in G1/S phase of the cell cycle over those in G0 phase in synchronized rat 3Y1 fibroblasts. (Keyword) Amidophosphoribosyltransferase / Amino Acid Sequence / Animals / Base Sequence / Carboxy-Lyases / Cell Cycle / DNA, Complementary / Gene Expression Regulation, Enzymologic / Molecular Sequence Data / Rats / Rats, Wistar / Sequence Alignment (Link to Publication Site) ● Publication site (DOI): 10.1016/0167-4781(95)00036-G (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 7742366 ● Search Scopus @ Elsevier (PMID): 7742366 ● Search Scopus @ Elsevier (DOI): 10.1016/0167-4781(95)00036-G (DOI: 10.1016/0167-4781(95)00036-G, PubMed: 7742366)
97.	Hideo Kaneko, Kiyoko Sugita, Nobutaka Kiyokawa, Koho Iizuka, Koji Takada, Masahiro Saito, Katsuhiko Yoshimoto, Mitsuo Itakura, Yasuo Kokai and Junichiro Fujimoto : Lack of CD54 Expression and Mutation of p53 Gene Relate to the Prognosis of Childhood Burkitt's Lymphoma., Leukemia and Lymphoma, Vol.18, 179-184, 1995.
98.	Takehiko Kimura, Katsuhiko Yoshimoto, Yutaka Yokogoshi and Shiro Saito : Mutations in the Cysteine-Rich Region of the RET Proto-Oncogene in Patients Diagnosed as Having Sporadic Medullary Thyroid Carcinoma., Endocrine Journal, Vol.42, No.4, 517-525, 1995. (Summary) Medullary thyroid carcinoma (MTC) and pheochromocytoma appear in either a sporadic or a hereditary form as components of multiple endocrine neoplasia (MEN). Many germline mutations of the RET proto-oncogene have been reported in patients with MEN 2A and 2B, and familial MTC (FMTC). To elucidate the etiological roles in tumorigenesis of sporadic MTCs and pheochromocytomas, mutations in the cysteine-rich region of the RET proto-oncogene were analyzed by using polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) analysis. Exons 10 and 11 were studied in genomic DNAs from 3 clinically apparent sporadic MTCs, MTCs and pheochromocytomas from 2 patients with MEN 2A, 1 with FMTC, 4 with MEN 2B, 3 with neurofibromatosis type 1 (NF1), 12 sporadic pheochromocytomas and an MTC cell line, TT. All tumors from two patients with MEN 2A and one patient with FMTC had mutations at codon 618 and 634 as well as their leukocytes, reflecting their germline mutations. In this region, no mutations were detected in any tumors from patients with MEN 2B and NF1, and sporadic pheochromocytomas. But mutations were detected and identified in 3 clinically apparent sporadic MTCs and TT cells. A 6 base pair (bp) deletion causing the loss of a cysteine residue at codon 634 and a mutation causing substitution from cysteine to tyrosine at codon 634 were detected in 2 sporadic MTCs as somatic events. In a female patient diagnosed as having sporadic MTC, a mutation at codon 618 was detected not only in tumor tissues, but also in her leukocytes, suggesting a germline mutation of the RET proto-oncogene.(ABSTRACT TRUNCATED AT 250 WORDS) (Keyword) Adrenal Gland Neoplasms / Aged / Alleles / Base Sequence / Carcinoma, Medullary / Cysteine / DNA, Neoplasm / Exons / Female / Germ-Line Mutation / Humans / Leukocytes / Male / Middle Aged / Molecular Sequence Data / Pheochromocytoma / Polymerase Chain Reaction / Proto-Oncogenes / Thyroid Neoplasms / Tumor Cells, Cultured (Tokushima University Institutional Repository) ● Metadata: 111692 (Link to Publication Site) ● Publication site (DOI): 10.1507/endocrj.42.517 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 8556059 ● Search Scopus @ Elsevier (PMID): 8556059 ● Search Scopus @ Elsevier (DOI): 10.1507/endocrj.42.517 (Tokushima University Institutional Repository: 111692, DOI: 10.1507/endocrj.42.517, PubMed: 8556059)
99.	Yasumi Shintani, Katsuhiko Yoshimoto, Hideaki Horie, Toshiaki Sano, Yoshiko Kanesaki, Emiko Hosoi, Yutaka Yokogoshi, Hiroshi Bando, Hiroyuki Iwahana, Seiji Kannuki, Keizo Matsumoto, Mitsuo Itakura and Shiro Saito : Two Different Pituitary Adenomas in a Patient with Multiple Endocrine Neoplasia Type 1Associated with Growth Hormone-Releasing Hormone-Producing Pancreatic Tumor: Clinical and Genetic Features., Endocrine Journal, Vol.42, No.3, 331-340, 1995. (Summary) The clinical and genetic features of a 43-year-old male patient with multiple endocrine neoplasia type 1 were reported. He developed hyperparathyroidism, a GHRH-producing pancreatic tumor, and acromegaly between 1980 and 1983. Because his pituitary gland increased in size even after resecting the GHRH-producing pancreatic tumor, transsphenoidal hypophysectomy was performed six years later. The pituitary contained two histologically-different adenomas composed of somatotroph cells and null cells. Genetic analyses revealed loss of heterozygosity on chromosome 11 in common in the pituitary adenomas, the pancreatic endocrine tumors, and a parathyroid hyperplasia. On the other hand, mutations of ras, p53, Gs alpha, and Gi2 alpha genes were not found in these tumors. The loss of the tumor suppressor gene on chromosome 11q12-13 was involved in the formation of two pituitary adenomas, two pancreatic endocrine functioning tumors, and a parathyroid hyperplasia in this patient, but the tumorigenic factors in the specific endocrine organs remain to be studied. (Keyword) Acromegaly / Adenoma / Adult / Base Sequence / Chromosomes, Human, Pair 11 / DNA Mutational Analysis / Genes, Tumor Suppressor / Growth Hormone-Releasing Hormone / Heterozygote / Humans / Hyperparathyroidism / Male / Molecular Sequence Data / Multiple Endocrine Neoplasia Type 1 / Pancreatic Neoplasms / Pituitary Neoplasms / Polymorphism, Restriction Fragment Length (Tokushima University Institutional Repository) ● Metadata: 111462 (Link to Publication Site) ● Publication site (DOI): 10.1507/endocrj.42.331 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 7670561 ● Search Scopus @ Elsevier (PMID): 7670561 ● Search Scopus @ Elsevier (DOI): 10.1507/endocrj.42.331 (Tokushima University Institutional Repository: 111462, DOI: 10.1507/endocrj.42.331, PubMed: 7670561)
100.	Chen-Yu Zhang, Yutaka Yokogoshi, Katsuhiko Yoshimoto, Yuichi Fujinaka, Kazuya Matsumoto and Shiro Saito : Point Mutation of the Somatostatin Receptor 2 Gene in the Human Small Cell Lung Cancer Cell line COR-L103., Biochemical and Biophysical Research Communications, Vol.210, No.3, 805-815, 1995.
101.	Mika Ohta, Setsuko Ii, Takashi Yamaoka, Kazuo Ono, Yasuo Kokai, Jun-ichiro Fujimoto, Hiroyuki Iwahana, Katsuhiko Yoshimoto and Mitsuo Itakura : Galactose-Induced Albuminuria in Transgenic Mice Expressing Human Aldose Reductase., Nutrition Research, Vol.15, No.9, 1343-1353, 1995. (Link to Publication Site) ● Publication site (DOI): 10.1016/0271-5317(95)02009-K (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/0271-5317(95)02009-K (DOI: 10.1016/0271-5317(95)02009-K)
102.	Hiroyuki Iwahana, Kyo Adzuma, Yoko Takahashi, Rumi Katashima, Katsuhiko Yoshimoto and Mitsuo Itakura : Multiple Fluorescence-Based PCR-SSCP Analysis with Postlabeling., Genome Research, Vol.4, 275-282, 1995.
103.	Katsuhiko Yoshimoto, Chisato Kosugi, Sachiko Hamaguchi, Takehiko Kimura, Hiroyuki Iwahana, Akira Miyauchi and Mitsuo Itakura : Tumor-Specific Mutations in the Tyrosine Kinase Domain of the RET Proto-Oncogene in Pheochromocytomas of Sporadic Type., Endocrine Journal, Vol.42, No.2, 265-270, 1995. (Summary) Sporadic pheochromocytomas, sporadic medullary thyroid carcinomas (MTCs), pheochromocytomas and/or MTCs in multiple endocrine neoplasia (MEN) 2A or 2B were screened for mutations in the tyrosine kinase domain of the RET proto-oncogene by direct sequencing of PCR-amplified products or sequencing subcloned DNAs from PCR-products. All tumors of 4 MEN 2B patients were confirmed to contain a heterozygous missense mutation at codon 918 (ATG-->ACG; Met-->Thr) of the RET proto-oncogene as well as their leukocytes. The same tumor-specific mutations at codon 918 were also found in 5/16 (31%) sporadic pheochromocytomas. These results suggest that mutations of the RET proto-oncogene in its tyrosine kinase domain play a role not only as the predisposing gene for MEN 2B, but also as a tumorigenic factor for pheochromocytomas of sporadic type. (Keyword) Adolescent / Adult / Aged / Base Sequence / Carcinoma, Medullary / DNA, Neoplasm / Drosophila Proteins / Female / Humans / Male / Middle Aged / Molecular Sequence Data / Multiple Endocrine Neoplasia Type 2a / Mutation / Pheochromocytoma / Polymerase Chain Reaction / Protein-Tyrosine Kinases / Proto-Oncogene Proteins / Proto-Oncogene Proteins c-ret / Receptor Protein-Tyrosine Kinases / Thyroid Neoplasms (Tokushima University Institutional Repository) ● Metadata: 111690 (Link to Publication Site) ● Publication site (DOI): 10.1507/endocrj.42.265 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 7627271 ● Search Scopus @ Elsevier (PMID): 7627271 ● Search Scopus @ Elsevier (DOI): 10.1507/endocrj.42.265 (Tokushima University Institutional Repository: 111690, DOI: 10.1507/endocrj.42.265, PubMed: 7627271)
104.	Masaki Tanaka, Kyo Adzuma, Miki Iwami, Katsuhiko Yoshimoto, Yasumasa Monden and Mitsuo Itakura : Human Calgizzarin; One Colorectal Cancer-Related Gene Selected by a Large Scale Random cDNA Sequencing and Northern Blot Analysis., Cancer Letters, Vol.89, 195-200, 1995. (Tokushima University Institutional Repository) ● Metadata: 113515 (Tokushima University Institutional Repository: 113515)
105.	Masaki Tanaka, Rumi Katashima, Daisuke Murakami, Kyo Adzuma, Yoko Takahashi, Akira Tomonari, Hiroyuki Iwahana, Katsuhiko Yoshimoto and Mitsuo Itakura : Molecular Cloning of a Group of Mouse Pancreatic Islet B Cell and Glucose Concentration-Related Genes by Random cDNA Sequencing., Diabetologia, Vol.38, 381-386, 1995.
106.	Chen-Yu Zhang, Yutaka Yokogoshi, Katsuhiko Yoshimoto, Yuichi Fujinaka, Kazuya Matsumoto and Shiro Saito : Point mutation of the somatostatin receptor 2 gene in the human small cell lung cancer cell line COR-L103, Biochemical and Biophysical Research Communications, Vol.210, 805-815, 1995.
107.	Yoshiaki Kubo, Yoshio Urano, Katsuhiko Yoshimoto, Hiroyuki Iwahana, Kosaku Fukuhara, Seiji Arase and Mitsuo Itakura : p53 Gene Mutations in Human Skin Cancers and Precancerous Lesions: Comparison with Immunohistochemical Analysis., The Journal of Investigative Dermatology, Vol.102, No.4, 440-444, 1994.
108.	Maki Moritani, Katsuhiko Yoshimoto, Fumi Tashiro, Chikara Hashimoto, Jun-ichi Miyazaki, Setsuko Ii, Eiji Kudo, Hiroyuki Iwahana, Yoshio Hayashi, Toshiaki Sano and Mitsuo Itakura : Transgenic Expression of IL-10 in Pancreatic Islet A cells Accelerates Autoimmune Insulitis and Diabetes in Non-Obese Diabetic Mice., International Immunology, Vol.6, No.12, 1927-1936, 1994.
109.	Hiroyuki Iwahana, Toshiyuki Tsujisawa, Rumi Katashima, Katsuhiko Yoshimoto and Mitsuo Itakura : PCR with End Trimming and Cassette Ligation: A Rapid Method to Clone Exon-Intron Boundaries and a 5'-Upstream Sequence of Genomic DNA Based on a cDNA Sequence., Genome Research, Vol.4, No.1, 19-25, 1994.
110.	Hiroyuki Iwahana, Katsuhiko Yoshimoto, Toshiyuki Tsujisawa and Mitsuo Itakura : T-Cassette Ligation: A Method for Direct Sequencing and Cloning of PCR-Amplified DNA Fragments., Genome Research, Vol.3, 219-224, 1994.
111.	Hiroyuki Iwahana, Katsuhiko Yoshimoto, Noriko Mizusawa, Eiji Kudo and Mitsuo Itakura : Multiple Fluorescence-Based PCR-SSCP Analysis., BioTechniques, Vol.16, No.2, 296-305, 1994.
112.	Hiroyuki Iwahana, Noriko Mizusawa, Setsuko Ii, Katsuhiko Yoshimoto and Mitsuo Itakura : An End-Trimming Method to Amplify Adjacent cDNA Fragments by PCR., BioTechniques, Vol.16, No.1, 94-98, 1994.
113.	Katsuhiko Yoshimoto and Shiro Saito : Critical Commentary to "MEN 1 with Mediastinal Carcinoid"., Pathology, Research and Practice, Vol.189, No.9, 1097-1099, 1993.
114.	Katsuhiko Yoshimoto, Hiroyuki Iwahana and Mitsuo Itakura : Relatively Good Prognosis of Multiple Endocrine Neoplasia Type 2B in Japanese: Review of Cases in Japan and Analysis of Genetic Changes in Tumors., Endocrine Journal, Vol.40, No.6, 649-657, 1993. (Summary) Since 1968, a total of 23 patients with multiple endocrine neoplasia type 2B (MEN 2B) have been identified in Japan. The mean age at diagnosis was 20.3 years (range, 6 to 39 years). All patients had neuromas and bumpy lips. All patients underwent thyroidectomy for medullary thyroid carcinoma (MTC). Ten of 23 patients had pheochromocytomas. One patient died of cerebral bleeding at the age of 43, 2 patients died of MTC at the age of 35 and 12. Five-, 10-, and 15-year survival rates were 100%, 92%, and 88%, respectively. The clinical course of MTC in MEN 2B in Japanese is not so aggressive when compared with about a 50% 10-year survival reported for Caucasians. Genetic analysis of 4 MTC and 1 pheochromocytoma from 4 patients with MEN 2B revealed no common changes in regard to loss of heterozygosity on 21 chromosomes or point mutations of the ras, Gs alpha, or p53 genes. (Keyword) Adolescent / Adrenal Gland Neoplasms / Adult / Asian Continental Ancestry Group / Carcinoma, Medullary / Cerebral Hemorrhage / Child / Chromosome Aberrations / Chromosomes, Human, Pair 10 / European Continental Ancestry Group / Female / Genes, p53 / Genes, ras / Humans / Japan / Lip Neoplasms / Male / Multiple Endocrine Neoplasia Type 2b / Neuroma / Pheochromocytoma / Prognosis / Survival Rate / Thyroid Neoplasms (Tokushima University Institutional Repository) ● Metadata: 111689 (Link to Publication Site) ● Publication site (DOI): 10.1507/endocrj.40.649 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 7951533 ● Search Scopus @ Elsevier (PMID): 7951533 ● Search Scopus @ Elsevier (DOI): 10.1507/endocrj.40.649 (Tokushima University Institutional Repository: 111689, DOI: 10.1507/endocrj.40.649, PubMed: 7951533)
115.	Eiji Kudo, Kunio Ii, Hiroyuki Iwahana, Katsuhiko Yoshimoto, Kazuo Hizawa and Mitsuo Itakura : PCR-SSCP Screening of b-Amyloid Precursor Protein Mutations in Two Japanese Pedigrees with Familial Early Onset Alzheimer's Disease., Biomed Res, Vol.14, No.3, 223-231, 1993. (Tokushima University Institutional Repository) ● Metadata: 111720 (Tokushima University Institutional Repository: 111720)
116.	Katsuhiko Yoshimoto, Hiroyuki Iwahana, Ayumi Fukuda, Toshiaki Sano, Shiro Saito and Mitsuo Itakura : Rare Mutation of Gs Alpha Subunit Gene in Human Endocrine Tumors: Mutation Detection by Polymerase Chain Reaction-Primer-Introduced Restriction Analysis., Cancer, Vol.72, No.4, 1386-1393, 1993. (Summary) The Gs alpha (Gs alpha) gene can be activated to the putative oncogene gsp by specific point mutations at codons 201 or 227. Such mutations have been reported in growth hormone (GH)-secreting pituitary adenomas and thyroid tumors. To clarify the role of Gs alpha gene in human endocrine tumors, 197 tumors were screened for point mutations at codons 201 or 227 of the Gs alpha gene. Mutations were detected by primer-introduced restriction analysis (PIRA) of the polymerase chain reaction (PCR) product of genomic DNA. These Gs alpha mutations were present in 4 of 53 pituitary adenomas (4 of 43 GH-secreting adenomas; 1 of these 4 was a GH- and prolactin-secreting adenoma from a patient with familial multiple endocrine neoplasia Type 1), 4 of 66 thyroid tumors (4 of 30 papillary carcinomas), and 1 of 19 adrenocortical adenomas (1 of 6 aldosterone-secreting adenomas). In contrast, none of these Gs alpha mutations were detected in parathyroid tumors, endocrine pancreatic tumors, or pheochromocytomas. Gs alpha mutations at these two loci may play a role in the pathogenesis of a small population of GH-secreting pituitary adenomas, papillary thyroid carcinomas, and adrenocortical adenomas, but that they are not involved in the pathogenesis of other types of endocrine tumors. (Keyword) Acromegaly / Adrenal Gland Neoplasms / Adult / Aged / Base Sequence / Female / GTP-Binding Proteins / Growth Hormone-Releasing Hormone / Humans / Male / Middle Aged / Molecular Sequence Data / Pancreatic Neoplasms / Parathyroid Neoplasms / Pituitary Neoplasms / Point Mutation / Polymerase Chain Reaction / Restriction Mapping / Thyroid Neoplasms (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 8339229 ● Search Scopus @ Elsevier (PMID): 8339229 (PubMed: 8339229)
117.	Hiroyuki Iwahana, Takashi Yamaoka, Masakazu Mizutani, Noriko Mizusawa, Setsuko Ii, Katsuhiko Yoshimoto and Mitsuo Itakura : Molecular Cloning of Rat Amidophosphoribosyltransferase., The Journal of Biological Chemistry, Vol.268, No.10, 7225-7237, 1993.
118.	Hiroyuki Iwahana, Jun Oka, Noriko Mizusawa, Eiji Kudo, Setsuko Ii, Katsuhiko Yoshimoto, Edward W Holmes and Mitsuo Itakura : Molecular Cloning of Human Amidophosphoribosyltransferase., Biochemical and Biophysical Research Communications, Vol.190, No.1, 192-200, 1993.
119.	Katsuhiko Yoshimoto, Hiroyuki Iwahana, Ayumi Fukuda, Toshiaki Sano, Kiyonori Katsuragi, Moritoshi Kinoshita, Shiro Saito and Mitsuo Itakura : Ras Mutations in Endocrine Tumors: Mutation Detection by PCR-SSCP., Japanese Journal of Cancer Research, Vol.83, No.10, 1057-1062, 1992. (Tokushima University Institutional Repository) ● Metadata: 114361 (Tokushima University Institutional Repository: 114361)
120.	Hiroyuki Iwahana, Katsuhiko Yoshimoto, Toshio Shigekiyo, Akira Shirakami, Shiro Saito and Mitsuo Itakura : Molecular and Genetic Analysis of a Compound Heterozygote for Dysprothrombinemia of Prothrombin Tokushima and Hypoprothrombinemia., American Journal of Human Genetics, Vol.51, 1386-1395, 1992.
121.	Akira Tomonari, Hiroyuki Iwahara, Katsuhiko Yoshimoto, Toshio Shigekiyo, Shiro Saito and Mitsuo Itakura : Two New Nonsense Mutations in Type Ia Antithrombin III Deficiency at Leu 140 and Arg 197., Thromb Haemostas, Vol.68, No.4, 455-459, 1992.
122.	Hiroyuki Iwahana, Noriko Mizusawa, Katsuhiko Yoshimoto and Mitsuo Itakura : Detection of a New Polymorphism of the Human Prothrombin (F2) Gene by Combination of PASA and Mutated Primer-Mediated PCR-RFLP., Human Genetics, Vol.90, 325-326, 1992.
123.	Katsuhiko Yoshimoto, Hiroyuki Iwahana, Ayumi Fukuda, Shiro Saito and Mitsuo Itakura : Role of p53 Gene Mutations for Endocrine Tumorigenesis: Mutation Detection by Polymerase Chain Reaction-Single Strand Conformation Polymorphism., Cancer Research, Vol.52, No.18, 5061-5064, 1992.
124.	Hiroyuki Iwahana, Katsuhiko Yoshimoto and Mitsuo Itakura : Highly Polymorphic Region of the Human Prothrombin (F2) Gene., Human Genetics, Vol.89, No.1, 123-124, 1992.
125.	Hiroyuki Iwahana, Katsuhiko Yoshimoto and Mitsuo Itakura : Detection of a Single Base Substitution of the Gene for Prothrombin Tokushima: The Application of PCR-SSCP for the Genetic and Molecular Analysis of Dysprothrombinemia., International Journal of Hematology, Vol.55, No.1, 93-100, 1992. (Summary) The genetic and molecular basis of a mutant prothrombin of 'prothrombin Tokushima' was studied by polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) and PCR-restriction fragment length polymorphism (PCR-RFLP) analyses. The abnormal gene was detected by altered migration by PCR-SSCP and by the loss of an MspI site by PCR-RFLP. The gene for prothrombin Tokushima was shown to be inherited from the mother of the proband. Sequencing analysis using PCR-amplified genomic DNA clarified a substitution of thymine (T) for cytosine (C) at position 9,490, changing arginine (Arg) to tryptophan (Trp) at position 418 of the polypeptide chain. This point mutation is assumed to be the molecular basis of prothrombin Tokushima, firstly, because of the absence of distinct changes in Southern blot analysis of the proband's DNA (using a full-length human prothrombin cDNA as a probe), secondly, because it has the same molecular weight as the abnormal gene product, and, thirdly, because of the absence of other amino acid abnormalities in the proteolytic peptide-fragments. It is concluded that PCR-SSCP and PCR-RFLP were useful for detecting the abnormal gene and for directly diagnosing the carrier status of dysprothrombinemia. This is the first report of gene analysis of dysprothrombinemia. (Keyword) Amino Acid Sequence / Base Sequence / Molecular Sequence Data / Mutation / Nucleic Acid Conformation / Polymerase Chain Reaction / Polymorphism, Genetic / Polymorphism, Restriction Fragment Length / Prothrombin (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 1349838 ● Search Scopus @ Elsevier (PMID): 1349838 (PubMed: 1349838)
126.	Hiroyuki Iwahana, Katsuhiko Yoshimoto and Mitsuo Itakura : Detection of Point Mutations by SSCP of PCR-Amplified DNA after Endonuclease Digestion., BioTechniques, Vol.12, No.1, 64-66, 1992.
127.	Shigeki Yamamoto, Isao Morimoto, Takashi Fujihira, Kenichi Watanabe, Kazuya Zeki, Katsuhiko Yoshimoto, Fujio Zese and Sumiya Eto : A Kindred of Multiple Endocrine Neoplasia Type 2B., Endocrinologia Japonica, Vol.39, No.1, 25-30, 1992. (Tokushima University Institutional Repository) ● Metadata: 111687 (Tokushima University Institutional Repository: 111687)
128.	Hiroyuki Iwahana, Katsuhiko Yoshimoto and Mitsuo Itakura : NcoI RFLP in the Human Prothrombin (F2) Gene., Nucleic Acids Research, Vol.19, No.15, 4309, 1991.
129.	高田幸伸, 板東浩, Katsuhiko Yoshimoto, 山崎柳一, Toshiaki Sano and Shiro Saito : 胆嚢摘出後に高カルシウム血症性クリーゼを来たした原発性副甲状腺機能亢進症の1例, Internal Medicine, Vol.68, 183-186, 1991.
130.	長宅芳男, 橋本浩三, 平沢龍登, 槙野博史, 太田善介, 大枝忠史, 大森弘之, 小松原正吉, 村上正和, 吉野正, Katsuhiko Yoshimoto, 脇谷勇夫 and 三宅淳史 : MEN 2A (Sipple 症候群) の一例, 腫瘍と感染, Vol.4, No.2, 83-89, 1991.
131.	Katsuhiko Yoshimoto and Shiro Saito : 本邦における多発性内分泌腺腫瘍症1型の実態調査, 日本内分泌学会雑誌, Vol.67, No.7, 764-774, 1991. (Tokushima University Institutional Repository) ● Metadata: 111696 (Tokushima University Institutional Repository: 111696)
132.	Katsuyuki Kubo, Katsuhiko Yoshimoto, Yutaka Yokogoshi, Masaru Tsuyuguchi and Shiro Saito : Loss of Heterozygosity on Chromosome 1p in Thyroid Adenoma and Medullary Carcinoma, but not in Papillary Carcinoma., Japanese Journal of Cancer Research, Vol.82, 1097-1103, 1991. (Tokushima University Institutional Repository) ● Metadata: 114360 (Tokushima University Institutional Repository: 114360)
133.	Katsuhiko Yoshimoto, Hiroyuki Iwahana, Katsuyuki Kubo, Shiro Saito and Mitsuo Itakura : Allele Loss on Chromosome 11 in a Pituitary Tumor from a Patient with Multiple Endocrine Neoplasia Type I., Japanese Journal of Cancer Research, Vol.82, 886-889, 1991. (Tokushima University Institutional Repository) ● Metadata: 114359 (Tokushima University Institutional Repository: 114359)
134.	Yuka Uno, Toshio Shigekiyo, Katsuhiko Yoshimoto, Shiro Saito and Kyoji Inomoto : 先天性anti-thrombin III (ATIII) 欠乏症家系におけるATIII遺伝子のDNA解析, 日本血栓止血会誌, Vol.1, 512-519, 1990. (Tokushima University Institutional Repository) ● Metadata: 111697 (Tokushima University Institutional Repository: 111697)
135.	Yutaka Yokogoshi, Katsuhiko Yoshimoto and Shiro Saito : Loss of Heterozygosity on Chromosomes 1 and 11 in Sporadic Pheochromocytomas., Japanese Journal of Cancer Research, Vol.81, 632-638, 1990. (Tokushima University Institutional Repository) ● Metadata: 114358 (Tokushima University Institutional Repository: 114358)
136.	Katsuhiko Yoshimoto, Ryuichi Yamasaki, Hideki Sakai, Uichiro Tezuka, Masanori Takahashi, Masayoshi Iizuka, Takao Sekiya and Shiro Saito : Ectopic Production of Parathyroid Hormone by Small Cell Lung Cancer in a Patient with Hypercalcemia., The Journal of Clinical Endocrinology and Metabolism, Vol.68, No.5, 976-981, 1989.
137.	松本直也, Katsuhiko Yoshimoto, 岡川和人, 小阪昌明 and Shiro Saito : Vinca-Alcaloidsにより紅皮症を来したと思われるHodgkin病の一症例, Japanese Journal of Cancer and Chemotherapy, Vol.16, No.6, 2297-2300, 1989. (Tokushima University Institutional Repository) ● Metadata: 111704 (Tokushima University Institutional Repository: 111704)
138.	Katsuhiko Yoshimoto, Masayoshi Iizuka, Hiroyuki Iwahana, Ryuichi Yamasaki, Haruhiko Saito, Shiro Saito and Takao Sekiya : Loss of the Same Allele of HRAS1 and D11S151 in Two Independent Pancreatic Cancers from a Patient with Multiple Endocrine Neoplasia Type 1., Cancer Research, Vol.49, 2716-2721, 1989.
139.	Katsuhiko Yoshimoto, Hiroyuki Iwahara, Yutaka Yokogoshi, Shiro Saito, Masahiro Shiraishi, Takao Sekiya, Michael M Gottesman and Ira Pasitan : A polymorphic HindIII site within the human multidrug resistance gene 1 (MDR1)., Nucleic Acids Research, Vol.16, No.24, 11850, 1988.
140.	Ryuichi Yamasaki, Haruhiko Saito, Toshiaki Sano, Kazuto Kameyama, Katsuhiko Yoshimoto, Eiji Hosoi, Mitsuhiro Matsumura, Kunihiko Harada and Shiro Saito : Ectopic Growth Hormone-Releasing Hormone (GHRH) Syndrome in a Case with Multiple Endocrine Neoplasia Type 1., Endocrinologia Japonica, Vol.35, No.1, 97-109, 1988. (Tokushima University Institutional Repository) ● Metadata: 111685 (Tokushima University Institutional Repository: 111685)
141.	Katsuhiko Yoshimoto, Masahiko Shiraishi, Setsuo Hirohashi, Shojiro Morinaga, Yukio Shimosato, Takashi Sugimura and Takao Sekiya : Rearrangement of the c-myc Gene in Two Giant Cell Carcinoma of the Lung., Japanese Journal of Cancer Research, Vol.77, 731-735, 1986. (Tokushima University Institutional Repository) ● Metadata: 114357 (Tokushima University Institutional Repository: 114357)
142.	Katsuhiko Yoshimoto, Setsuo Hirohashi and Takao Sekiya : Increased Expression of the c-myc Gene without Gene Amplification in Human Lung Cancer and Colon Cancer Cell Lines., Japanese Journal of Cancer Research, Vol.77, 540-545, 1986. (Tokushima University Institutional Repository) ● Metadata: 114355 (Tokushima University Institutional Repository: 114355)
143.	Toshikazu Nakamura, Katsuhiko Yoshimoto, Yasuo Nakayama, Yumiko Tomita and Akira Ichihara : Reciprocal Modulation of Growth and Differentiated Functions of Mature Rat Hepatocytes in Primary Culture by Cell-Cell Contact and Cell Membranes., Proceedings of the National Academy of Sciences of the United States of America, Vol.80, No.23, 7229-7233, 1983.
144.	Katsuhiko Yoshimoto, Toshikazu Nakamura and Akira Ichihara : Reciprocal Effects of Epidermal Growth Factor on Key Lipogenic Enzymes in Primary Cultures of Adult Rat Hepatocytes., --- Induction of Glucose-6-Phosphate Dehydrogenase and Suppression of Malic Enzyme and Lipogenesis. ---, The Journal of Biological Chemistry, Vol.258, No.20, 12355-12360, 1983.
145.	Katsuhiko Yoshimoto, Toshikazu Nakamura, Shingo Niimi and Akira Ichihara : Hormonal Regulation of Translatable mRNA of Glucose-6-Phosphate Dehydrogenase in Primary Cultures of Adult Rat Hepatocytes., Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression, Vol.741, No.1, 143-149, 1983. (Summary) The quantity of translatable mRNA of glucose-6-phosphate dehydrogenase (D-glucose-6-phosphate: NADP+ 1-oxidoreductase, EC 1.1.1.49) in primary cultures of adult rat hepatocytes subjected to different hormonal conditions was determined with a reticulocyte-lysate, cell-free system. The level of glucose-6-phosphate dehydrogenase mRNA was about 5-fold higher in the presence of insulin than in its absence. This increase of glucose-6-phosphate dehydrogenase mRNA reached a maximum 12 h after the addition of insulin. The maximum level of induction of glucose-6-phosphate dehydrogenase mRNA required 10(-8) M insulin. Glucagon and triiodothyronine had no effect on the glucose-6-phosphate dehydrogenase mRNA level. The increase of glucose-6-phosphate dehydrogenase activity correlated with the increase in level of mRNA of this enzyme. This suggests that the changes in glucose-6-phosphate dehydrogenase activity in response to the above hormonal changes are primarily due to changes in the amount of mRNA coding for this enzyme. (Keyword) Animals / Cell-Free System / Cells, Cultured / Glucagon / Glucosephosphate Dehydrogenase / Insulin / Kinetics / Liver / Protein Biosynthesis / RNA, Messenger / Rabbits / Rats / Reticulocytes (Link to Publication Site) ● Publication site (DOI): 10.1016/0167-4781(83)90021-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 6351922 ● Search Scopus @ Elsevier (PMID): 6351922 ● Search Scopus @ Elsevier (DOI): 10.1016/0167-4781(83)90021-0 (DOI: 10.1016/0167-4781(83)90021-0, PubMed: 6351922)
146.	Toshikazu Nakamura, Katsuhiko Yoshimoto, Kazushi Aoyama and Akira Ichihara : Hormonal Regulations of Glucose-6-Phosphate Dehydrogenase and Lipogenesis in Primary Cultures of Rat Hepatocytes., The Journal of Biochemistry, Vol.91, 681-693, 1982. (Tokushima University Institutional Repository) ● Metadata: 111698 (Tokushima University Institutional Repository: 111698)

Review, Commentary:

1.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa and Shinji Ono : Carney complex (CNC), 臨床画像, Vol.31, No.10, 31-32, 2015. (Tokushima University Institutional Repository) ● Metadata: 111702 (Tokushima University Institutional Repository: 111702)
2.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa and 小野信二 : Hyperparathyroidism-Jaw Tumor Syndrome, Shikoku Dental Research, Vol.27, No.1, 35-39, Jun. 2014. (Tokushima University Institutional Repository) ● Metadata: 109852 (Tokushima University Institutional Repository: 109852)
3.	Katsuhiko Yoshimoto, Noriko Mizusawa, Takeo Iwata and Shinji Ono : Familial hyperparathyroidism, Endocrinology, Diabetology & Metabolism, Vol.37, No.4, 380-386, Oct. 2013. (Keyword) familial isolated hyperparathyroidism / familial hypocalciuric hypercalcemia / hyperparathyroidism-jaw tumor syndrome / CDC73 / parafibromin (Tokushima University Institutional Repository) ● Metadata: 111716 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050302172853579264 (Tokushima University Institutional Repository: 111716, CiNii: 1050302172853579264)
4.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa and Shinji Ono : The AIP gene and pituitary tumors, ホルモンと臨床, Vol.60, No.8, 627-632, Aug. 2012. (Tokushima University Institutional Repository) ● Metadata: 114320 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050020697876034688 (Tokushima University Institutional Repository: 114320, CiNii: 1050020697876034688)
5.	藤本寛太, 浜本芳之, 松岡敦子, 森可南子, 龍岡久登, 河崎祐貴子, 本庶祥子, Shozo Yamada, Takeo Iwata, Katsuhiko Yoshimoto and 越山裕行 : 家族性先端巨大症2家系におけるAIP遺伝子の検討, Folia endocrinologica Japonica, Vol.88, No.Suppl. June, 11-14, Jun. 2012. (Tokushima University Institutional Repository) ● Metadata: 111700 (Tokushima University Institutional Repository: 111700)
6.	Noriko Mizusawa, Takeo Iwata and Katsuhiko Yoshimoto : 【遺伝性内分泌腫瘍の基礎と臨床遺伝カウンセリングに必要な知識】家族性副甲状腺機能亢進症の基礎と臨床, ホルモンと臨床, Vol.57, No.3, 255-261, Mar. 2009. (Keyword) 顎腫瘍(病理学) カルシウム代謝障害(診断,遺伝学) 甲状腺機能亢進症(実験的) *上皮小体機能亢進症(診断,遺伝学) 上皮小体腫瘍(病理学) 免疫組織化学ノックアウトマウス遺伝学的検査腫瘍抑制蛋白質低カルシウム尿性高カルシウム血症-家族性(診断,遺伝学) HRPT2 Protein ヒトマウス動物特集 (Tokushima University Institutional Repository) ● Metadata: 114318 (Tokushima University Institutional Repository: 114318)
7.	Katsuhiko Yoshimoto and Shozo Yamada : Clinical and molecular genetics of familiar acromegaly, ホルモンと臨床, Vol.57, No.3, 263-268, Mar. 2009. (Keyword) シグナルトランスダクション血統下垂体腫瘍(診断,遺伝学) 腺腫(診断,遺伝学) 変異遺伝学的検査 *下垂体腺腫-成長ホルモン産生(診断,遺伝学) Carney症候群(診断,遺伝学) ヒト特集 (Tokushima University Institutional Repository) ● Metadata: 114319 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050302172852747136 (Tokushima University Institutional Repository: 114319, CiNii: 1050302172852747136)
8.	Katsuhiko Yoshimoto, Takeo Iwata and Noriko Mizusawa : アディポサイトカインと生活習慣病, Shikoku Dental Research, Vol.20, No.2, 261-263, 2008. (Tokushima University Institutional Repository) ● Metadata: 109771 (Tokushima University Institutional Repository: 109771)
9.	HM Golam, Takeo Iwata, Noriko Mizusawa, Zhi-Rong Qian, Shozo Yamada, Toshiaki Sano and Katsuhiko Yoshimoto : Role of cyclin-dependent kinase inhibitors in pituitary tumorigenesis: an update, Shikoku Acta Medica, Vol.64, 225-231, 2008. (Tokushima University Institutional Repository) ● Metadata: 110181 (Tokushima University Institutional Repository: 110181)
10.	Takeo Iwata, Noriko Mizusawa, Golam Md Hossain and Katsuhiko Yoshimoto : 癌抑制因子パラフィブロミンはSV40 large T抗原存在下では細胞増殖促進に働く, ホルモンと臨床増刊号, Vol.56, 147-155, 2008. (Tokushima University Institutional Repository) ● Metadata: 114317 (Tokushima University Institutional Repository: 114317)
11.	Katsuhiko Yoshimoto : メタボリックシンドロームって何?, DENTAL DIAMOND, Vol.32, No.138, 76-79, Jan. 2007.
12.	水越常徳, 佐藤裕信, 高橋裕樹, 今井浩三, 鈴木やすよ, 内野眞也, 首藤茂, 野口志郎 and Katsuhiko Yoshimoto : HRPT2遺伝子変異を認めた家族性孤発性副甲状腺機能亢進症(FIHP)の一例, 日本内分泌学会雑誌, Vol.82, 42-45, 2006. (Tokushima University Institutional Repository) ● Metadata: 111701 (Tokushima University Institutional Repository: 111701)
13.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa, 長尾大輔, Md.Golam Hossain, 露口勝, Toshiaki Sano and 内野眞也 : 家族性副甲状腺機能亢進症2家系におけるHRPT2遺伝子変異の解析,, ホルモンと臨床, Vol.54, 138-142, 2006. (Tokushima University Institutional Repository) ● Metadata: 114316 (Tokushima University Institutional Repository: 114316)
14.	泉山肇, 土肥賢, 山本満千, 松下美加, 名和田久礼, 今井泰平, 山崎弘幸, Katsuhiko Yoshimoto and 平田結喜緒 : 心房粘液腫による脳塞栓を発症したCarney's complex(CNC)の一例, ACTH RELATED PEPTIDES, Vol.13, 253-260, Feb. 2003.
15.	Katsuhiko Yoshimoto : 内分泌腫瘍における腫瘍発生機序とホルモン分泌の調節異常, Shikoku Dental Research, Vol.15, No.2, 221-226, Feb. 2003.
16.	Katsuhiko Yoshimoto : Multiple endocrine neoplasia, MEN, 日本内科学会雑誌, Vol.91, No.4, 119-123, Apr. 2002.
17.	Katsuhiko Yoshimoto : 副甲状腺ホルモン産生腫瘍, 内分泌·糖尿病科, Vol.14, No.2, 125-131, Feb. 2002. (Tokushima University Institutional Repository) ● Metadata: 111715 (Tokushima University Institutional Repository: 111715)
18.	Mitsuo Itakura, 山岡孝, 森谷眞紀, 片島るみ, Eiji Kudo, 日野聡史, 岩花弘之 and Katsuhiko Yoshimoto : 痛風·核酸に関わる代謝調節の解析分子生物学から個体レベルの解析に向けて遺伝子改変動物とゲノム多型解析, Gout and Nucleic Acid Metabolism, Vol.26, No.2, 151-153, 2002.
19.	Katsuhiko Yoshimoto : 家族性下垂体腫瘍の基礎と臨床, Folia endocrinologica Japonica, Vol.77, No.Supplement-1, 13-16, Jan. 2001. (Tokushima University Institutional Repository) ● Metadata: 111699 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050302172853588608 (Tokushima University Institutional Repository: 111699, CiNii: 1050302172853588608)
20.	Katsuhiko Yoshimoto : Multiple Endocrine Neoplasia Type 1: From Bedside to Benchside., The Journal of Medical Investigation : JMI, Vol.47, No.3-4, 108-117, Aug. 2000. (Summary) Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder characterized by the combined occurrence of parathyroid, pancreatic endocrine, and anterior pituitary tumors. MEN1 has two characteristics; a hormone excess and a sometimes lethal outcome due to malignant tumors. The recent identification of the MEN1 gene has opened the door to a much deeper understanding of this syndrome. Germline MEN1 mutations have been identified in most MEN1 families. They were not found, however, in families with familial pituitary tumors. Thus, studies with the MEN1 gene helped to establish that mutation of some other gene(s) is likely causative of the MEN1 phenocopy. These recent advances provide for the identification of mutant MEN1 gene carriers who are at a high risk of developing MEN1. The protein encoded by the MEN1 gene has been shown to function in the regulation of JunD-activated transcription but much still remains to be elucidated. (Keyword) Genes, Tumor Suppressor / Humans / Multiple Endocrine Neoplasia Type 1 / Mutation / Neoplasm Proteins / Pancreatic Neoplasms / Parathyroid Neoplasms / Pituitary Neoplasms / Proto-Oncogene Proteins (Tokushima University Institutional Repository) ● Metadata: 26954 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11019489 ● Search Scopus @ Elsevier (PMID): 11019489 (Tokushima University Institutional Repository: 26954, PubMed: 11019489)
21.	Toshiaki Sano and Katsuhiko Yoshimoto : 症例解説「多発性内分泌腫瘍症1型 multiple endocrine neoplasia 1 (MEN1)」, 病理と臨床, Vol.18, No.1, 56-57, Jan. 2000.
22.	Katsuhiko Yoshimoto : 多発性内分泌腫瘍症1型および2A型, 日本内科学会雑誌, Vol.88, No.7, 42-47, Jan. 1999.
23.	Katsuhiko Yoshimoto : トランスジェニックマウスを用いた副甲状腺腫瘍化機構の解析, BIOClinica, Vol.14, No.9, 81-84, Jan. 1999.
24.	Katsuhiko Yoshimoto : 先端巨大症, Molecular Medicine, Vol.35, 417-418, Jan. 1998.
25.	Katsuhiko Yoshimoto : MENの遺伝子変異と疫学, Journal of Medical Technology, Vol.42, No.7, 751-757, Jan. 1998.
26.	Andrew Arnold and Katsuhiko Yoshimoto : Gene Defects and Clinical Disorders of the Parathyroids, --- Primary Hyperparathyroidism ---, Curr Opin Endocrinol Diabetes, Vol.4, No.6, 417-426, Jun. 1997.
27.	青木晃, 萱嶋信介, 永瀬晃正, 大島智, 伊東貞三, 安田浩子, 鈴木節, 松熊晋, 桑原紀之, 塚田俊彦, 山口建, Katsuhiko Yoshimoto and Shiro Saito : 躁鬱病として治療中に発見されたMEN 1型の1症例, ホルモンと臨床, Vol.45, 242-246, Jan. 1997. (Tokushima University Institutional Repository) ● Metadata: 114484 (Tokushima University Institutional Repository: 114484)
28.	Katsuhiko Yoshimoto : 膵内分泌腫瘍の遺伝子異常, 臨床消化器内科, Vol.12, No.9, 1277-1283, Jan. 1997. (Tokushima University Institutional Repository) ● Metadata: 111722 (Tokushima University Institutional Repository: 111722)
29.	Katsuhiko Yoshimoto : 多発性内分泌腫瘍症, 病理と臨床, Vol.15, 134, Jan. 1997.
30.	山田正三, Katsuhiko Yoshimoto, Toshiaki Sano, 高田浩次, Mitsuo Itakura, 臼井雅昭 and 寺本明 : 家族性下垂体腺腫を呈した1家族の遺伝子解析, ホルモンと臨床, Vol.45, 30-33, Jan. 1997. (Tokushima University Institutional Repository) ● Metadata: 114451 (Tokushima University Institutional Repository: 114451)
31.	Katsuhiko Yoshimoto, Chisato Kosugi, 木村建彦, 岩花弘之, 山田正三, Toshiaki Sano, Shiro Saito and Mitsuo Itakura : 下垂体腺腫におけるヘテロ接合性消失およびp16遺伝子変異の解析, ホルモンと臨床, Vol.45, 26-29, Jan. 1997. (Tokushima University Institutional Repository) ● Metadata: 114315 (Tokushima University Institutional Repository: 114315)
32.	Katsuhiko Yoshimoto, Chisato Kosugi, 木村建彦, 岩花弘之, 山田正三, Toshiaki Sano and Mitsuo Itakura : 孤発性下垂体腺腫におけるマイクロサテライト解析による第11染色体のヘテロ接合性消失の検出, ホルモンと臨床, Vol.44, 73-75, Jan. 1996. (Tokushima University Institutional Repository) ● Metadata: 114314 (Tokushima University Institutional Repository: 114314)
33.	Katsuhiko Yoshimoto and Shiro Saito : 多発性内分泌腫瘍症, Internal Medicine, Vol.77, No.6, 1505, Jan. 1996.
34.	Shiro Saito, 宮恵子, 土橋孝之, 板東浩, 新谷保実, Toshiaki Sano, Katsuhiko Yoshimoto, 岩花弘之 and Takashi Yamaoka : 臨床医学の展望「内分泌学」, Japan Medical Journal, No.3748, 19-34, Jan. 1996.
35.	Katsuhiko Yoshimoto : 多発性内分泌腫瘍症, 病理と臨床, Vol.14, 43-47, Jan. 1996.
36.	Katsuhiko Yoshimoto and Shiro Saito : ホルモン合成異常症-ペプチドホルモン, ホルモンと臨床, Vol.44, No.1, 3-7, Jan. 1996. (Tokushima University Institutional Repository) ● Metadata: 114313 (Tokushima University Institutional Repository: 114313)
37.	Katsuhiko Yoshimoto and Shiro Saito : 家族性下垂体腫瘍, Nihon Rinsho. Japanese Journal of Clinical Medicine, Vol.53, No.11, 71-76, Jan. 1995. (Tokushima University Institutional Repository) ● Metadata: 111531 (Tokushima University Institutional Repository: 111531)
38.	Katsuhiko Yoshimoto : 褐色細胞腫, medicina, Vol.32, No.12, 423-424, Jan. 1995.
39.	猿井宏, 奥村昇司, 嘉村正徳, 宅野洋, 石塚達夫, 安田圭吾, 鷹尾博司, 梅本敬夫, 深田代造, 下川邦泰 and Katsuhiko Yoshimoto : 嚢胞性グルカゴノーマを発症した多発性内分泌腫瘍症I型の1例, ホルモンと臨床, Vol.43, 183-188, Jan. 1995. (Tokushima University Institutional Repository) ● Metadata: 114449 (Tokushima University Institutional Repository: 114449)
40.	Chisato Kosugi, Katsuhiko Yoshimoto, 木村建彦, 岩花弘之, 宮内昭 and Mitsuo Itakura : 孤発性褐色細胞腫におけるRET遺伝子チロシンキナーゼ部位の変異, ホルモンと臨床, Vol.43, 164-168, Jan. 1995. (Tokushima University Institutional Repository) ● Metadata: 114448 (Tokushima University Institutional Repository: 114448)
41.	Katsuhiko Yoshimoto : G蛋白異常による内分泌疾患, 内分泌·糖尿病科, Vol.1, No.1, 57-63, Jan. 1995. (Tokushima University Institutional Repository) ● Metadata: 111714 (Tokushima University Institutional Repository: 111714)
42.	Katsuhiko Yoshimoto : 多発性内分泌腫瘍症の遺伝子診断, Journal of Clinical and Experimental Medicine, Vol.174, No.5, 494-498, Jan. 1995.
43.	Shiro Saito, 宮恵子, 土橋孝之, 板東浩, 新谷保実, Toshiaki Sano, Katsuhiko Yoshimoto, 岩花弘之 and Takashi Yamaoka : 臨床医学の展望「内分泌学」, Japan Medical Journal, No.3698, 3-13, Jan. 1995.
44.	Katsuhiko Yoshimoto and Shiro Saito : 副甲状腺細胞, Nihon Rinsho. Japanese Journal of Clinical Medicine, Vol.53, No.4, 7-12, Jan. 1995. (Tokushima University Institutional Repository) ● Metadata: 111530 (Tokushima University Institutional Repository: 111530)
45.	Katsuhiko Yoshimoto and Shiro Saito : 多発性内分泌腫瘍症の診断基準·病型分類, Internal Medicine, Vol.75, No.6, 1625-1628, Jan. 1995.
46.	Katsuhiko Yoshimoto : PCR-SSCP法, Nihon Rinsho. Japanese Journal of Clinical Medicine, 463-466, Jan. 1994. (Tokushima University Institutional Repository) ● Metadata: 111529 (Tokushima University Institutional Repository: 111529)
47.	Katsuhiko Yoshimoto : 内分泌腺腫瘍の遺伝子異常, Journal of Medical Technology, Vol.38, No.11, 221, Jan. 1994.
48.	Katsuhiko Yoshimoto : 多内分泌腫瘍MEN2A型，MEN2B型の分子遺伝学研究の動向, Nihon Rinsho. Japanese Journal of Clinical Medicine, Vol.52, No.4, 237-242, Jan. 1994. (Tokushima University Institutional Repository) ● Metadata: 111528 (Tokushima University Institutional Repository: 111528)
49.	Katsuhiko Yoshimoto : パラクライン作用を解析するためのトランスジェニックマウス, BIO Clinica, Vol.9, No.8, 58-61, Jan. 1994.
50.	Katsuhiko Yoshimoto and Shiro Saito : 多発性内分泌腫瘍症における遺伝子異常, medicina, Vol.31, No.2, 416-419, Jan. 1994.
51.	Katsuhiko Yoshimoto, 岩花弘之, Toshiaki Sano and Mitsuo Itakura : マイクロサテライト解析による多発性内分泌腫瘍症1型(MEN 1)腫瘍における第11染色体の欠失の検出, ホルモンと臨床, Vol.24, 262-265, Jan. 1994. (Tokushima University Institutional Repository) ● Metadata: 114312 (Tokushima University Institutional Repository: 114312)
52.	Katsuhiko Yoshimoto and Mitsuo Itakura : 糖尿病の遺伝子治療, 治療の最前線, Vol.1, No.3, 116-120, Jan. 1994.
53.	Katsuhiko Yoshimoto and Mitsuo Itakura : 遺伝子治療への展望, nanoGIGA, Vol.19, No.4, 114-119, Jan. 1994. (Tokushima University Institutional Repository) ● Metadata: 111723 (Tokushima University Institutional Repository: 111723)
54.	Katsuhiko Yoshimoto : 内分泌腺の腫瘍化に関する遺伝子異常の解析, BIOmedica, Vol.8, No.11, 45-49, Jan. 1993.
55.	Katsuhiko Yoshimoto : PCR-SSCPを用いた遺伝子解析, 治療学, Vol.27, No.2, 85-88, Jan. 1993. (Tokushima University Institutional Repository) ● Metadata: 111718 (Tokushima University Institutional Repository: 111718)
56.	Shiro Saito and Katsuhiko Yoshimoto : 異所性PTH産生腫瘍, CLINICAL CALCIUM, Vol.2, No.5, 74-78, Jan. 1992.
57.	Katsuhiko Yoshimoto : 膵内分泌腫瘍の遺伝子異常, 胆と膵, Vol.13, No.3, 247-251, Jan. 1992. (Tokushima University Institutional Repository) ● Metadata: 111717 (Tokushima University Institutional Repository: 111717)
58.	横井健治, Katsuhiko Yoshimoto, 鈴木まどか, 板東浩, 張辰宇, 山崎柳一 and Shiro Saito : 家族性多発性内分泌腺症1型の1家系2症例, ホルモンと臨床, Vol.40, 180-183, Jan. 1992. (Tokushima University Institutional Repository) ● Metadata: 114447 (Tokushima University Institutional Repository: 114447)
59.	坂本幸裕, Katsuhiko Yoshimoto, 横井健治, Toshiaki Sano and Shiro Saito : 酢酸オクトレオチドによりカルシトニン分泌が抑制された内分泌腺腫瘍症(MEN)2B型の1例, ホルモンと臨床, Vol.40, 180-183, Jan. 1992. (Tokushima University Institutional Repository) ● Metadata: 114310 (Tokushima University Institutional Repository: 114310)
60.	Katsuhiko Yoshimoto : Single strand conformation polymorphism, Metabolism and Disease, Vol.28, No.9, 53-61, Jan. 1991. (Tokushima University Institutional Repository) ● Metadata: 111710 (Tokushima University Institutional Repository: 111710)
61.	Katsuhiko Yoshimoto : 膵内分泌腫瘍の遺伝子異常, Metabolism and Disease, Vol.28, No.7, 23-30, Jan. 1991. (Tokushima University Institutional Repository) ● Metadata: 111709 (Tokushima University Institutional Repository: 111709)
62.	Katsuhiko Yoshimoto, 山崎柳一, 横越浩, 坂井秀樹, 手束卯一郎, 高橋正倫 and Shiro Saito : 異所性PTH産生により高Ca血症を来した肺癌の一例, ホルモンと臨床, Vol.38, 303-306, Jan. 1990. (Tokushima University Institutional Repository) ● Metadata: 114309 (Tokushima University Institutional Repository: 114309)
63.	板東浩, 堀江秀茂, 友成章, 新谷保実, Katsuhiko Yoshimoto, 山崎柳一 and Shiro Saito : 放射線療法と化学療法の視床下部下垂体に及ぼす影響を検討した鞍上部胚芽腫の1例, ホルモンと臨床, Vol.37, 73-77, Jan. 1989. (Tokushima University Institutional Repository) ● Metadata: 114308 (Tokushima University Institutional Repository: 114308)
64.	山崎柳一, 宮崎修一, 木村成明, Takao Mitsui, 三橋信次, Katsuhiko Yoshimoto, 齋藤晴比古, Toshiaki Sano and Shiro Saito : GHRH産生膵腫瘍により先端巨大症を惹起したと思われるMEN 1型の症例, ホルモンと臨床, Vol.37, 6-11, Jan. 1989. (Tokushima University Institutional Repository) ● Metadata: 114414 (Tokushima University Institutional Repository: 114414)
65.	齋藤晴比古, Toshiaki Sano, 山崎柳一, Eiji Hosoi, Katsuhiko Yoshimoto, 宮崎修一, 岩花弘之 and 三橋信次 : SomatostatinおよびGHRH産生腫瘍, 第6回下垂体腫瘍Workshop講演集, 111-117, May 1988.
66.	Shiro Saito, Katsuhiko Yoshimoto and 齋藤晴比古 : 腫瘍における異所性ホルモン産生と遺伝子発現, Japanese Journal of Cancer and Chemotherapy, Vol.12, 1-12, Jan. 1985. (Tokushima University Institutional Repository) ● Metadata: 111703 (Tokushima University Institutional Repository: 111703)
67.	Katsuhiko Yoshimoto and 中村敏一 : 肝細胞におけるリポタンパク合成のホルモン及び細胞内脂質による調節, The Medical Frontline, Vol.37, 833-838, Jan. 1982. (Tokushima University Institutional Repository) ● Metadata: 111721 (Tokushima University Institutional Repository: 111721)

Proceeding of International Conference:

1.	Yuki Iwawaki, Noriko Mizusawa, Yoritoki Tomotake, Tetsuo Ichikawa and Katsuhiko Yoshimoto : Mechanical stress - responsive microRNA, The 3rd ASEAN plus and TOKUSHIMA Joint International Conference, Makassar, Indonesia, Dec. 2014.
2.	Katsuhiko Yoshimoto : Mechanisms of tumorigenesis in GH adenomas, 2nd Pituitary Expert Meeting in Asia (PEMA) Seoul, Aug. 2013.
3.	Noriko Mizusawa, Takeo Iwata and Katsuhiko Yoshimoto : Profile of microRNA inhuman saliva, Asean Plus Tokushima Joint International Conference, Dec. 2012.
4.	T Fukui, N Fukuhara, H Nishioka, N Kobayashi, N Inoshita, N Yoshida, H Suzuki, A Takeshita, Y Takeuchi, Shozo Yamada, Takeo Iwata and Katsuhiko Yoshimoto : Clinical and histological characteristics of giant GH producing pituitary adenomas, The Joint 15th International Congress of Endocrinology and the 14th European Congress of Endocrinology- ICE/ECE2012, May 2012.
5.	Shima Nazatul Wan, Noriko Mizusawa, Takeo Iwata and Katsuhiko Yoshimoto : Analysis of microRNA in saliva and submandibular gland cell lines., International Joint Symposium: The University of Tokushima, Universitas Gadjah Mada, Niigata University, Denpasar, Bali, Dec. 2010.
6.	Kyoko Ishimoto, Takeo Iwata, Katsuhiko Yoshimoto and Eiji Tanaka : Functional analysis of a novel adipokine, D-dopachrome tautomerase, in preadipocytes., International Joint Symposium: The University of Tokushima, Universitas Gadjah Mada, Niigata University, Denpasar, Bali, Dec. 2010.
7.	Katsuhiko Yoshimoto, Md. Golam Hossain, Takeo Iwata, Noriko Mizusawa, Shima Wan Nazatul Schadan, Toru Okutsu, Kyoko Ishimoto, Zhi-Rong Qian, Toshiaki Sano and Shozo Yamada : Down-regulated expression of p18INK4C in pituitary adenomas., 14th International Congress of Endocrinology, Kyoto, Mar. 2010.
8.	Zhi-Rong Qian, Toshihito Tanahashi, Katsuhiko Yoshimoto, Shozo Yamada, Sakurako Katsuura, Wang EL, Kazuhito Rokutan and Toshiaki Sano : MicroRNA Expression Abnormalities in Pituitary Adenomas Are Associated with Distinctive Pathologic Features and May Contribute to Tumorigenesis., 99th Annual Meeting of United States and Canadian Academy of Pathology, Washington, D.C., Mar. 2010.
9.	Zhi-Rong Qian, Wang EL, Katsuhiko Yoshimoto, Shozo Yamada and Toshiaki Sano : Characterization of estrogen receptor beta 1 in human pituitary adenomas, 99th Annual Meeting of United States and Canadian Academy of Pathology, Washington, D.C., Mar. 2010.
10.	Takeo Iwata, Masamichi Kuwajima, Akiko Sukeno, Naozumi Ishimaru, Yoshio Hayashi, M Wabitsch, Noriko Mizusawa, Mitsuo Itakura and Katsuhiko Yoshimoto : YKL-40 secreted from macrophages infiltrating into adipose tissue inhibits degradation of type I collagen., International symposium on diabetes, Tokyo, Mar. 2009.
11.	Shima Nazatul Wan, Noriko Mizusawa, Takeo Iwata and Katsuhiko Yoshimoto : Effect of Liver X Receptor (LXR) Agonist on GLP-1 Expression., The International Symposium on Oral Sciences to Improve The Quality of Life, Tokushima, Sep. 2008.
12.	Golam Md. Hossain, Takeo Iwata, Noriko Mizusawa and Katsuhiko Yoshimoto : Compressive force-induced inhibition of adipocyte differentiation is mediated through down-regulatioin of PPAR2., The International Symposium on Oral Sciences to Improve The Quality of Life, Tokushima, Sep. 2008.
13.	Golam Md. Hossain, Takeo Iwata, Noriko Mizusawa, Shozo Yamada, Zhi-Rong Qian, Toshiaki Sano and Katsuhiko Yoshimoto : Mutational analysis and gene expression profile of CDKN2C/p18INK4C in pituitary adenomas., TThe 2nd International Symposium on "The Future Direction of Oral Sciences in the 21st Century"-Oral Sciences for Our Healthy Life-, Tokushima, Dec. 2007.
14.	Golam Md. Hossain, Takeo Iwata, Shozo Yamada, Noriko Mizusawa, Toshiaki Sano and Katsuhiko Yoshimoto : Mutation analysis of AIP in isolated familial somatotropinomas and sporadic growth hormone-secreting adenomas., The 1st International Symposium and Workshop The Future Direction of Oral Sciences in the 21st Century, Awaji, Mar. 2007.
15.	Daisuke Nagao, Katsuhiko Yoshimoto and Tetsuo Ichikawa : Compressing force induces Hsp25 in a mouse osteoblast-like cell line., IADR General Session & Exhibition, Brisbane, Jun. 2006.
16.	Daisuke Nagao, Katsuhiko Yoshimoto, Yoritoki Tomotake, Megumi Watanabe, Y Yoshijima and Tetsuo Ichikawa : Gene expression in a mouse osteoblast like cell line in response to compressing force., 11th International College of Prosthodontists, Crete, Greece, May 2005.
17.	Zhi-Rong Qian, Toshiaki Sano, Katsuhiko Yoshimoto, Asa L. Sylvia, Mitsuyoshi Hirokawa and Hisanori Uehara : DNA methyltransferase 1 (DNMT1) protein overexpression correlates with tumor invasion and DNA hypermethylation of multiple tumor suppressor genes in human pituitary adenomas., 96th Annual Meeting of American Association of Cancer Research, Anaheim, Apr. 2005.
18.	Shinya Uchino, Hiroyuki Yamashita, Shiro Noguchi, Tsunenori Mizukoshi and Katsuhiko Yoshimoto : Germline mutation of the HRPT2 gene in Japanese FIHP families, MEN2004, Bethesda, Jun. 2004.
19.	Yamasaki Hiroyuki, Noriko Mizusawa, Shinji Nagahiro, Shozo Yamada, Toshiaki Sano, Mitsuo Itakura and Katsuhiko Yoshimoto : GH-secreting pituitary adenomas infrequently contain inactivating mutations of PRKAR1A and LOH of 2p16 and 17q23-24., 85th annual meeting of the endocrine society, Philadelphia, Jun. 2003.
20.	Toshiaki Sano, Xu Bing, Katsuhiko Yoshimoto, Yamasaki Hiroyuki, Mitsuyoshi Hirokawa and Shozo Yamada : Down-regulation of E-cadherin and Catenins in Human Pituitary Growth Hormone Cell Adenomas with Prominent Fibrous Bodies., 8th International Pituitary Pathology Meeting, Delphi and Athens, Oct. 2001.
21.	Toshinori Sakai, Shinsuke Katoh, Koichi Sairyo, Chisato Tanaka, Rumi Katashima, Katsuhiko Yoshimoto and Mitsuo Itakura : An SNP in the 3region of the Collagen11 Alpha 2 Gene is Associated with Susceptibility to OPLL., 47th Annual Meeting of Orthopaedic Research Society, San Francisco, Feb. 2001.
22.	T. Abe, Katsuhiko Yoshimoto, M. Taniyama, K. Hanakawa, H. Izumiyama, Mitsuo Itakura and K. Matsumoto : A Germline Mutation of the Multiple Endocrine Neoplasia Type 1 (MEN1) Gene in Japanese Prolactinoma Variant of MEN1., Annual Meeting of the American Association of Neurological Surgeons, San Francisco, Apr. 2000.
23.	Y. Hosokawa, Katsuhiko Yoshimoto, R. Bronson, T. Wang, E.V. Schmidt and A. Arnold : Mouse Model for Primary Hyperparathyroidism: Parathyroid-targeted Overexpression of Cyclin D1/PRAD1 Oncogene., 2nd Cold Spring Harbor Meeting on Cancer Genetics & Tumor Suppressor Genes, Cold Spring Harbor, New York, Aug. 1998.
24.	Y. Hosokawa, Katsuhiko Yoshimoto, R. Bronson, T. Wang, E.V. Schmidt and A. Arnold : Chronic Hyperparathyroidism in Transgenic Mice with Parathyroid Targeted Overexpression of CyclinD1/PRAD1., The 19th Annual Meeting of American Society for Bone and Mineral Research, Cincinnati, Sep. 1997.
25.	Y. Imanishi, H. Tahara, I.B. Salusky, W.G. Goodman, R.D. Gaz, M.L. Brandi, E. Sarfati, T.B. Drueke, A.P. Smith, Katsuhiko Yoshimoto and A. Arnold : Distinct Molecular Pathogenesis in Different Categories of Benign Hyperparathyroidism., The 19th Annual Meeting of American Society for Bone and Mineral Research, Cincinnati, Sep. 1997.
26.	Mitsuo Itakura, Maki Moritani, Setsuko Ii, Takashi Yamaoka, Hiroyuki Iwahana and Katsuhiko Yoshimoto : Approaches to Develop Gene Therapy for Diabetes., The 12th International Symposium of Federation of Asian and Oceanian Biochemists and Molecular Biologists: Gene Regulation of Biological Functions, Tokushima, Jul. 1996.
27.	Setsuko Ii, M. Ohta, Y. Takahashi, Y. Tano, Y. Kokai, Hiroyuki Iwahana, Katsuhiko Yoshimoto and Mitsuo Itakura : Effect of Transgenic Expression of Aldose Reductase (AR) on Diabetic Proteinuria and Retinopathy., The 15th International Diabetes Federation Congress, Kobe, Nov. 1994.
28.	A. Tomonari, Katsuhiko Yoshimoto, M. Tanaka, Hiroyuki Iwahana and Mitsuo Itakura : Cis-Elements of Human Insulin Gene Involved in Glucose-Responsive Transcription in a Mouse Islet B Cell Line of MIN6., The 15th International Diabetes Federation Congress, Kobe, Nov. 1994.
29.	M. Tanaka, Rumi Katashima, D. Murakami, A. Tomonari, Hiroyuki Iwahana, Katsuhiko Yoshimoto and Mitsuo Itakura : Molecular Cloning of a Group of Pancreatic Islet B cell- and Glucose Concentration-Specific Genes by Random cDNA Sequencing., The 15th International Diabetes Federation Congress, Kobe, Nov. 1994.
30.	Maki Moritani, Katsuhiko Yoshimoto, Hiroyuki Iwahana and Mitsuo Itakura : Effect of IL-10 on Immunological Rejection of Islet B cells by Lymphocytes., The 15th International Diabetes Federation Congress, Kobe, Nov. 1994.
31.	J. Miyazaki, C. Hashimoto, F. Tashiro, Maki Moritani, Katsuhiko Yoshimoto and Mitsuo Itakura : Early-Onset Diabetes Induced in NOD Mice by Transgenic Expression of IL-10 in A cells or SV40 T antigen in B cells., The 15th International Diabetes Federation Congress, Satellite Symposium, "Lessons from Animal Diabetes", Oomiya, Nov. 1994.
32.	Kunio Ii, Eiji Kudo, K. Hizawa, Hiroyuki Iwahana, Katsuhiko Yoshimoto, Setsuko Ii and Mitsuo Itakura : Early Onset Familial Alzheimer's Disease (AD) in the Largest Family with AD in Japan. - Histopathological, Immunohistochemical and Amyloid Precursor Protein (APP) Gene Analysis Studies., The XIIth International Congress of Neuropathology, Toronto, Sep. 1994.
33.	Maki Moritani, Katsuhiko Yoshimoto, J. Miyazaki, F. Tashiro, Setsuko Ii, Eiji Kudo, Hiroyuki Iwahana, Yoshio Hayashi, Toshiaki Sano and Mitsuo Itakura : (Workshop) Local Production of IL-10 in Pancreatic Islet A-Cells in Transgenic NOD Mice Accelerates Autoimmune Insulitis and Diabetes., Combined Meeting of the 8th International Lymphokine Workshop and The 4th International Workshop on Cytokines, Osaka, Oct. 1993.
34.	Y. Uno, A. Tomonari, T. Shigekiyo, Katsuhiko Yoshimoto, T. Inoue and Shiro Saito : DNA Analysis of Antithrombin III Deficiency., XIIIth Congress of the International Society on Thrombosis and Haematostasis, Amsterdam, Jun. 1991.
35.	Katsuhiko Yoshimoto, K. Kubo, Hiroyuki Iwahana, R. Yamasaki, Shiro Saito and Mitsuo Itakura : Molecular Basis for Tumorigenesis in Multiple Endocrine Neoplasia (MEN), FRONTIERS IN MOLECULAR ENDOCRINOLOGY" in GUNMA INTERNATIONAL ENDOCRINE SYMPOSIUM, Maebashi, Jan. 1991.
36.	R. Yamasaki, Haruhiko Saito, Katsuhiko Yoshimoto, S. Miyazaki, Hiroshi Bandou, S. Kimura, Eiji Hosoi, Y. Shintani, S. Mitsuhashi, H. Iwahana, Toshiaki Sano and Shiro Saito : Growth hormone-releasing hormone (GHRH)-secreting pancreatic tumor associated with multiple endocrine neoplasia type 1., 8th International Congress of Endocrinology, Kyoto, Jul. 1988.
37.	Katsuhiko Yoshimoto, Y. Yokogoshi, H. Iwahana, R. Yamasaki, Haruhiko Saito, M. Iizuka, T. Sekiya and Shiro Saito : Allelic deletion of the region in the short arm of chromosome 11 in pancreatic tumors from a patient with multiple endocrine neoplasia type 1., 8th International Congress of Endocrinology, Kyoto, Jul. 1988.

Proceeding of Domestic Conference:

1.	Nanaka Murata, Mima Hashimoto, Noriko Mizusawa and Katsuhiko Yoshimoto : マイクロRNAの細胞増殖への影響, 四国歯学会第56回例会・徳島県歯科医学大会, Feb. 2020.
2.	Mima Hashimoto, Nanaka Murata, Noriko Mizusawa and Katsuhiko Yoshimoto : 唾液マイクロRNAの機能解析, 四国歯学会第56回例会・徳島県歯科医学大会, Feb. 2020.
3.	Noriko Mizusawa, Yuki Iwawaki and Katsuhiko Yoshimoto : 唾液中に存在するマイクロRNAのプロファイリング, 四国歯学会第56回例会・徳島県歯科医学大会, Feb. 2020.
4.	福原紀章, Takeo Iwata, 井下尚子, Katsuhiko Yoshimoto, 福原宏和, 辰島啓太, 岡田満夫, 竹下章, 伊藤純子, 竹内靖博 and 西岡宏 : 頭蓋咽頭腫の病理亜型診断の方法と意義, 第29回臨床内分泌代謝Update (高知), Nov. 2019.
5.	Noriko Mizusawa and Katsuhiko Yoshimoto : マイクロRNAプロファイリングによるヒト顎下腺細胞株での上皮間葉系変換の解析, 第11回日本RNAi研究会, Aug. 2019.
6.	Noriko Mizusawa, Nagakatsu Harada, Takeo Iwata and Katsuhiko Yoshimoto : 膵beta細胞機能に関与するPrss53の解析, 第62回日本糖尿病学会年次学術集会, May 2019.
7.	Katsuhiko Yoshimoto : シンポジウム1 「がんゲノム医療時代の遺伝性内分泌腫瘍」1. 家族性下垂体腫瘍, 第92回日本内分泌学会学術総会, May 2019.
8.	Noriko Mizusawa, Nagakatsu Harada, Takeo Iwata and Katsuhiko Yoshimoto : Prss53は膵ベータ細胞のミトコンドリア機能を介した細胞維持に関与する, 第22回日本臨床内分泌病理学会学術総会, Sep. 2018.
9.	本田壮一 and Katsuhiko Yoshimoto : 地域での内分泌病理との接点—副甲状腺や副腎腫瘍の症例より, 第22回日本臨床内分泌病理学会学術総会, Sep. 2018.
10.	西岡宏, 井下尚子, Takeo Iwata, Katsuhiko Yoshimoto, 御神本雅亮, 福原紀章 and 岡田満夫 : 頭蓋咽頭腫・ラトケ嚢胞の病理と外科治療, 第22回日本臨床内分泌病理学会学術総会, Sep. 2018.
11.	本田壮一, Yoshihiro Suzuki, 小原聡彦, 竹田勝則, 北市雅代, 小笠原卓, 清久泰司, Ken-ichi Aihara and Katsuhiko Yoshimoto : 地域での内分泌診療∼高カルシウム血症の2症例より∼, 第18回日本内分泌学会四国支部学術集会, Sep. 2018.
12.	Katsuhiko Yoshimoto : 下垂体腫瘍と遺伝子, 第20回後期家族性腫瘍セミナー, Mar. 2018.
13.	Katsuhiko Yoshimoto : 家族性内分泌腫瘍:副甲状腺・下垂体腫瘍を中心に, 第8回大阪副甲状腺ホルモン研究会学術集会, Jan. 2018.
14.	中崎真理, 小原聡彦, Yoshihiro Suzuki, 竹田勝則, 北市雅代, 白川光雄, Kenji Tani and Katsuhiko Yoshimoto : 在宅医療での栄養サポートを考える, 第17回日本プライマリ・ケア学会四国ブロック支部大会/第24回四国地域医学研究会合同学術集会, Nov. 2017.
15.	Takeo Iwata and Katsuhiko Yoshimoto : 脂肪組織におけるD-dopachrome tautomerase遺伝子の転写調節, 第21回日本内分泌病理学会学術総会, Oct. 2017.
16.	Takeo Iwata and Katsuhiko Yoshimoto : AMPK/mTOR 経路は脂肪組織での D-dopachrome tautomerase 遺伝子の転写を調節する, 第59回歯科基礎医学会学術大会・総会, Sep. 2017.
17.	Noriko Mizusawa, Takeo Iwata and Katsuhiko Yoshimoto : ヒト顎下腺細胞株 NS-SV-AC における miR-1290 の機能解析, 第59回歯科基礎医学会学術大会・総会, Sep. 2017.
18.	Katsuhiko Yoshimoto : 下垂体腫瘍と遺伝子, 第20回前期家族性腫瘍セミナー, Aug. 2017.
19.	Shinji Ono, Takeo Iwata, Noriko Mizusawa, Shozo Yamada and Katsuhiko Yoshimoto : 非機能性腺腫および ACTH 腺腫における 14q32 領域遺伝子の発現低下, 第27回間脳下垂体腫瘍学会, Feb. 2017.
20.	本田壮一, 小原聡彦, 梅本良雄, Yoshihiro Suzuki, 竹田勝則, 橋本崇代, Hirofumi Oka, Teruyoshi Kageji and Katsuhiko Yoshimoto : 地域におけるがん診療の実践, 第254回徳島医学会学術集会, Feb. 2017.
21.	Takeo Iwata and Katsuhiko Yoshimoto : 分化脂肪細胞における D-dopachrome tautomerase 遺伝子の転写調節, 第58回歯科基礎医学会学術大会・総会, Aug. 2016.
22.	Ohtuka Ryo, Nagakatsu Harada, Noriko Mizusawa, Katsuhiko Yoshimoto, Kazuchika Nishitsuji, Kazumi Takaishi, 豊中屋, Hiroshi Sakaue and Hiroshi Kitahata : GADD34のC末端領域を欠損したCHO-K1細胞の樹立, 第253回徳島医学会学術集会, Jul. 2016.
23.	本田壮一, 小原聡彦, Katsuhiko Yoshimoto and Masataka Sata : FREED試験に参加する意義を考える, 第114回日本内科学会四国地方会, May 2016.
24.	Katsuhiko Yoshimoto : 教育講演13「家族性下垂体腺腫の病因」, 第89回日本内分泌学会学術総会, Apr. 2016.
25.	加藤朋子, 波床朋信, 村上隆亮, 米光新, 武呂誠司, 藤澤一朗, Takeo Iwata, Katsuhiko Yoshimoto, 井下尚子, 山田尚三 and 隠岐尚吾 : 内分泌異常と線維性骨異形成症の合併から，McCune-Albright症候群と診断した一例, 第89回日本内分泌学会学術総会, Apr. 2016.
26.	Katsuhiko Yoshimoto : 特別講演:下垂体腺腫の分子病理学, 第61回成長ホルモン研究会, Feb. 2016.
27.	Noriko Mizusawa, Takeo Iwata and Katsuhiko Yoshimoto : miR-222はRNA-binding protein 24 を標的として顎下腺細胞株NS-SV-ACの細胞増殖に関与する, 第38回日本分子生物学会年会, Dec. 2015.
28.	Katsuhiko Yoshimoto : 下垂体腫瘍発生と原因遺伝子, 第25回臨床内分泌代謝Update, Nov. 2015.
29.	白川光雄, 本田壮一 and Katsuhiko Yoshimoto : 原発性副甲状腺機能亢進症に対する2年間にわたる抗RANKL抗体の投与経験, 第29回日本臨床内科医学会, Oct. 2015.
30.	Katsuhiko Yoshimoto : 下垂体NETのoverview-分子生物学的視点から, AMED革新的がん医療実用化研究事業領域1 研究課題名:「希少がんである神経内分泌腫瘍の個別化医療開発に向けたがん抑制遺伝子 PHLDA3 の機能解析」第1回班会議, Sep. 2015.
31.	Takeo Iwata, 栗林恭子 and Katsuhiko Yoshimoto : D-dopachrome tautomerase 遺伝子転写における FOXO1 と PGC1α の関与, 第57回歯科基礎医学会学術大会・総会, Sep. 2015.
32.	薮内さつき, Hiromi Nakae, Daisuke Hinode, Hiroki Iga, Kazumi Ozaki, Yasuhiko Shirayama, Miwa Matsuyama, Masami Yoshioka, Shizuko Yanagisawa, Natsumi Fujiwara, Akari Watanabe, Tokiko Doi, Fumiaki Kawano and Katsuhiko Yoshimoto : 歯学部学生の情動知能に対する高齢者交流学習の効果, 第34回日本歯科医学教育学会総会および学術大会鹿児島市, Jul. 2015.
33.	Katsuhiko Yoshimoto : シンポジウム「下垂体腺腫の診断と治療Update 2015」下垂体腺腫の腫瘍化機構, 第88回日本内分泌学会学術総会東京, Apr. 2015.
34.	Katsuhiko Yoshimoto : シンポジウム「MEN1の基礎と臨床」腫瘍発生分子機構のoverview, 第88回日本内分泌学会学術総会東京, Apr. 2015.
35.	本田壮一, Kenji Tani, 白川光雄, 橋本崇代, 小原聡彦, Masashi Akaike and Katsuhiko Yoshimoto : 医学生実習を受け入れて(第2報), 第250回徳島医学会学術集会, Feb. 2015.
36.	Ray S. Furuya, 齋藤隆仁, keiji Ido, Takayoshi Miyazaki, Kazuhiko Aiba, Norikazu Miyoshi, Hideo Araki, Daisuke Hinode, Katsuhiko Yoshimoto and Namie Sasaki : 徳島大学における「大学入門講座・読書レポート2014」の試み:読書からアカデミック・ライティングへ-, 平成26年度 FD推進プログラム大学教育カンファレンス in 徳島, Dec. 2014.
37.	薮内さつき, Hiromi Nakae, Daisuke Hinode, Yuko Takeuchi, Hiroki Iga, Kazumi Ozaki, Yasuhiko Shirayama, Miwa Matsuyama, Shizuko Yanagisawa, Masami Yoshioka, Kaya Yoshida, Natsumi Fujiwara, Akari Watanabe, Tokiko Doi, Masanori Nakano, Fumiaki Kawano and Katsuhiko Yoshimoto : 地域育成型歯学教育プログラムの評価(第2報)地域福祉体験学習における教育効果の変化, 平成26年度FD推進プログラム大学教育カンファレンスin徳島, 62-63, Dec. 2014.
38.	肥塚諒, 玉那覇民子, 菱田藍, 橡谷真由, 大畑洋子, 槇野久士, 島津章, Takeo Iwata, Katsuhiko Yoshimoto, 井下尚子, Shozo Yamada and 岸本一郎 : PRKAR1A を含む広範な胚細胞性欠失を認めた下垂体性巨人症の一例, 第24回臨床内分泌代謝Update さいたま市, Nov. 2014.
39.	Shinji Ono, Takeo Iwata, Noriko Mizusawa, 岩脇有軌 and Katsuhiko Yoshimoto : ACTH 産生腺腫で低発現を認めた miR-551b の腺腫発症への関与, 第56回歯科基礎医学会学術大会・総会福岡, Sep. 2014.
40.	Takeo Iwata, Kyoko Ishimoto and Katsuhiko Yoshimoto : 前駆脂肪細胞における D-dopachrome tautomerase 遺伝子の転写調節, 第56回歯科基礎医学会学術大会・総会福岡, Sep. 2014.
41.	岩脇有軌, Noriko Mizusawa, Takeo Iwata, Shinji Ono, Yoritoki Tomotake, Tetsuo Ichikawa and Katsuhiko Yoshimoto : メカニカルストレス応答性 miR-494-3p による FGFR2 発現の抑制, 第56回歯科基礎医学会学術大会・総会福岡, Sep. 2014.
42.	白川光雄, 本田壮一, Katsuhiko Yoshimoto and Toshio Matsumoto : 抗ランクル抗体を投与した原発性副甲状腺機能亢進症の1例, 第14回日本内分泌学会四国地方会徳島, Sep. 2014.
43.	本田壮一, 四宮秀美, 小原聡彦, 白川光雄, 伊藤祐司 and Katsuhiko Yoshimoto : 原発性アルドステロン症のスクリーニングの試み, 第14回日本内分泌学会四国地方会徳島, Sep. 2014.
44.	Shinji Ono, Takeo Iwata, Noriko Mizusawa, Shozo Yamada and Katsuhiko Yoshimoto : 成長ホルモン産生腺腫におけるPRKACA遺伝子活性化変異の検討, 第14回日本内分泌学会四国地方会徳島, Sep. 2014.
45.	Noriko Mizusawa, 岩脇有軌, Takeo Iwata and Katsuhiko Yoshimoto : ヒト顎下腺細胞株を用いた miRNA 標的遺伝子の解析, 第6回日本RNAi研究会・第1回細胞外小胞学会広島, Aug. 2014.
46.	薮内さつき, Hiromi Nakae, Daisuke Hinode, Hiroki Iga, Kazumi Ozaki, Yasuhiko Shirayama, Miwa Matsuyama, Shizuko Yanagisawa, Masami Yoshioka, Yumi Hoshimo, Natsumi Fujiwara, Akari Watanabe, Fumiaki Kawano and Katsuhiko Yoshimoto : 高齢者交流学習後の歯学部生の高齢者イメージの変化・北九州, The Journal of Japanese Dental Education Association, 105, Jul. 2014.
47.	本田壮一, 小原聡彦, Kenji Tani, 白川光雄, Masashi Akaike and Katsuhiko Yoshimoto : 医学生実習を受け入れて-5年間の経験よりー, 第110回日本内科学会四国地区支部主催四国地方会徳島, Jun. 2014.
48.	肥塚諒, 玉那覇民子, 菱田藍, 橡谷真由, 大畑洋子, 槇野久士, 島津章, Takeo Iwata, Katsuhiko Yoshimoto, 井下尚子, Shozo Yamada and 岸本一郎 : 下垂体腫瘍組織にPRKAR1A遺伝子の体細胞変異を認めた下垂体巨人症の一例, 第86回京都内分泌同好会京都, Mar. 2014.
49.	本田壮一, 小原聡彦, 橋本崇代 and Katsuhiko Yoshimoto : 地域におけるがん診療のプライマリ・ケア, 第13回プライマリ・ケア連合学会四国ブロック支部大会高知, Oct. 2013.
50.	Takeo Iwata, Hisaaki Taniguchi, Masamichi Kuwajima, Noriko Mizusawa and Katsuhiko Yoshimoto : D-dopachrome tautomeraseの脂肪細胞への作用, 第17回日本内分泌病理学会学術総会横浜, Oct. 2013.
51.	本田壮一, Katsuhiko Yoshimoto, Hiroyuki Iwahana and 関谷剛男 : 国立がんセンターでのリサーチ・レジデントとしての経験を振り返る, 第72回日本癌学会学術集会横浜, Oct. 2013.
52.	Takeo Iwata, Kyoko Ishimoto, Noriko Mizusawa and Katsuhiko Yoshimoto : D-dopachrome tautomeraseのインスリン抵抗性改善機序に関連する分子の探索, 第55回歯科基礎医学会学術大会・総会岡山, Sep. 2013.
53.	小野信二, Takeo Iwata, Noriko Mizusawa and Katsuhiko Yoshimoto : 下垂体腺腫における miRNA 発現解析, 第55回歯科基礎医学会学術大会・総会岡山, Sep. 2013.
54.	岩脇有軌, Noriko Mizusawa, Takeo Iwata, 小野信二, Yoritoki Tomotake, Tetsuo Ichikawa and Katsuhiko Yoshimoto : 機械的刺激応答性miRNAの同定, 第5回日本RNAi研究会広島, Aug. 2013.
55.	本田壮一, 小原聡彦, 橋本崇代, Katsuhiko Yoshimoto and Toshio Matsumoto : 長期臥床の入院患者の増加—骨粗鬆症—, 第247回徳島医学会学術集会, Aug. 2013.
56.	本田壮一, 小原聡彦, 新谷保実 and Katsuhiko Yoshimoto : 急性冠症候群への糖尿病の関与—「海部プロジェクト」自験例より—, 第56回日本糖尿病学会年次学術集会, May 2013.
57.	Katsuhiko Yoshimoto : ホルモンとがん, 第42回四国歯学会例会, Mar. 2013.
58.	Toshiyuki Suge, Naoto Noguchi, Takashi Matsuo, Katsuhiko Yoshimoto and Tetsuo Ichikawa : 日本大学松戸歯学部臨床実習視察報告, 第42回四国歯学会例会, Mar. 2013.
59.	Keiji Oishi, Hisahiro Takeuchi, Takashi Matsuo, Katsuhiko Yoshimoto and Tetsuo Ichikawa : 広島大学臨床実習視察報告, 第42回四国歯学会例会, Mar. 2013.
60.	Katsuhiko Yoshimoto : 遺伝性・家族性の下垂体腫瘍の基礎と臨床, 第22回臨床内分泌代謝Update, Jan. 2013.
61.	福井崇人, 福原紀章, 西岡宏, 井下尚子, 鈴木尚宣, 竹下章, 竹内靖博, Takeo Iwata, Katsuhiko Yoshimoto and Shozo Yamada : GH産生巨大下垂体腺腫の臨床的および組織学的特徴の検討, 日本脳神経外科学会第71回学術総会, Oct. 2012.
62.	福井崇人, 福原紀章, 西岡宏, 井下尚子, 鈴木尚宣, 竹下章, 竹内靖博, Takeo Iwata, Katsuhiko Yoshimoto and Shozo Yamada : GH産生巨大下垂体腺腫の臨床的および組織学的特徴の検討, 第8回アクロメガリーフォーラム, Oct. 2012.
63.	Mao Kawakami, 杉本明日奈, 杉本明日奈, 堀川絵里子, Fumiaki Kawano and Katsuhiko Yoshimoto : 診療室で行う総合模型実習の試み, 第31回日本歯科医学教育学会総会・学術大会および記念大会, Jul. 2012.
64.	薮内さつき, Hiromi Nakae, Daisuke Hinode, Yuko Takeuchi, Hiroki Iga, Kazumi Ozaki, Masaru Hada, Yasuhiko Shirayama, Miwa Matsuyama, Masami Yoshioka, Atsuko Nakamichi, Yumi Hoshimo, Natsumi Fujiwara, Masanori Nakano, Fumiaki Kawano and Katsuhiko Yoshimoto : 高齢社会を担う地域育成型歯学教育:専門教育終了時の授業アンケートから考察される教育効果, 第31回日本歯科医学教育学会総会および学術大会プログラム・抄録集, 124, Jul. 2012.
65.	本田壮一, 小原聡彦, 新谷保実 and Katsuhiko Yoshimoto : 溺死した糖尿病2症例の検討-津波対策を含めて-, 第55回日本糖尿病学会年次学術集会, May 2012.
66.	安藤明彦, 長坂昌一郎, 高橋仁麗, 野牛宏晃, 大須賀淳一, Noriko Mizusawa, Katsuhiko Yoshimoto and 石橋俊 : 原発性アルドステロン症・サブクリニカルCushing症候群を合併した家族性副甲状腺機能亢進症の1例, 第85回日本内分泌学会学術総会, Apr. 2012.
67.	竹本潤哉, 佐久間一基, 京原麻由, 滝口朋子, 橋本直子, 松澤陽子, 齋藤淳, 大村昌夫, Katsuhiko Yoshimoto, Shozo Yamada and 西川哲男 : AIP遺伝子変異を認めなかった家族性下垂体腺腫の一例, 第12回日本内分泌学会関東甲信越支部学術集会, Mar. 2012.
68.	藤本寛太, 浜本芳之, 河崎祐貴子, 本庶祥子, 森可南子, 龍岡久登, Shozo Yamada, Takeo Iwata, Katsuhiko Yoshimoto and 越山裕行 : 家族性先端巨大症2家系におけるAIP遺伝子の検討, 第21回臨床内分泌代謝Update, Jan. 2012.
69.	中江弘美, 薮内さつき, Daisuke Hinode, Hiroki Iga, Fumiaki Kawano and Katsuhiko Yoshimoto : 学外体験学習における教育管理システムの運用とその効果, 平成23年度全学FD大学教育カンファレンス in 徳島, Jan. 2012.
70.	安藤明彦, 長坂昌一郎, 齋藤芽里, 山崎智行, 高橋仁麗, 野牛宏晃, 大須賀淳一, Noriko Mizusawa, Katsuhiko Yoshimoto and 石橋俊 : 原発性アルドステロン症・サブクリニカルCushing症候群を合併した家族性副甲状腺機能亢進症の一例, 第39回内分泌代謝研究会, Dec. 2011.
71.	藤本寛太, 浜本芳之, 河崎祐貴子, 本庶祥子, 森可南子, 龍岡久登, Shozo Yamada, Takeo Iwata, Katsuhiko Yoshimoto and 越山裕行 : 家族性先端巨大症2家系におけるAIP遺伝子の検討, 第7回アクロメガリフォーラム, Nov. 2011.
72.	Katsuhiko Yoshimoto : 家族性先端巨大症2家系におけるAIP遺伝子の検討:コメント発表家族性下垂体腺腫, 第7回アクロメガリフォーラム, Nov. 2011.
73.	Takeo Iwata, Kyoko Ishimoto, Noriko Mizusawa and Katsuhiko Yoshimoto : D-dopachrome tautomeraseは肥満マウスでのインスリン抵抗性を改善する, 第53回歯科基礎医学会学術大会(岐阜), Oct. 2011.
74.	Nazatul Wan Shima, Noriko Mizusawa, Takeo Iwata and Katsuhiko Yoshimoto : Analysis of miRNAs in saliva, 第84回日本生化学会大会, Sep. 2011.
75.	本田壮一, 新谷保実, 白川光雄, 小原聡彦 and Katsuhiko Yoshimoto : 高齢者糖尿病の診療の問題点—自験症例からの考察—, 第25回日本臨床内科医学会, Sep. 2011.
76.	Daisuke Hinode, 薮内さつき, 中江弘美, Hiroki Iga, Fumiaki Kawano and Katsuhiko Yoshimoto : 地域育成型歯学教育を推進するための教育管理ネットワークシステムの構築とその活用, 第30回日本歯科医学教育学会総会・学術大会および記念大会, Jul. 2011.
77.	Hidehiko Hosoki, Hiroki Iga, Fumiaki Kawano and Katsuhiko Yoshimoto : A Questionnaire Survey to the Dental Students about Periodical Health Examination, 日本歯科医学教育学会, 136, Jul. 2011. (Keyword) health / student / enquête
78.	Noriko Mizusawa, Takeo Iwata, Nagakatsu Harada, Shima Nazatul Wan, Mitsuo Itakura and Katsuhiko Yoshimoto : マウス膵島におけるisletasinの機能解析, 第54回日本糖尿病学会年次学術集会(札幌), May 2011.
79.	Takeo Iwata, Hisaaki Taniguchi, Masamichi Kuwajima, Kyoko Ishimoto, Noriko Mizusawa and Katsuhiko Yoshimoto : D-dopachrome tautomeraseは脂肪細胞での脂質代謝を制御する, 第54回日本糖尿病学会年次学術集会(札幌), May 2011.
80.	本田壮一, 新谷保実, 小原聡彦 and Katsuhiko Yoshimoto : 高齢者糖尿病の診療の問題点-自験症例よりー, 第84回日本内分泌学会学術総会, Apr. 2011.
81.	Kan Nagao, Natsumi Fujiwara, Tomoko Kimura, Akihiro Yasue, Masami Yoshioka, Yoichiro Miyake, Katsuhiko Yoshimoto and Tetsuo Ichikawa : 東京医科歯科大学の臨床実習視察報告, 四国歯学会第38回例会, Mar. 2011.
82.	Hisahiro Takeuchi, Toshiyuki Suge, Yukihiro Momota, Kazumi Ozaki, Atsuko Nakamichi, Yoichiro Miyake, Katsuhiko Yoshimoto and Tetsuo Ichikawa : 日本歯科大学臨床実習視察報告, 第38回四国歯学会例会, Mar. 2011.
83.	薮内さつき, 中江弘美, Daisuke Hinode, Yuko Takeuchi, Hiroki Iga, Masanori Nakano, Hideo Yoshida, Masaru Hada, Kazumi Ozaki, Masami Yoshioka, Kaya Yoshida, Atsuko Nakamichi, Yumi Hoshimo, Natsumi Fujiwara, Fumiaki Kawano and Katsuhiko Yoshimoto : 徳島大学教育GP「高齢社会を担う地域育成型歯学教育」授業アンケートから考察される教育効果, 平成22年度全学FD大学教育カンファレンス in 徳島, Jan. 2011.
84.	Rie Kido, Noriko Mizusawa, Shima Nazatul Wan, Takeo Iwata and Katsuhiko Yoshimoto : マウス膵島の単離, 126回徳島生物学会, Dec. 2010.
85.	都島由希子, 宮章博, 舛岡裕雄, 薮田智範, 福島光浩, 友田智哲, 木原実, 井上博之, 東山卓也, 高村勇貴, 伊藤康弘, 小林薫, Katsuhiko Yoshimoto, Mitsuyoshi Hirokawa and 宮内昭 : 再発を来した副甲状腺機能亢進症顎腫瘍症候群の一例, 第43回日本甲状腺外科学会学術集会, Oct. 2010.
86.	Kyoko Ishimoto, Takeo Iwata, Katsuhiko Yoshimoto and Eiji Tanaka : 前駆脂肪細胞における新規アディポカインD-dopachrome tautomeraseの作用解析, 第69回日本矯正歯科学会, Sep. 2010.
87.	都島由希子, 宮章博, 舛岡裕雄, 薮田智範, 福島光浩, 友田智哲, 木原実, 井上博之, 東山卓也, 高村勇貴, 伊藤康弘, 小林薫, Katsuhiko Yoshimoto, Mitsuyoshi Hirokawa and 宮内昭 : 再発を来した副甲状腺機能亢進症顎腫瘍症候群の一例, 第94回神戸甲状腺研究会, Sep. 2010.
88.	Shima Nazatul Wan, Noriko Mizusawa, Takeo Iwata and Katsuhiko Yoshimoto : 唾液microRNAの解析, 第52回歯科基礎医学会学術大会・総会, Sep. 2010.
89.	Takeo Iwata, Kyoko Ishimoto, Noriko Mizusawa and Katsuhiko Yoshimoto : D-dopachrome tautomeraseは脂肪細胞での中性脂肪量を制御する, 第52回歯科基礎医学会学術大会・総会, Sep. 2010.
90.	Kyoko Ishimoto, Takeo Iwata, Katsuhiko Yoshimoto and Eiji Tanaka : D -dopachrome tautomeraseが脂肪分化に及ぼす影響, 第52回歯科基礎医学会学術大会・総会, Sep. 2010.
91.	Kyoko Ishimoto, Takeo Iwata, Eiji Tanaka and Katsuhiko Yoshimoto : 新規アディポカインD-dopachrome tautomeraseの抗肥満作用についての検討, 第10回日本内分泌学会四国支部学術集会, Sep. 2010.
92.	薮内さつき, Hiroki Iga, 中江弘美, Daisuke Hinode, Masanori Nakano, Hideo Yoshida, Masaru Hada, Kazumi Ozaki, Masami Yoshioka, Atsuko Nakamichi, Yumi Hoshimo, Fumiaki Kawano and Katsuhiko Yoshimoto : 「人間力の向上」を目指した教育プログラム-「高齢者交流学習」-, 第29回日本歯科医学教育学会, Jul. 2010.
93.	Takeo Iwata, Md. Golam Hossain, Noriko Mizusawa and Katsuhiko Yoshimoto : 持続的圧縮力は前駆脂肪細胞からの脂肪細胞への分化を抑制する, 第53回日本糖尿病学会年次学術集会, May 2010.
94.	Noriko Mizusawa, Takeo Iwata, Shima Nazatul Wan and Katsuhiko Yoshimoto : LXRアゴニストによるプログルカゴン遺伝子産生への影響, 第53回日本糖尿病学会年次学術集会, May 2010.
95.	Zhi-Rong Qian, 王路, 中園雅彦, Toshihito Tanahashi, Katsuhiko Yoshimoto, Yoshimi Bando, Eiji Kudo, Mitsuo Shimada and Toshiaki Sano : High Expression of TLR4/MyD88 Signals Correlates with Poor Prognosis in Colorectal Cancer., 第99回日本病理学会総会, Apr. 2010.
96.	Hiroki Iga, Masanori Nakano, Daisuke Hinode, Kazumi Ozaki, Hisahiro Takeuchi, Katsuhiko Yoshimoto and Yoshio Hayashi : 口腔保健学を基軸とした国際的社会福祉教育プログラムの構築に向けて, 平成21年度全学FD 徳島大学教育カンファレンス, Mar. 2010.
97.	中江弘美, Daisuke Hinode, 薮内さつき, Yuko Takeuchi, Hiroki Iga, Masanori Nakano, Hideo Yoshida, Masaru Hada, Kazumi Ozaki, Masami Yoshioka, Atsuko Nakamichi, Yumi Hoshimo, Naoko Matsumoto, Fumiaki Kawano and Katsuhiko Yoshimoto : 地域育成型歯学教育プログラムの評価 -地域福祉体験学習の取り組みを通して-, 平成21年度全学FD 徳島大学教育カンファレンス, Mar. 2010.
98.	Zhi-Rong Qian, 王路, Katsuhiko Yoshimoto, Shozo Yamada and Toshiaki Sano : 下垂体性腺腫のER beta1，2の発現とDNAのhypermethylationおよび機能分析について, 第20回日本間脳下垂体腫瘍学会, Feb. 2010.
99.	Zhi-Rong Qian, Toshihito Tanahashi, Katsuhiko Yoshimoto, Shozo Yamada, Sakurako Katsuura, Kazuhito Rokutan and Toshiaki Sano : MicroRNA Expression Abnormalities in Pituitary Adenomas are Associated with Distinctive Pathologic Features and May Contribute to Tumorigenesis, 第55回日本病理学会秋期特別総会, Nov. 2009.
100.	Daisuke Hinode, 中江弘美, Hiroki Iga, Masanori Nakano, Hideo Yoshida, Masaru Hada, Kazumi Ozaki, Masami Yoshioka, Atsuko Nakamichi, Yumi Hoshimo, Naoko Matsumoto, Fumiaki Kawano and Katsuhiko Yoshimoto : 「高齢社会を担う地域育成型歯学教育」—地域福祉体験学習の取り組みと教育効果—, 第28回日本歯科医学教育学会総会および学術大会, Nov. 2009.
101.	Zhi-Rong Qian, Toshihito Tanahashi, Katsuhiko Yoshimoto, Shozo Yamada, Sakurako Katsuura, Kazuhito Rokutan and Toshiaki Sano : MicroRNA expression abnormalities in pituitary adenomas are associated with distinctive pathologic features and may contribute to tumorigenesis, 第13回日本内分泌病理学会学術総会, Oct. 2009.
102.	Takeo Iwata, Hisaaki Taniguchi, Masamichi Kuwajima and Katsuhiko Yoshimoto : 脂肪細胞におけるD-dopachrome tautomeraseの機能解析, 第30回日本肥満学会, Oct. 2009.
103.	Takeo Iwata, Naozumi Ishimaru, Yoshio Hayashi, Noriko Mizusawa and Katsuhiko Yoshimoto : 脂肪組織におけるYKL-40の役割, 第51回歯科基礎医学会学術大会, Sep. 2009.
104.	Shima Nazatul Wan, Noriko Mizusawa, Takeo Iwata and Katsuhiko Yoshimoto : Liver X receptorアゴニストによる消化管ホルモン発現調節, 第51回歯科基礎医学会学術大会, Sep. 2009.
105.	Takeo Iwata, Hisaaki Taniguchi, Masamichi Kuwajima and Katsuhiko Yoshimoto : D-dopachrome tautomeraseの抗肥満作用解析, 第28回分子病理研究会, Jul. 2009.
106.	Noriko Mizusawa, Takeo Iwata, Shima Nazatul Wan and Katsuhiko Yoshimoto : LXRアゴニスト T0901317によるプログルカゴン遺伝子発現への影響, 第52回日本糖尿病学会年次学術集会, May 2009.
107.	畠山節子, 堤玲子, Noriko Mizusawa, Katsuhiko Yoshimoto, 安本茂 and 武田泰典 : hTERTおよびcdk4遺伝子導入による不死化歯原性上皮細胞の樹立, 日本組織培養学会第82回大会, May 2009.
108.	王路, Zhi-Rong Qian, Mustafizur Md. Rahman, Katsuhiko Yoshimoto, Shozo Yamada, Eiji Kudo and Toshiaki Sano : Overexpression of HMGA1 correlates with tumor invasiveness and proliferation in pituitary adenomas, 第98回日本病理学会年総会, May 2009.
109.	Zhi-Rong Qian, 王路, Mustafizur Md. Rahman, Katsuhiko Yoshimoto, Shozo Yamada, Eiji Kudo and Toshiaki Sano : Tumor-specific down-regulation of ER-1 and ER-2 in Human Pituitary Adenomas, 第98回日本病理学会年総会, May 2009.
110.	Katsuhiko Yoshimoto : メインシンポジウム3 下垂体腺腫:最近の展開 2. 家族性成長ホルモン産生腺腫, 第82回日本内分泌学会学術総会, Apr. 2009.
111.	Zhi-Rong Qian, 王路, Mustafizur Md. Rahman, Katsuhiko Yoshimoto, Radia Sultana, Shozo Yamada, Eiji Kudo and Toshiaki Sano : Tumor-specific down-regulation of ER-1 and ER- 2 in human pituitary adenomas., 第19回日本間脳下垂体腫瘍学会, Feb. 2009.
112.	王路, Zhi-Rong Qian, Mustafizur Md. Rahman, Katsuhiko Yoshimoto, Shozo Yamada, Eiji Kudo and Toshiaki Sano : Increased expression of HMGA1 correlates with tumor invasiveness and proliferation in human pituitary adenomas., 第19回日本間脳下垂体腫瘍学会, Feb. 2009.
113.	Golam Md. Hossain, Takeo Iwata, Noriko Mizusawa, Shozo Yamada, Zhi-Rong Qian, Toshiaki Sano and Katsuhiko Yoshimoto : Mutations, gene expression and CpG methylation status of cyclin-dependent kinase inhibitor p18INK4C in human pituitary adenomas., 第238回徳島医学会学術集会, Feb. 2009.
114.	Daisuke Hinode, Yuko Takeuchi, Hiroki Iga, Masanori Nakano, Hideo Yoshida, Masaru Hada, Kazumi Ozaki, Masami Yoshioka, Kaya Yoshida, Yumi Hoshimo, Naoko Matsumoto, Fumiaki Kawano and Katsuhiko Yoshimoto : 高齢社会を担う地域育成型歯学教育 -初年次教育における達成課題-, 平成20年度全学FD 徳島大学教育カンファレンス, Jan. 2009.
115.	Takeo Iwata, Noriko Mizusawa, Mitsuo Itakura and Katsuhiko Yoshimoto : YKL-40とMMP-1は脂肪組織のリモデリングに関与する, 第29回日本肥満学会, Oct. 2008.
116.	小野信二, Shima Nazatul Wan, Noriko Mizusawa and Katsuhiko Yoshimoto : インクレチン発現におけるLXR合成アゴニストの影響, 第50回歯科基礎医学会学術大会・総会, Sep. 2008.
117.	安永佳世, Noriko Mizusawa, 畠山節子 and Katsuhiko Yoshimoto : isletasinの機能解析, 第50回歯科基礎医学会学術大会・総会, Sep. 2008.
118.	Golam Md. Hossain, Takeo Iwata, Noriko Mizusawa, Shozo Yamada, Zhi-Rong Qian, Toshiaki Sano and Katsuhiko Yoshimoto : Mutations, gene expression and CpG methylation status of cyclin-dependent kinase inhibitor p18INK4C in human pituitary adenomas., 第237回徳島医学会学術集会, Aug. 2008.
119.	Noriko Mizusawa, Takeo Iwata and Katsuhiko Yoshimoto : LXRアゴニストによるインクレチン発現への影響,, 第81回日本内分泌学会学術総会, May 2008.
120.	Feng Yun Yuan, Zhi-Rong Qian, Toshiaki Sano, Katsuhiko Yoshimoto, Shozo Yamada and Eiji Kudo : The pi-class glutathione S-transferase (GSTP1) may be a novel tumor suppressor gene in pituitary tumorigenesis., 第81回日本内分泌学会学術総会, May 2008.
121.	Katsuhiko Yoshimoto, Golam Hossain, Takeo Iwata, Noriko Mizusawa, 内野眞也, 鈴木やすよ, 水越常徳, 田原英樹, 櫻井晃洋, 紅粉睦男, 八代享, 鈴木眞一, 松野彰, 西岡宏 and 田村哲郎 : 家族性副甲状腺機能亢進症家系および家族性下垂体腺腫家系におけるp27Kip1遺伝子解析, 第81回日本内分泌学会学術総会, May 2008.
122.	Takeo Iwata, Noriko Mizusawa, Toshiaki Sano, Mitsuo Itakura and Katsuhiko Yoshimoto : マクロファージ培養上清が脂肪前駆細胞株SGBSのMMP発現に与える影響, 第28回日本肥満学会, Oct. 2007.
123.	Yuan Feng Yun, Zhi-Rong Qian, Toshiaki Sano, Katsuhiko Yoshimoto, Shozo Yamada and Eiji Kudo : The pi-class glutathione S-transferase (GSTP1) may be a novel tumor suppressor gene in pituitary tumorigenesis., 第11回日本内分泌病理学会学術総会, Oct. 2007.
124.	Zhi-Rong Qian, Toshiaki Sano, Shozo Yamada, Yuan Feng Yun, Katsuhiko Yoshimoto and Eiji Kudo : Reduced expression of the let-7 microRNAs in human pituitary adenomas in association with pituitary tumorigenesis through regulating HMGA2., 第11回日本内分泌病理学会学術総会, Oct. 2007.
125.	吉田将紀, Nagakatsu Harada, 原小百合, 尹雲潔, Katsuhiko Yoshimoto and Yutaka Nakaya : 新規グリセロール-3-リン酸アシルトランスフェラーゼ(xGPAT1)の遺伝子クローニング, 第28回日本肥満学会, Oct. 2007.
126.	Takeo Iwata, Noriko Mizusawa, Yutaka Taketani, Mitsuo Itakura and Katsuhiko Yoshimoto : 副甲状腺癌抑制因子パラフィブロミンはSV40 large T抗原存在下では細胞増殖促進に働く, 第32回日本比較内分泌学会大会, Oct. 2007.
127.	Noriko Mizusawa, 畠山節子 and Katsuhiko Yoshimoto : isletasin遺伝子の膵β細胞特異的発現と細胞内局在, 第49回歯科基礎医学会学術大会・総会, Aug. 2007.
128.	Golam Md. Hossain, Takeo Iwata, Noriko Mizusawa, Katsuhiko Yoshimoto, Shozo Yamada and Toshiaki Sano : Mutation analysis of AIP gene in isolated familial somatotropinomas and sporadic growth hormone-secreting adenomas., 第235回徳島医学会学術集会, Aug. 2007.
129.	Takeo Iwata, Shozo Yamada, Noriko Mizusawa, Golam Md. Hossain, 西岡宏, 松野彰, Toshiaki Sano and Katsuhiko Yoshimoto : 家族性および孤発性 GH産生腺腫におけるAIP遺伝子解析, 第80回日本内分泌学会学術総会, Jun. 2007.
130.	Noriko Mizusawa, Takeo Iwata and Katsuhiko Yoshimoto : 膵β細胞に高発現するisletasin遺伝子の解析, 第50回日本糖尿病学会年次学術集会, May 2007.
131.	関澤直子, 神山隆治, 泉山肇, 土井賢, 田中啓之, 明石巧, Katsuhiko Yoshimoto and 平田結喜緒 : 不明熱を契機に発見されたプロラクチノーマに心粘液腫を合併した一例:carney complex?, 第7回日本内分泌学会関東甲信越支部学術集会, Feb. 2007.
132.	Takeo Iwata, Noriko Mizusawa, Yutaka Taketani, Mitsuo Itakura and Katsuhiko Yoshimoto : 癌抑制因子パラフィブロミンはSV40 large T抗原存在下では細胞増殖促進に働く, 第10回日本内分泌病理学会学術総会, Nov. 2006.
133.	Katsuhiko Yoshimoto, Noriko Mizusawa, Takeo Iwata, Toshiaki Sano and 露口勝 : 副甲状腺機能亢進症-顎腫瘍症候群におけるHRPT2変異, 第6回日本内分泌学会四国地方会, Sep. 2006.
134.	Katsuhiko Yoshimoto : 特別講演メタボリックシンドローム, 第27回日本歯内療法学会学術大会徳島大会, Jul. 2006.
135.	Noriko Mizusawa, Nagakatsu Harada, Takeo Iwata, 国香清, Maki Moritani, Yutaka Taketani, Mitsuo Itakura and Katsuhiko Yoshimoto : 膵β細胞に高発現する新規蛋白Isletasinの機能解析, 第49回日本糖尿病学会年次学術集会, May 2006.
136.	Katsuhiko Yoshimoto, Noriko Mizusawa, Takeo Iwata, Toshiaki Sano, 露口勝, 内野眞也, 野口志郎, 鈴木やすよ, 水越常徳, 田原英樹, 櫻井晃洋, 紅粉睦男, 八代享, 鈴木眞一 and 藤澤正人 : 家族性副甲状腺機能亢進症家系および孤発性副甲状腺腺腫症例におけるHRPT2遺伝子変異,, 第79回日本内分泌学会学術総会, May 2006.
137.	Zhi-Rong Qian, Toshiaki Sano, Asa L Sylvia, Katsuhiko Yoshimoto, Shozo Yamada, Eiji Kudo and Mitsuyoshi Hirokawa : Tumor suppressor genes methylation analysis and DNA methyltransferase inhibitors treatment in HP75 cell., 第79回日本内分泌学会学術総会, May 2006.
138.	Takeo Iwata, Noriko Mizusawa, Yutaka Taketani, Mitsuo Itakura and Katsuhiko Yoshimoto : 副甲状腺癌抑制遺伝子産物パラフィブロミンとSV40 large T抗原の相互作用による癌化機構, 第79回日本内分泌学会学術総会, May 2006.
139.	水越常徳, 佐藤裕信, 高橋裕樹, 今井浩三, 鈴木やすよ, 内野眞也, 首藤茂, 野口志郎 and Katsuhiko Yoshimoto : HRPT2遺伝子変異を認めた家族性孤発性副甲状腺機能亢進症(FIHP)の一例, 第16回臨床内分泌代謝UPDATE, Mar. 2006.
140.	Zhi-Rong Qian, Toshiaki Sano, Katsuhiko Yoshimoto, Shozo Yamada, Eiji Kudo and Mitsuyoshi Hirokawa : Promoter methylation and differential expression of estrogen receptor-beta in pituitary adenomas., 第16回日本間脳下垂体腫瘍学会, Feb. 2006.
141.	Zhi-Rong Qian, Toshiaki Sano, Katsuhiko Yoshimoto, Shozo Yamada, Eiji Kudo and Mitsuyoshi Hirokawa : Promoter methylation and differential expression of pi-class glutathione S-transferase (GSTP1) in pituitary adenomas., 第9回日本内分泌病理学会学術総会, Oct. 2005.
142.	Takeo Iwata and Katsuhiko Yoshimoto : 副甲状腺癌抑制遺伝子産物パラフィブロミンとSV40 large T抗原の相互作用, 第64回日本癌学会学術総会, Sep. 2005.
143.	本田壮一, 新谷保実, 中川洋一 and Katsuhiko Yoshimoto : 地域での糖尿病予防の経験, 第231回徳島医学会学術集会, Aug. 2005.
144.	Takeo Iwata, Noriko Mizusawa, Yutaka Taketani, Mitsuo Itakura and Katsuhiko Yoshimoto : Under40 Panel Discussion 副甲状腺癌抑制遺伝子産物パラフィブロミンと相互作用する蛋白の同定, 第78回日本内分泌学会学術総会, Jul. 2005.
145.	Zhi-Rong Qian, Toshiaki Sano, Katsuhiko Yoshimoto, Shozo Yamada and Mitsuyoshi Hirokawa : Methylation analysis of the cell cycle control genes in human pituitary tumors., 第78回日本内分泌学会学術総会, Jul. 2005.
146.	佐藤絢香, 中山耕之介, 渡邉昌樹, 犬飼浩一, 武市潔, 澤貴広, 泉田太郎, 和田誠基, Katsuhiko Yoshimoto, 内野眞也, 板橋明 and 片山茂裕 : 原発性副甲状腺機能亢進症姉妹例, 第78回日本内分泌学会学術総会, Jul. 2005.
147.	Katsuhiko Yoshimoto, Noriko Mizusawa, Takeo Iwata, 露口勝, Toshiaki Sano and 内野眞也 : 家族性副甲状腺機能亢進症2家系におけるHRPT2遺伝子変異の解析, 第78回日本内分泌学会学術総会, Jul. 2005.
148.	Noriko Mizusawa, Takeo Iwata, Mitsuo Itakura and Katsuhiko Yoshimoto : ヒトインスリン遺伝子発現調節におけるGC2-GC1配列の役割, 第48回日本糖尿病年次学術集会, May 2005.
149.	Zhi-Rong Qian, Toshiaki Sano, Katsuhiko Yoshimoto, Shozo Yamada, Hidehisa Horiguchi and Mitsuyoshi Hirokawa : Analysis of DNA methyltransferase 1 (DNMT1) expression in human pituitary tumors, 第15回日本間脳下垂体腫瘍学会, Feb. 2005.
150.	水越常徳, 佐藤裕信, 高橋裕樹, 今井浩三, 鈴木やすよ, 内野眞也, 首藤茂, 野口志郎 and Katsuhiko Yoshimoto : HRPT2遺伝子変異を認めた家族性副甲状腺機能亢進症の一例, 第4回日本内分泌学会北海道地方会, Nov. 2004.
151.	Zhi-Rong Qian, Toshiaki Sano, Katsuhiko Yoshimoto, Shozo Yamada, Hidehisa Horiguchi, Mitsuyoshi Hirokawa and Asa L Sylvia : Methylation and expression of the cell cycle control genes in human pituitary tumors, 第8回日本内分泌病理学会総会, Nov. 2004.
152.	内野眞也, 野口志郎, 山下弘幸, 渡辺紳, 小川尚洋, 鈴木やすよ, 水越常徳 and Katsuhiko Yoshimoto : MEN1遺伝子変異陰性の家族性副甲状腺機能亢進症におけるHRPT2遺伝子変異, 第37回甲状腺外科研究会, Oct. 2004.
153.	井上紀子, Yasuko Ishikawa, Yoshiko Nakae, Fumiaki Kawano and Katsuhiko Yoshimoto : 耳下腺小葉間導管におけるAQP5の細胞内移動に及ぼす糖尿病の影響, 第46回基礎歯科学会学術大会・総会, Sep. 2004.
154.	Akiko Matsumura, 橋本理恵, 宇野和美, Kazuko Okada, Yutaka Nakaya and Katsuhiko Yoshimoto : 頭頸部悪性腫瘍患者の栄養管理, 徳島NST研究会, Jun. 2004.
155.	内野眞也, 首藤茂, 野口志郎, 水越常徳 and Katsuhiko Yoshimoto : 家族性副甲状腺機能亢進症におけるHRPT2遺伝子変異, 第10回家族性腫瘍研究会学術集会, Jun. 2004.
156.	井上紀子, Yasuko Ishikawa, Masayuki Shono and Katsuhiko Yoshimoto : 糖尿病における唾液分泌低下機序, 第28回例会・第23回総会四国歯学会, Jun. 2004.
157.	Katsuhiko Yoshimoto : ワ-クショップ「多発性内分泌腫瘍症1・2型の基礎と臨床」遺伝性内分泌腫瘍について, 第16回日本内分泌外科学会総会, May 2004.
158.	Noriko Mizusawa, Chisato Kosugi, Nagakatsu Harada, Mitsuo Itakura and Katsuhiko Yoshimoto : 膵β細胞とα細胞のHox遺伝子およびホメオティック遺伝子発現の差異, 第47回日本糖尿病学会年次学術総会, May 2004.
159.	Zhi-Rong Qian, Toshiaki Sano, Katsuhiko Yoshimoto, Shozo Yamada, Noriko Mizusawa, 石塚明, Hidehisa Horiguchi and Mitsuyoshi Hirokawa : Aberrant methylation of the CDH13 gene in pituitary adenomas, 第14回日本間脳下垂体腫瘍学会, Feb. 2004.
160.	Akiko Matsumura, 橋本理恵, 宇野和美, 佐賀啓子, 国清紀子, 山田静恵, Yasuko Takahashi, Toshiya Okahisa, Katsuhiko Yoshimoto and Yutaka Nakaya : (シンポジウム) NST導入により何がかわったか: NSTによる頭頸部悪性腫瘍患者の栄養管理, 第7回日本病態栄養学会年次学術集会, Jan. 2004.
161.	Zhi-Rong Qian, Toshiaki Sano, Katsuhiko Yoshimoto, Shozo Yamada, Noriko Mizusawa, Ishizuka Akira, Hidehisa Horiguchi and Mitsuyoshi Hirokawa : Inactivation of RASSF1A tumor suppressor gene by aberrant promoter methylation in human pituitary adenomas, 第7回日本内分泌病理学会総会, Oct. 2003.
162.	Noriko Mizusawa, Nagakatsu Harada and Katsuhiko Yoshimoto : 膵β細胞特異的に発現するisletasin遺伝子の解析, 第46回日本糖尿病学会年次学術総会, May 2003.
163.	藤井俊充, 泉山肇, 土肥賢, 名和田久礼, 吉本貴宣, 今井泰平, 山崎弘幸, Katsuhiko Yoshimoto and 平田結喜緒 : 心房粘液腫による脳塞栓を発症したCarney's complex (CNC)の遺伝子解析, 第76回日本内分泌学会学術総会, May 2003.
164.	Katsuhiko Yoshimoto : (シンポジウム) 種々のsyndromeに伴う甲状腺疾患「基礎のoverview」, 第76回日本内分泌学会学術総会, May 2003.
165.	山崎弘幸, Teruyoshi Kageji, Shinji Nagahiro, Shozo Yamada, Toshiaki Sano and Katsuhiko Yoshimoto : GH 産生下垂体腺腫におけるPRKAR1A遺伝子異常の解析, 第20回日本脳腫瘍学会, Nov. 2002.
166.	山崎弘幸, Teruyoshi Kageji, Shinji Nagahiro, Shozo Yamada, Toshiaki Sano and Katsuhiko Yoshimoto : GH 産生下垂体腺腫におけるPRKAR1A遺伝子異常の解析, 第6回日本内分泌病理学会総会, Oct. 2002.
167.	Katsumi Tsuchiya, Tetsuo Sakai, Hideo Matsuo, Akira Nomura, Shunhan Koh, Seishi Mizuno, Rika Yoshie, Katsuhiko Yoshimoto and Akira Wakizaka : Differences of the gene expression with different histological types in the growth hormone-releasing pituitary tumors estimated by the DNA chip technology., 第75回日本生化学会大会, Oct. 2002.
168.	隈晴二, 徐冰, Katsuhiko Yoshimoto, 宮内昭, Mitsuyoshi Hirokawa and Toshiaki Sano : 甲状腺乳頭癌cribriform-morular variantにみられたβ-catenin遺伝子(CTNNB1) exon 3のsomatic mutation, 第92回日本病理学会年総会, Oct. 2002.
169.	井上紀子, Yasuko Ishikawa and Katsuhiko Yoshimoto : 耳下腺に局在するbeta-アドレナリン受容体と細胞内情報伝達系のストレプトゾトシン誘発性糖尿病による動態, 第44回基礎歯科医学会学術大会・総会, Oct. 2002.
170.	Katsuhiko Yoshimoto : (ワークショップ) 内分泌腫瘍の基礎と臨床:最近の知見「内分泌腫瘍の基礎:内分泌機能と腫瘍発生の機序」, 第2回日本内分泌学会四国地方会, Sep. 2002.
171.	本田壮一, Chisato Kosugi, Shozo Yamada, Toshiaki Sano and Katsuhiko Yoshimoto : 下垂体腺腫におけるRB遺伝子変異とメチル化の解析, 第75回日本内分泌学会学術総会, Jun. 2002.
172.	Katsuhiko Yoshimoto : 内分泌腺腫瘍から学ぶ, 四国歯学会第26回例会・第21回総会, Jun. 2002.
173.	Noriko Mizusawa, 友成章, Chisato Kosugi, 小倉真琴, Nagakatsu Harada, Izumi Ohigashi, Mitsuo Itakura and Katsuhiko Yoshimoto : ヒトインスリン遺伝子のグルコ-ス応答性転写調節に及ぼすGG配列の役割, 第45回日本糖尿病学会年次学術総会, May 2002.
174.	隈晴二, Xu Bing, Mitsuyoshi Hirokawa, Katsuhiko Yoshimoto, 三木仁司, 高橋正倫 and Toshiaki Sano : Ki-ras gene mutation in spindle epithelial tumor with thymus-like differenriation of the thyroid, 第91回日本病理学会総会, Mar. 2002.
175.	Zhi-Rong Qian, Li Chei Chiun, 山崎弘幸, Noriko Mizusawa, Katsuhiko Yoshimoto, Shozo Yamada, Hidehisa Horiguchi, Shingo Wakatsuki, Mitsuyoshi Hirokawa and Toshiaki Sano : Expression of E-cadherin and alpha-, beta-, and gamma-catenins in Human Pituitary Prolactinomas, 第91回日本病理学会総会, Mar. 2002.
176.	Mitsuo Itakura, Takashi Yamaoka, Maki Moritani, Rumi Katashima, Eiji Kudo, 日野聡史, Hiroyuki Iwahana and Katsuhiko Yoshimoto : 痛風・核酸に関する代謝調節の解析，分子生物学から個体レベルの解析に向けて-遺伝子改変動物とゲノム多型解析, 第35回日本痛風・核酸代謝学会総会, Feb. 2002.
177.	Zhi-Rong Qian, Li Chei Chiun, 山崎弘幸, Noriko Mizusawa, Katsuhiko Yoshimoto, Shozo Yamada and Toshiaki Sano : Expression of E-cadherin and alpha-, beta-, and gamma-catenins in Human Pituitary Prolactinomas, 第12回日本間脳下垂体腫瘍学会, Feb. 2002.
178.	山崎弘幸, Noriko Mizusawa, Chisato Kosugi, Nagakatsu Harada, Izumi Ohigashi, 本田壮一, Shozo Yamada, Toshiaki Sano, Teruyoshi Kageji, Shinji Nagahiro and Katsuhiko Yoshimoto : GH下垂体腺腫におけるPRKAR1A遺伝子異常の解析, 第12回日本間脳下垂体腫瘍学会, Feb. 2002.
179.	本田壮一, Chisato Kosugi, Shozo Yamada, 木村敏彦, Nagakatsu Harada, Izumi Ohigashi, Noriko Mizusawa, 山崎弘幸, Toshiaki Sano and Katsuhiko Yoshimoto : 下垂体腺腫における網膜芽細胞腫 (RB)遺伝子異常の解析, 第12回日本間脳下垂体腫瘍学会, Feb. 2002.
180.	Zhi-Rong Qian, Li Chei Chiun, 山崎弘幸, Noriko Mizusawa, Katsuhiko Yoshimoto, Shozo Yamada and Toshiaki Sano : Expression of E-cadherin and alpha-, beta-, and gamma-catenins in Human Pituitary Prolactinomas, 第224回徳島医学会学術集会 (平成13年度冬期), Feb. 2002.
181.	Noriko Mizusawa, 友成章, Chisato Tanaka, Nagakatsu Harada, Izumi Ohigashi, Mitsuo Itakura and Katsuhiko Yoshimoto : インスリン遺伝子のグルコース応答性転写調節に及ぼすCG配列の役割, 第24回日本分子生物学会年会, Dec. 2001.
182.	Chisato Tanaka, 内野眞也, 野口志郎 and Katsuhiko Yoshimoto : MEN1遺伝子の体細胞変異による両アレルの不活化, 第60回日本癌学会総会, Sep. 2001.
183.	山崎弘幸, Norio Nakajima, Teruyoshi Kageji, Shinji Nagahiro, Hidehisa Horiguchi, 関貫聖二, Yasuhisa Kanematsu and Katsuhiko Yoshimoto : Glioblastomaの一兄弟例, 第15回中国四国脳腫瘍研究会, Aug. 2001.
184.	山崎誠司, 松村敏信, Seiki Tashiro, Katsuhiko Yoshimoto, Maki Moritani and Mitsuo Itakura : 膵α細胞にTGF-β1を発現させた膵島移植モデルにおける免疫寛容の誘導, 第56日本消化器外科学会, Jul. 2001.
185.	Katsuhiko Yoshimoto, Chisato Tanaka and Arnold Andrew : 卵巣癌における異所性PTH産生機構の解析, 第74回日本内分泌学会学術総会, Jun. 2001.
186.	Izumi Ohigashi, 長谷川朋子, Nagakatsu Harada, Chisato Tanaka and Katsuhiko Yoshimoto : DNAマイクロアレイを用いた膵島α細胞およびβ細胞に特異的に発現する遺伝子の検索, 第44回日本糖尿病学会年次学術総会, Apr. 2001.
187.	Nagakatsu Harada, Izumi Ohigashi, Chisato Tanaka, Mitsuo Itakura and Katsuhiko Yoshimoto : 膵β細胞における発現プロファイルの解析および新規遺伝子のクローニング, 第44回日本糖尿病学会年次学術総会, Apr. 2001.
188.	Chisato Tanaka, Nagakatsu Harada, Izumi Ohigashi, Mitsuo Itakura and Katsuhiko Yoshimoto : グルカゴン遺伝子の転写調節に関わる新規蛋白の同定とその解析, 第44回日本糖尿病学会年次学術総会, Apr. 2001.
189.	西村有子, Maki Moritani, Rumi Katashima, Takashi Yamaoka, Katsuhiko Yoshimoto, Naoyuki Kamatani and Mitsuo Itakura : 家族性若年性高尿酸血症性腎症 (FJHN)の疾患遺伝子の解析, 第34回日本痛風・核酸代謝学会総会, Feb. 2001.
190.	Rumi Katashima, Hiroyuki Iwahana, Takashi Yamaoka, Maki Moritani, Katsuhiko Yoshimoto, 小関しおり, 多比良和誠 and Mitsuo Itakura : ラットアミドホスホリボシルトランスフェラーゼ (ATase) のmRNAを標的とするリボザイムを用いたラット線維芽細胞株の細胞増殖についての検討, 第34回日本痛風・核酸代謝学会総会, Feb. 2001.
191.	Izumi Ohigashi, Nagakatsu Harada, Chisato Tanaka and Katsuhiko Yoshimoto : cyclin D1の異常は副甲状腺細胞の増殖とホルモン分泌異常を引き起こす, 第222回徳島医学会学術集会 (平成12年度冬期), Jan. 2001.
192.	Mitsuo Itakura, Maki Moritani, 片島るみ, YanHui Ying, Takashi Yamaoka, 伊井節子, Katsuhiko Yoshimoto and Naoyuki Kamatani : 痛風のゲノム解析, 第34回日本痛風・核酸代謝学会総会, 2001.
193.	笹原賢司, Takashi Yamaoka, Maki Moritani, Katsuhiko Yoshimoto, Yasuhiro Kuroda and Mitsuo Itakura : 新規Regファミリ-遺伝子``INGAPrP''のクロ-ニングと組織特異的発現, 日本糖尿病学会中国四国地方会38回総会, Oct. 2000.
194.	Toshinori Sakai, 井形高明, Shinsuke Katoh, Koichi Sairyo, Chisato Tanaka, Rumi Katashima, Katsuhiko Yoshimoto and Mitsuo Itakura : SNPsを用いたOPLL疾患感受性遺伝子に関する解析, 第15回日本整形外科学会基礎学術集会, Sep. 2000.
195.	Toshinori Sakai, 井形高明, Shinsuke Katoh, Koichi Sairyo, Chisato Tanaka, Rumi Katashima, Katsuhiko Yoshimoto and Mitsuo Itakura : SNPsを用いたOPLL疾患感受性遺伝子に関する解析, 第12回徳大脊椎外科カンファレンス, Aug. 2000.
196.	Takashi Yamaoka, Katsuhiko Yoshimoto and Mitsuo Itakura : FGF-8による膵島細胞の肝細胞への分化誘導, 第73回日本内分泌学術総会, Jun. 2000.
197.	Noriko Mizusawa, Katsuhiko Yoshimoto, Hiroyuki Iwahana, 清水新司, 久保田美子, 平野浩子, Mitsuo Itakura and 堀内三郎 : ヒトCAD遺伝子上流調節領域の構造決定と解析, 第66回日本生化学会東北支部会例会, Jun. 2000.
198.	Setsuko Ii, 山本千恵美, Mitsuo Itakura, 張春花, Katsuhiko Yoshimoto and Mitsuo Itakura : ヒトアルド-ス還元酵素発現およびソルビト-ル脱水素酵素欠損マウスにおける糖尿病性蛋白尿の解析, 第43回日本糖尿病学会年次学術総会, May 2000.
199.	長谷川朋子, Katsuhiko Yoshimoto, 大塚理司, Setsuko Ii, Maki Moritani, Takashi Yamaoka and Mitsuo Itakura : 膵ランゲルハンス島β細胞およびα細胞におけるHOX遺伝子発現の解析, 第43回日本糖尿病学会年次学術総会, May 2000.
200.	Takashi Yamaoka, Katsuhiko Yoshimoto and Mitsuo Itakura : Reg-1トランスジェニックマウスに認められた糖尿病と腫瘍形成, 第43回日本糖尿病学会年次学術総会, May 2000.
201.	阿部琢巳, Katsuhiko Yoshimoto, 谷山松雄, 望月由武人, 小林信介, 花川一郎, 泉山仁, Mitsuo Itakura and 松本清 : A germline mutation of the multiple endocrine neoplasia type 1 (MEN 1) gene in Japanese prolactinoma variant of MEN1., 第10 回日本間脳下垂体腫瘍学会(宮崎), Feb. 2000.
202.	Mitsuo Itakura, Maki Moritani, Rumi Katashima, YanHui Ying, Takashi Yamaoka, Setsuko Ii, Katsuhiko Yoshimoto and Naoyuki Kamatani : 痛風のゲノム解析, 第33回日本・核酸代謝学会総会, Feb. 2000.
203.	阿部琢巳, Katsuhiko Yoshimoto, 谷山松男, 望月由武人, 小林信介, 花川一郎, 神保洋之, 泉山仁, Mitsuo Itakura and 松本清 : MEN1遺伝子の変異を検出した家族性プロラクチノ-マの一家系, 第58回日本脳神経外科学会総会(東京), Oct. 1999.
204.	西岡達矢, 山崎弘実, 近沢宏明, 細川貴規, 武田京子, 公文義雄, 橋本浩三, Katsuhiko Yoshimoto, Chisato Tanaka and Mitsuo Itakura : プロラクチン上昇を伴った原発性副甲状腺機能亢進症におけるMEN1遺伝子の解析, 第80回日本内科学会四国地方会(高知), Jun. 1999.
205.	阿部琢巳, Katsuhiko Yoshimoto, 谷山松男, 花川一郎, 泉山仁, 富田基郎, Mitsuo Itakura and 松本清 : MEN1遺伝子の変異を検出した家族性プロラクチノ-マの1家系, 第5回家族性腫瘍研究会学術集会(東京), Jun. 1999.
206.	Katsuhiko Yoshimoto : (シンポジウム)「家族性腫瘍の診断・治療の現状と将来の問題点」多発性内分泌腫瘍症, 第5回家族性腫瘍研究会学術集会(東京), Jun. 1999.
207.	Takashi Yamaoka, Katsuhiko Yoshimoto and Mitsuo Itakura : グルカゴンプロモ-タ-/インタ-フェロン-γ-トランスジェニックマウス(IFN-γ-Tg)に認められたβ細胞のアポト-シスと膵島リモデリング, 第72回日本内分泌学会学術総会(横浜), May 1999.
208.	Mitsuo Itakura, Maki Moritani, Takashi Yamaoka, Setsuko Ii and Katsuhiko Yoshimoto : Strategy of SNPs-based discovery of disease-related genes as the possible targets of drug development,, 第73回日本薬理学会(横浜), May 1999.
209.	Maki Moritani, Katsuhiko Yoshimoto, Toshiaki Sano, 宮崎純一, 菊谷仁 and Mitsuo Itakura : 膵ラ島A細胞に発現させた活性型 TGF-β1による糖尿痛発症の抑制機構, 第28回日本免疫学会総会・学術集会(神戸), Dec. 1998.
210.	Katsuhiko Yoshimoto, 細川好孝, Mitsuo Itakura and Andrew Arnold : 副甲状腺にcyclin D1を過剰発現させたトランスジェニックマウスにおける副甲状腺腺腫, 第57回日本癌学会総会(横浜), Sep. 1998.
211.	Katsuhiko Yoshimoto, Chisato Tanaka, 木村建彦, Yang Peng, Maki Moritani, Takashi Yamaoka, Shozo Yamada, Toshiaki Sano and Mitsuo Itakura : MEN1遺伝子の異常:孤発性下垂体腺腫における解析, 第71回日本内分泌学会学術総会(福岡), Jun. 1998.
212.	Chisato Tanaka, Katsuhiko Yoshimoto, Shozo Yamada, 西岡宏, Maki Moritani, Takashi Yamaoka and Mitsuo Itakura : MEN1遺伝子の異常:「多発性内分泌腫瘍症I型」，「家族性下垂体腺腫」および「家族性副甲状腺機能亢進症」における解析, 第71回日本内分泌学会学術総会(福岡), Jun. 1998.
213.	Maki Moritani, Katsuhiko Yoshimoto, 菊谷仁, Toshiaki Sano, 宮崎純一 and Mitsuo Itakura : 膵ラ島A細胞に発現させた活性型TGF-β1によるNODマウスにおける糖尿病発症の抑制効果, 第27回日本免疫学会総会・学術集会(札幌), Oct. 1997.
214.	Takashi Yamaoka, 出原千代子, 近藤麻木, Katsuhiko Yoshimoto and Mitsuo Itakura : Amidophosphoribosyltransferase(ATase)の細胞密度依存的発現を司るプロモーター領域の同定, 第70回日本生化学会(金沢), Sep. 1997.
215.	Noriko Mizusawa, 藤村美和, Hiroyuki Iwahana, Rumi Katashima, Katsuhiko Yoshimoto, 堀内三郎 and Mitsuo Itakura : ヒトCAD遺伝子のゲノム構造の解析, 第70回日本生化学会(金沢), Sep. 1997.
216.	Mitsuo Itakura, Maki Moritani, Setsuko Ii, Takashi Yamaoka and Katsuhiko Yoshimoto : (シンポジウム) 糖尿病の分子機構-多面的アプローチ，Animal Models of Gene Therapy of Diabetes, 第70回日本生化学会(金沢), Sep. 1997.
217.	Takashi Yamaoka, Takaya Matsushita, 出原干代子, 山田健人, Katsuhiko Yoshimoto and Mitsuo Itakura : アクチビンのドミナントネガテイブ(優性阻害)受容体を膵β細胞で発現するトランスジェニックマウス(dnActRⅡ-Tg)に認められた膵島形成不全, 第70回日本内分泌学会学術総会(東京), Jun. 1997.
218.	Chisato Tanaka, Katsuhiko Yoshimoto, 木村建彦, Shozo Yamada and Mitsuo Itakura : 下垂体腺腫における第12番染色体のallelic imbalanceとp27KIP1遺伝子異常の解析, 第70回日本内分泌学会学術総会(東京), Jun. 1997.
219.	Maki Moritani, Katsuhiko Yoshimoto, Toshiaki Sano, 宮崎純一 and Mitsuo Itakura : 膵ラ島A細胞に活性型TGF-β1を発現させたNODトランスジェニックマウス(Tg)における糖尿病発症の抑制効果, 第40回日本糖尿病学会年次学術集会(東京), May 1997.
220.	Takashi Yamaoka, Takaya Matsushita, 出原千代子, 山田健人, Katsuhiko Yoshimoto, 秦順一 and Mitsuo Itakura : アクチビンのドミナントネガティブ(優性阻害)受容体を膵β細胞で発現するトランスジェニックマウス(dnActRⅡ-Tg)に認められた膵島形成不全, 第40回日本糖尿病学会年次学術集会(東京), May 1997.
221.	Hiroyuki Iwahana, Maki Moritani, Katsuhiko Yoshimoto, Toshiaki Sano and 菊谷仁 : (ワークショップ) 膵島β細胞障害のメカニズムとその予防，5. IL-10遺伝子を導入したNODマウスの膵ラ島特異的Th1リンパ球の養子移入によるNODマウスのⅠ型糖尿病発症抑制, 第40回日本糖尿病学会年次学術集会(東京), May 1997.
222.	藤村美和, Hiroyuki Iwahana, Katsuhiko Yoshimoto and Mitsuo Itakura : ヒトCAD遺伝子のゲノム構造の解析, 第30回日本プリン・ピリミジン代謝学会総会(東京), Mar. 1997.
223.	近藤麻木, Takashi Yamaoka, Hiroyuki Iwahana, Katsuhiko Yoshimoto and Mitsuo Itakura : プリン体のde novo生合成経路とサルべージ経路:両経路の相互調節機構と細胞増殖に対する寄与, 第30回日本プリン・ピリミジン代謝学会総会(東京), Mar. 1997.
224.	Hiroyuki Iwahana, 藤村美和, Setsuko Ii, Maki Moritani, Takashi Yamaoka, Katsuhiko Yoshimoto, 石塚俊治, 喜多和子, 富永眞一, 橘正道 and Mitsuo Itakura : ヒト・ホスホリボシルピロリン酸(PRPP)合成酵素39kDa結合蛋白質(PAP39)遺伝子のP1プラスミドとPCRを用いたゲノム構造の解析, 第30回日本プリン・ピリミジン代謝学会総会(東京), Mar. 1997.
225.	Hiroyuki Iwahana, Rumi Katashima, 井上明子, 藤村美和, 高橋陽子, Takashi Yamaoka, Katsuhiko Yoshimoto, 富永眞一 and Mitsuo Itakura : 産生過剰型痛風患者におけるアミドホスホリボシルトランスフェラーゼ(ATase)の多色蛍光PCR-SSCPを用いた遺伝子解析, 第30回日本プリン・ピリミジン代謝学会総会, Mar. 1997.
226.	Rumi Katashima, Hiroyuki Iwahana, 藤村美和, 山崎篤子, 石塚俊治, 喜多和子, 橘正道, Katsuhiko Yoshimoto and Mitsuo Itakura : ヒト・ホスホリボシルピロリン酸(PRPP)合成酵素の41kDa結合蛋白質のcDNAクローニング, 第30回日本プリン・ピリミジン代謝学会総会(東京), Mar. 1997.
227.	出原千代子, Takashi Yamaoka, Hiroyuki Iwahana, Katsuhiko Yoshimoto and Mitsuo Itakura : amidophosphoribosyltransferase(ATase)の細胞密度依存的発現を司るプロモーター領域の同定, 第30回日本プリン・ピリミジン代謝学会総会(東京), Mar. 1997.
228.	Maki Moritani, Katsuhiko Yoshimoto, Toshiaki Sano, 菊谷仁 and Mitsuo Itakura : IL-10導入膵ラ島特異Th1細胞の養子移入によるIFN-γ抑制を介するⅠ型糖尿病の遺伝子治療の動物モデル, 第26回日本免疫学会総会・学術集会(横浜), Nov. 1996.
229.	Hiroshi Bandou, Shiro Saito, 島健二, Mitsuo Itakura, Masamichi Kuwajima, Ken Saito, Haruhiko Saito, 小松まち子, 長瀬教夫, 亀山和人, 西村典三, 中西嘉巳, 山野利尚, 山崎正行, 滝下佳寛, 米田和夫, 小原卓爾, 野間善彦, Katsuhiko Yoshimoto, 矢木文和, 吉田健三, 増田和彦, 折野和人, 市川和佳 and 中矢修一郎 : 徳島県における糖尿病患者の現状, 日本糖尿病学会中国四国地方会第34回総会(宇部), Oct. 1996.
230.	Shozo Yamada, Katsuhiko Yoshimoto, 高田浩次, Mitsuo Itakura and 臼井雅昭 : 下垂体腺腫の遺伝子異常:マイクロサテライト解析によるヘテロ接合性の消失の検討, 第55回日本脳神経外科学会総会(富山), Oct. 1996.
231.	Hiroyuki Iwahana, 藤村美和, 安田后希, Setsuko Ii, Maki Moritani, Takashi Yamaoka, Katsuhiko Yoshimoto, 石塚俊治, 喜多和子, 橘正道 and Mitsuo Itakura : ヒト・ホスホリボシルピロリン酸(PRPP)合成酵素の39kDa結合蛋白質(PAP39)遺伝子のゲノム構造の解析, 第69回日本生化学会・第19回日本分子生物学会(札幌), Aug. 1996.
232.	Takashi Yamaoka, 近藤麻木, Setsuko Ii, 近藤麻木, Hiroyuki Iwahana, Katsuhiko Yoshimoto and Mitsuo Itakura : 遺伝子欠損株と導入株を用いた細胞増殖に対するプリン体de novo生合成経路の律速性, 第69回日本生化学会・第19回日本分子生物学会(札幌), Aug. 1996.
233.	藤村美和, Hiroyuki Iwahana, Setsuko Ii, 近藤麻木, Maki Moritani, 高橋陽子, Takashi Yamaoka, Katsuhiko Yoshimoto and Mitsuo Itakura : ヒトCAD cDNAのPCRを用いた遺伝子クローニング, 第69回日本生化学会・第19回日本分子生物学会(札幌), Aug. 1996.
234.	Katsuhiko Yoshimoto : (ミニシンポジウム) Ⅲ. 分子生物学の進歩と医療現場の変貌，1.医学に応用できる分子生物学的手法, 第213回徳島医学会(平成8年度夏期総会), Jul. 1996.
235.	Chisato Tanaka, Katsuhiko Yoshimoto, 木村建彦, Hiroyuki Iwahana, Shozo Yamada, Toshiaki Sano and Mitsuo Itakura : 下垂体腺腫におけるp16/CDKN2遺伝子異常の解析, 第69回日本内分泌学会学術総会(大阪), Jul. 1996.
236.	Katsuhiko Yoshimoto and 木村建彦 : シンポジウムⅢ，MEN1型の臨床像および遺伝子異常, 第69回日本内分泌学会学術総会(大阪), Jul. 1996.
237.	笹原賢司, 東きよう, 大塚理司, 田中正喜, Hiroyuki Iwahana, Katsuhiko Yoshimoto and Mitsuo Itakura : Random sequencingにより培養マウス膵ラ島B細胞より得た新規cDNA cloneの全塩基配列と臓器特異的発現, 第39回日本糖尿病学会年次学術集会(福岡), May 1996.
238.	友成章, Katsuhiko Yoshimoto, Hiroyuki Iwahana, 宮崎純一 and Mitsuo Itakura : GGAAATモチーフ(GG1とGG2)によるヒトインスリン遺伝子(INS)の転写調節, 第39回日本糖尿病学会年次学術集会(福岡), May 1996.
239.	Setsuko Ii, 田島織絵, Takashi Yamaoka, Hiroyuki Iwahana, Katsuhiko Yoshimoto and Mitsuo Itakura : ヒトアルドース還元酵素(hAR)を発現するトランスジェニックマウス(hAR-Tg)の糖尿病性蛋白尿と腎組織におけるRedox, 第39回日本糖尿病学会年次学術集会(福岡), May 1996.
240.	Maki Moritani, Katsuhiko Yoshimoto, Hiroyuki Iwahana, 菊谷仁, 宮崎純一 and Mitsuo Itakura : NOD/scidマウスを用いる膵ラ島B細胞の破壊機序を検討する動物モデルの開発, 第39回日本糖尿病学会年次学術集会(福岡), May 1996.
241.	浅原貴志, 三村康男, Setsuko Ii, 東きよう, Katsuhiko Yoshimoto and Mitsuo Itakura : S化オリゴデオキシヌクレオチドのマウス硝子体内投与後の網膜組織への移行および安定性, 第100回日本眼科学会総会(京都), May 1996.
242.	藤村美和, Hiroyuki Iwahana, 高橋陽子, Takashi Yamaoka, Katsuhiko Yoshimoto and Mitsuo Itakura : ヒトCAD cDNAのPCRを用いた遺伝子クローニング, 第29回日本プリン・ピリミジン代謝学会総会(大阪), Feb. 1996.
243.	近藤麻木, Takashi Yamaoka, Hiroyuki Iwahana, Katsuhiko Yoshimoto and Mitsuo Itakura : プリン体de novo生合成経路とサルベージ経路:両経路のkey enzymeとその細胞増殖に対する寄与, 第29回日本プリン・ピリミジン代謝学会総会(大阪), Feb. 1996.
244.	高橋陽子, Hiroyuki Iwahana, Takashi Yamaoka, Katsuhiko Yoshimoto and Mitsuo Itakura : PCR法によるヒト・アミドホスホリボシルトランスフェラーゼ(ATase)のゲノム構造の解析, 第29回日本プリン・ピリミジン代謝学会総会(大阪), Feb. 1996.
245.	関貫聖二, 浜崎房光, 松本圭三, Toshiaki Sano, Katsuhiko Yoshimoto and Hiroshi Bandou : 下垂体腺腫の増大・再発に影響を及ぼす諸因子の検討, 第6回間脳下垂体腫瘍研究会(東京), Feb. 1996.
246.	高田浩次, Shozo Yamada, Katsuhiko Yoshimoto, Toshiaki Sano, 臼井雅昭 and 寺本明 : (シンポジウム)下垂体腫瘍の分子生物学:Acrogigantismを呈した兄弟例の遺伝子解析, 第6回間脳下垂体腫瘍研究会(東京), Feb. 1996.
247.	Katsuhiko Yoshimoto, Chisato Tanaka, 木村建彦, 大倉敏裕, Hiroyuki Iwahana, 山田正三, Toshiaki Sano, Shiro Saito and Mitsuo Itakura : (シンポジウム)下垂体腺腫におけるP16/CDKN2遺伝子変異の解析, 第6回間脳下垂体腫瘍研究会(東京), Feb. 1996.
248.	Hiroyuki Iwahana, 藤村美和, 高橋陽子, Katsuhiko Yoshimoto and Mitsuo Itakura : 内部標識による蛍光PCR-SSCP法を用いた遺伝子解析, 第16回日本分子生物学会年会(名古屋), Dec. 1995.
249.	Maki Moritani, Katsuhiko Yoshimoto, Toshiaki Sano, 菊谷仁 and Mitsuo Itakura : IL-10を発現する膵ラ島B細胞特異的Th1細胞の幼若NODマウスヘの養子移入による糖尿病発症の抑制, 第25回日本免疫学会総会・学術集会(福岡), Nov. 1995.
250.	Chisato Tanaka, Katsuhiko Yoshimoto, 木村建彦, 大倉敏裕, Hiroyuki Iwahana, Shiro Saito and Mitsuo Itakura : 下垂体腺腫におけるRET遺伝子の変異, 第68回日本内分泌学会秋期学術大会(山梨), Oct. 1995.
251.	木村建彦, Katsuhiko Yoshimoto, Chisato Tanaka, Hiroyuki Iwahana, Shiro Saito and Mitsuo Itakura : 副腎褐色細胞腫におけるRET遺伝子コドン768の変異, 第68回日本内分泌学会秋期学術大会(山梨), Oct. 1995.
252.	Katsuhiko Yoshimoto, Chisato Tanaka, 木村建彦, 本田壮一, Hiroyuki Iwahana, Shozo Yamada, Toshiaki Sano and Mitsuo Itakura : 孤発性下垂体腺腫におけるマイクロサテライト解析による第11染色体のヘテロ接合性消失の検討, 第68回日本内分泌学会秋期学術大会(山梨), Oct. 1995.
253.	Hiroyuki Iwahana, Rumi Katashima, Takashi Yamaoka, 本田壮一, Katsuhiko Yoshimoto and Mitsuo Itakura : ット・アミドホスホリボシルトランスフェラーゼに対するアンチセンスオリゴデオキシヌクレオチドの細胞増殖抑制効果について, 第54回日本癌学会総会(京都), Oct. 1995.
254.	木村建彦, Katsuhiko Yoshimoto, Chisato Tanaka, Hiroyuki Iwahana, Toshiaki Sano, 宮内昭, Shiro Saito and Mitsuo Itakura : 副甲状腺におけるRET遺伝子の変異, 第54回日本癌学会総会(京都), Oct. 1995.
255.	Takashi Yamaoka, 本田壮一, Hiroyuki Iwahana, Katsuhiko Yoshimoto and Mitsuo Itakura : アミドホスホリボシルトランスフェラーゼ(ATase)の細胞周期および細胞密度依存性の発現調節, 第68回日本生化学会大会(仙台), Sep. 1995.
256.	高橋陽子, Hiroyuki Iwahana, Takashi Yamaoka, Katsuhiko Yoshimoto and Mitsuo Itakura : YACライブラリーを用いたPCR法によるヒト・アミドホスホリボシルトランスフェラーゼ(ATase)のゲノム構造の解析, 第68回日本生化学会大会(仙台), Sep. 1995.
257.	Katsuhiko Yoshimoto, 木村建彦, 新谷保実, Hiroyuki Iwahana and Mitsuo Itakura : 多発性内分泌腫瘍症(MEN)における耐糖能異常, 第27回日本内科学会四国地方会(高知), Jun. 1995.
258.	木村建彦, Katsuhiko Yoshimoto, Chisato Tanaka, 濱口幸子, Hiroyuki Iwahana, Toshiaki Sano, 宮内昭, Shiro Saito and Mitsuo Itakura : 副甲状腺腫瘍におけるRET遺伝子の変異, 第68回日本内分泌学会学術総会(東京), Jun. 1995.
259.	Katsuhiko Yoshimoto : (シンポジウム)「甲状腺細胞制御系とその異常」，甲状腺髄様癌におけるRET遺伝子の変異, 第68回日本内分泌学会学術総会(東京), Jun. 1995.
260.	Katsuhiko Yoshimoto : 地方自治体における糖尿病教育-徳島市における実施状況-, 第38回日本糖尿病学会年次学術集会(大宮), May 1995.
261.	Maki Moritani, Katsuhiko Yoshimoto, Hiroyuki Iwahana, Hiroyuki Iwahana, Toshiaki Sano, 菊谷仁 and Mitsuo Itakura : (ワークショップ) 8. 糖尿病-個体レベルの分子生物学的アプローチIL-10遺伝子を導入したリンパ球を用いるI型糖尿病の体細胞遺伝子治療への取り組み, 第38回日本糖尿病学会年次学術集会(大宮), May 1995.
262.	Maki Moritani, Katsuhiko Yoshimoto, Hiroyuki Iwahana, Hiroyuki Iwahana, Toshiaki Sano, 菊谷仁 and Mitsuo Itakura : IL-10を発現する膵ラ島B細胞特異的T細胞の幼若NODマウスヘの養子移入による糖尿病発症の抑制効果, 第38回日本糖尿病学会年次学術集会(大宮), May 1995.
263.	濱口幸子, Katsuhiko Yoshimoto, Toshiaki Sano, Hiroyuki Iwahana, Yoshio Hayashi and Mitsuo Itakura : IFN-γを膵ランゲルハンス島(膵ラ島)A細胞で発現するトランスジェニックマウス(IFN-γ Tg)における耐糖能異常の出現, 第38回日本糖尿病学会年次学術集会(大宮), May 1995.
264.	友成章, Katsuhiko Yoshimoto, Hiroyuki Iwahana and Mitsuo Itakura : ヒトインスリン遺伝子(INS)のグルコース(Glc)応答性の転写調節に関与するDNAエレメントの検討, 第38回日本糖尿病学会年次学術集会(大宮), May 1995.
265.	Setsuko Ii, 大田美香, Takashi Yamaoka, Katsuhiko Yoshimoto, Hiroyuki Iwahana and Mitsuo Itakura : ヒトアルドース還元酵素(hAR)を発現するトランスジェニックマウス(hAR-Tg)の糖尿病状態におけるポリオール代謝, 第38回日本糖尿病学会年次学術集会(大宮), May 1995.
266.	堀江千昌, 堀江貴浩, 安田貢, 柴昌子, 横井孝文, 大黒隆司, 西角智子, 鎌村真子, 松永裕子, Hirohito Honda, Ichiro Shimizu, Susumu Ito, Hiroyuki Iwahana, Katsuhiko Yoshimoto and Mitsuo Itakura : 肝癌組織におけるC型肝炎ウイルス(HCV)ゲノムの高変異性, 第92回日本内科学会総会講演会(名古屋), Apr. 1995.
267.	Katsuhiko Yoshimoto, Hiroyuki Iwahana and Mitsuo Itakura : 糖尿病の体細胞遺伝子治療におけるHerpes Simplex Virus-thymidine kinase(HSV-tk)遺伝子を用いた安全装置の開発, 第92回日本内科学会総会講演会(名古屋), Apr. 1995.
268.	高橋陽子, Hiroyuki Iwahana, 東きよう, Rumi Katashima, 辻澤利行, 本田壮一, Takashi Yamaoka, Katsuhiko Yoshimoto and Mitsuo Itakura : ラット・アミドホスホリボシルトランスフェラーゼ(ATase)のゲノム構造の解析, 第28回日本プリン・ピリミジン代謝学会総会(東京), Feb. 1995.
269.	Hiroyuki Iwahana, 高橋陽子, 東きよう, Rumi Katashima, 辻澤利行, 本田壮一, Takashi Yamaoka, Katsuhiko Yoshimoto and Mitsuo Itakura : ラット・アミドホスホリボシルトランスフェラーゼ(ATase)のゲノム構造の解析, 第28回日本プリン・ピリミジン代謝学会総会(東京), Feb. 1995.
270.	Rumi Katashima, Hiroyuki Iwahana, Takashi Yamaoka, Katsuhiko Yoshimoto and Mitsuo Itakura : ラット・アミドホスホリボシルトランスフェラーゼ(ATase)に対するアンチセンスオリゴデオキシヌクレオチドの細胞増殖抑制効果について, 第28回日本プリン・ピリミジン代謝学会総会(東京), Feb. 1995.
271.	Takashi Yamaoka, 本田壮一, Hiroyuki Iwahana, Katsuhiko Yoshimoto and Mitsuo Itakura : アミドホスホリボシルトランスフェラーゼ(ATase)の細胞周期および細胞密度依存性の発現調節, 第28回日本プリン・ピリミジン代謝学会総会(東京), Feb. 1995.
272.	Hiroyuki Iwahana, Katsuhiko Yoshimoto and Mitsuo Itakura : バイオテクノロジーセミナー「最新技術の分子生物学への応用」，MF-PCR-SSCPによる遺伝子変異の解析, 第17回日本分子生物学会年会 (神戸), Dec. 1994.
273.	Hiroyuki Iwahana, 東きよう, 高橋陽子, Rumi Katashima, Katsuhiko Yoshimoto and Mitsuo Itakura : MF-PCR-SSCP:多種類の蛍光色素とコンピューター画像を用いた解析, 第17回日本分子生物学会年会(神戸), Dec. 1994.
274.	Maki Moritani, Katsuhiko Yoshimoto, 田代文, 橋本力, 宮崎純一, Hiroyuki Iwahana, Yoshio Hayashi, Toshiaki Sano and Mitsuo Itakura : 膵ランゲルハンス島(膵島)A細胞に発現させたIL-10による膵島炎促進の系統依存性, 第24回日本免疫学会総会・学術集会(京都), Nov. 1994.
275.	濱口幸子, Katsuhiko Yoshimoto, 小海康夫, Toshiaki Sano, Hiroyuki Iwahana, Yoshio Hayashi and Mitsuo Itakura : IFNγを膵ランゲルハンス島(膵ラ島)A細胞で発現するトランスジェニックマウス(IFNγTg)における耐糖能異常の出現, 第67回日本内分泌学会秋期学術大会(広島), Nov. 1994.
276.	Chisato Tanaka, Katsuhiko Yoshimoto, 木村建彦, Hiroyuki Iwahana, 宮内昭 and Mitsuo Itakura : 多発性内分泌腫瘍症2B型と孤発性の褐色細胞腫におけるRET遺伝子チロシンキナーゼ部位の変異, 第67回日本内分泌学会秋期学術大会(広島), Nov. 1994.
277.	閔洪中, Katsuhiko Yoshimoto, Hiroyuki Iwahana, Mitsuo Itakura, 北浦敬介, 長根芳文 and Keisuke Izumi : ニトロサミンによるラット肝・腎腫瘍のp53遺伝子の変異, 第53回日本癌学会総会(名古屋), Oct. 1994.
278.	田中正喜, 濱口幸子, 東きよう, Katsuhiko Yoshimoto, Hiroyuki Iwahana and Mitsuo Itakura : Random sequencingによる大腸癌細胞株(colo205)の遺伝子解析, 第53回日本癌学会総会(名古屋), Oct. 1994.
279.	Katsuhiko Yoshimoto, 村上理衣, Maki Moritani, 大田美香, Hiroyuki Iwahana and Mitsuo Itakura : 糖尿病の体細胞遺伝子治療におけるHerpes Simplex Virus thymidine kinase(HSV-tk)遺伝子を用いた安全装置の開発, 第32回日本糖尿病学会中国四国地方会(出雲), Oct. 1994.
280.	Hiroyuki Iwahana, Katsuhiko Yoshimoto and Mitsuo Itakura : テクニカルセミナー「生化学分析における自動化システムの最新技術」，多種類の蛍光色素とコンピューター画像を用いたMF-PCR-SSCP解析, 第67回日本生化学会大会 (大阪), Sep. 1994.
281.	本田壮一, Hiroyuki Iwahana, 辻澤利行, 安井理恵, Maki Moritani, Takashi Yamaoka, Katsuhiko Yoshimoto and Mitsuo Itakura : ラット・アミドホスホリボシルトランスフェラーゼ(ATase)遺伝子のゲノム構造と細胞周期依存性発現, 第67回日本生化学会大会(大阪), Sep. 1994.
282.	Hiroyuki Iwahana, 岡純, Noriko Mizusawa, Rumi Katashima, 村上大輔, Eiji Kudo, Setsuko Ii, Takashi Yamaoka, Katsuhiko Yoshimoto, Edward W. Holmes and Mitsuo Itakura : ヒト・アミドホスホリボシルトランスフェラーゼ(ATase)蛋白の精製とcDNAクローニング, 第67回日本生化学会大会(大阪), Sep. 1994.
283.	Katsuhiko Yoshimoto : (シンポジウム)「癌とホルモン」，内分泌腺の腫瘍化に関する遺伝子異常, 第67回日本内分泌学会学術総会(長崎), Jun. 1994.
284.	友成章, Katsuhiko Yoshimoto, 田中正喜, Hiroyuki Iwahana and Mitsuo Itakura : MIN6におけるヒトインスリン遺伝子(INS) のグルコース(Glc)応答性の転写調節, 第67回日本内分泌学会学術総会(長崎), Jun. 1994.
285.	Katsuhiko Yoshimoto, Maki Moritani, 田代文, 橋本力, 宮崎純一, Setsuko Ii, Eiji Kudo, Hiroyuki Iwahana, Yoshio Hayashi, Toshiaki Sano and Mitsuo Itakura : 膵ランゲルハンス島A細胞にIL-10を発現させたトランスジェニックNODマウスにおける糖尿病発症の促進, 第67回日本内分泌学会学術総会(長崎), Jun. 1994.
286.	Mitsuo Itakura, 大田美香, Setsuko Ii, Katsuhiko Yoshimoto, Hiroyuki Iwahana, 高橋幸男 and 田野保雄 : (サテライトシンボジウム)ヒトアルドース還元酵素(AR)を発現するトランスジェニックマウス(AR-Tg)における糖尿病性合併症の解析, 第37回日本糖尿病学会年次学術集会(徳島), May 1994.
287.	大田美香, Setsuko Ii, Katsuhiko Yoshimoto, Hiroyuki Iwahana, Mitsuo Itakura, 高橋幸男 and 田野保雄 : ヒトアルドース還元酵素(AR)を発現するトランスジェニックマウス(AR-Tg)における糖尿病性合併症の解析, 第37回日本糖尿病学会年次学術集会(徳島), May 1994.
288.	友成章, Katsuhiko Yoshimoto, 田中正喜, Hiroyuki Iwahana and Mitsuo Itakura : 成長ホルモン(GH)の発現系を用いたヒトインスリン遺伝子の転写調節の検討, 第37回日本糖尿病学会年次学術集会(徳島), May 1994.
289.	Katsuhiko Yoshimoto, Hiroyuki Iwahana and Mitsuo Itakura : インスリノーマにおける遺伝子異常の解析, 第37回日本糖尿病学会年次学術集会(徳島), May 1994.
290.	Maki Moritani, Katsuhiko Yoshimoto, 田代文, 橋本力, 宮崎純一, Setsuko Ii, Eiji Kudo, Hiroyuki Iwahana, Yoshio Hayashi, Toshiaki Sano and Mitsuo Itakura : (膵ランゲルハンス島(膵ラ島)A細胞にIL-10を発現させたトランスジェニックマウス(Tg)における糖尿病発症の促進, 第37回日本糖尿病学会年次学術集会(徳島), May 1994.
291.	Mitsuo Itakura, Maki Moritani, Katsuhiko Yoshimoto, 田代文, 橋本力, 宮崎純一, Setsuko Ii, Eiji Kudo, Hiroyuki Iwahana, Yoshio Hayashi and Toshiaki Sano : (ワークショップ)「トランスジェニック動物の糖尿病学への貢献」，IL-10を膵ラ氏島A細胞で発現するNODトランスジェニックマウス, 第37回日本糖尿病学会年次学術集会(徳島), May 1994.
292.	本田壮一, Hiroyuki Iwahana, 辻澤利行, 安井理恵, Maki Moritani, Katsuhiko Yoshimoto and Mitsuo Itakura : ラット・アミドホスホリボシルトランスフェラーゼ(ATase)mRNAの細胞周期依存性の発現とその調節, 第27回日本プリン・ピリミジン代謝学会総会(名古屋), Feb. 1994.
293.	辻澤利行, Hiroyuki Iwahana, 安井理恵, 本田壮一, Katsuhiko Yoshimoto and Mitsuo Itakura : ラット・アミドホスホリボシルトランスフェラーゼ(ATase, EC 2.4.2.14)ゲノムDNAのPCRを用いた遺伝子クローニング, 第27回日本プリン・ピリミジン代謝学会総会(名古屋), Feb. 1994.
294.	Hiroyuki Iwahana, 岡純, Noriko Mizusawa, Rumi Katashima, 村上大輔, Eiji Kudo, Setsuko Ii, Katsuhiko Yoshimoto, Edward W. Holmes and Mitsuo Itakura : ヒト・アミドホスホリボシルトランスフェラーゼ(ATase)蛋白の精製とcDNAクローニング, 第27回日本プリン・ピリミジン代謝学会総会(名古屋), Feb. 1994.
295.	柴田泰伸, 若槻真紀, 加部一行, Masashi Akaike, 新谷保実, Shiro Saito, Katsuhiko Yoshimoto, 川人智久, 筑後文雄, Takaki Hori and Tetsuya Kitagawa : 僧帽弁に粘液腫様変性が認められた先端巨大症合併MEN 1型の1例, 第208回徳島医学会(平成5年度冬期総会), Jan. 1994.
296.	安井理恵, Hiroyuki Iwahana, Setsuko Ii, 辻澤利行, 本田壮一, 田中正喜, Katsuhiko Yoshimoto and Mitsuo Itakura : ラット・アミドホスホリボシルトランスフェラーゼ(ATase)のcDNAクローニング, 第208回徳島医学会(平成5年度冬期総会), Jan. 1994.
297.	田中正喜, Rumi Katashima, Noriko Mizusawa, 村上大輔, 大塚理司, Katsuhiko Yoshimoto, Hiroyuki Iwahana and Mitsuo Itakura : Random sequencingによるマウス膵ランゲルハンス島B細胞(膵B細胞)の発現遺伝子群の解析, 第16回日本分子生物学会年会(千葉), Dec. 1993.
298.	Hiroyuki Iwahana, Katsuhiko Yoshimoto, Noriko Mizusawa, Eiji Kudo and Mitsuo Itakura : 多種類の蛍光色素とコンピューター画像を用いたMF-PCR-SSCP解析, 第16回日本分子生物学会年会(千葉), Dec. 1993.
299.	古味勝美, 堺恵理子, 美馬ミヨコ, 石原節子, 桜木照恵, 佐古多賀子, 井村由美子, 小笠恵子 and Katsuhiko Yoshimoto : 徳島市における糖尿病講座の実施状況, 第31回日本糖尿病学会中国四国地方会(松山), Nov. 1993.
300.	Katsuhiko Yoshimoto, Hiroyuki Iwahana, 村上理衣, 濱口幸子, Mitsuo Itakura, 久保克之 and Hiroshi Bandou : インスリノーマにおける遺伝子異常の解析, 第31回日本糖尿病学会中国四国地方会(松山), Nov. 1993.
301.	Maki Moritani, Katsuhiko Yoshimoto, 田代文, 橋本力, 宮崎純一, Setsuko Ii, Eiji Kudo, 岩花弘之, Yoshio Hayashi, Toshiaki Sano and Mitsuo Itakura : 膵ランゲルハンス島(膵ラ島)A細胞からIL-10を分泌するNODトランスジェニックマウス(Tg)における膵ラ島B細胞の自己免疫性破壊の促進, 第23回日本免疫学会総会・学術集会(仙台), Nov. 1993.
302.	Katsuhiko Yoshimoto, 岩花弘之, Toshiaki Sano and Mitsuo Itakura : マイクロサテライト解析による多発性内分泌腫瘍症1型(MEN I型)腫瘍における第11染色体欠失の検出, 第66回日本内分泌学会秋期学術大会(青森), Oct. 1993.
303.	閔洪中, Keisuke Izumi, Eiji Kudo, Katsuhiko Yoshimoto, 岩花弘之 and Mitsuo Itakura : LECラットの自然発生およびニトロサミン誘発肝腫瘍におけるp53およびras遺伝子の解析, 第52回日本癌学会総会(仙台), Oct. 1993.
304.	Katsuhiko Yoshimoto, 岩花弘之, Toshiaki Sano and Shiro Saito : マイクロサテライト解析による多発性内分泌腫瘍症1型腫瘍でのヘテロ接合性消失の検出, 第52回日本癌学会総会(仙台), Oct. 1993.
305.	新谷保実, Katsuhiko Yoshimoto, 金崎淑子, Masashi Akaike, 堀江秀茂, 細井恵美子, 横越浩, Hiroshi Bandou, 山崎柳一, 依田啓司, 松本圭蔵, Toshiaki Sano and Shiro Saito : MEN I型のGHRH産生膵腫瘍に見い出されたGH分泌下垂体腫瘍, 第66回日本内分泌学会学術総会(金沢), Jun. 1993.
306.	Katsuhiko Yoshimoto, 岩花弘之, Mitsuo Itakura, Toshiaki Sano, 久保克之, Shiro Saito and 露口勝 : 多発性内分泌腫瘍症2B型(MEN2B)の本邦における実態調査と腫瘍における遺伝子異常の解析, 第66回日本内分泌学会学術総会(金沢), Jun. 1993.
307.	村上理衣, Katsuhiko Yoshimoto, 大田美香, 岩花弘之, 中内啓光 and Mitsuo Itakura : 糖尿病の体細胞遺伝子治療法における分子生物学的安全装置の開発, 第36回日本糖尿病学会年次学術集会(仙台), May 1993.
308.	岩花弘之, Takashi Yamaoka, 水谷正一, Noriko Mizusawa, Eiji Kudo, Setsuko Ii, Katsuhiko Yoshimoto and Mitsuo Itakura : ラット・アミドホスホリボシルトランスフェラーゼ(ATase)酵素蛋白のアミノ酸配列とmRNAの組織別発現, 第26回日本プリン・ピリミジン代謝学会総会(仙台), Feb. 1993.
309.	岩花弘之, Noriko Mizusawa, Eiji Kudo, Setsuko Ii, Katsuhiko Yoshimoto and Mitsuo Itakura : ラット・アミドホスホリボシルトランスフェラーゼ(ATase)cDNAのPCRを用いた遺伝子クローニング, 第26回日本プリン・ピリミジン代謝学会総会(仙台), Feb. 1993.
310.	Noriko Mizusawa, 岩花弘之, Takashi Yamaoka, Eiji Kudo, Setsuko Ii, Katsuhiko Yoshimoto and Mitsuo Itakura : ラット・アミドホスホリボシルトランスフェラーゼ(ATase)のcDNAクローニング, 第64回日本生化学会大会(福岡), Oct. 1992.
311.	福田あゆみ, Katsuhiko Yoshimoto, 岩花弘之, Toshiaki Sano, Shiro Saito and Mitsuo Itakura : 内分泌腫瘍におけるrasおよびp53遺伝子異常の同定, 第65回日本内分泌学会総会(徳島), Jun. 1992.
312.	友成章, 宇野由佳, 重清俊雄, Shiro Saito, 岩花弘之, Katsuhiko Yoshimoto and Mitsuo Itakura : 先天性Antithrombin(AT)III欠乏症I型2家系におけるATIII遺伝子のLeu140およびArg197からstop codonへの新しい点突然変異, 第54回日本血液学会総会(東京), Apr. 1992.
313.	岩花弘之, Katsuhiko Yoshimoto, 重清俊雄, 白神あきら, Shiro Saito and Mitsuo Itakura : プロトロンビン異常症と低下症のダブルヘテロ接合体のPCR-SSCP法による遺伝子解析, 第89回日本内科講演会(東京), Apr. 1992.
314.	岩花弘之, Katsuhiko Yoshimoto, 重清俊雄, 白神あきら, Shiro Saito and Mitsuo Itakura : プロトロンビン異常症とプロトロンビン低下症のダブルヘテロ接合体のPCR-SSCP法による遺伝子解析, 第34回日本先天性代謝異常学会(東京), Nov. 1991.
315.	Katsuhiko Yoshimoto, 岩花弘之, Shiro Saito and Mitsuo Itakura : 内分泌腺腫瘍におけるras, Gsα, p53遺伝子の解析, 第64回日本内分泌学会秋期学術大会(前橋), Nov. 1991.
316.	Katsuhiko Yoshimoto, 岩花弘之, 久保克之, 露口勝, Shiro Saito and Mitsuo Itakura : 甲状腺腫瘍におけるras, gsp, gip2, p53遺伝子の解析, 第50回日本癌学会総会(東京), Sep. 1991.
317.	張辰宇, Katsuhiko Yoshimoto, 横越浩, 高田幸伸, Hiroshi Bandou and Shiro Saito : ヒトACTH産生培養細胞(COR-L103)におけるACTHの分泌動態と各種刺激因子に対する反応, 第64回日本内分泌学会学術総会(東京), Jun. 1991.
318.	Katsuhiko Yoshimoto, 久保克之, Mitsuo Itakura, 岩花弘之, 露口勝, Shiro Saito and Mitsuo Itakura : PCR-SSCP法による甲状腺腫瘍におけるras遺伝子の解析, 第64回日本内分泌学会学術総会(東京), Jun. 1991.
319.	岩花弘之, Katsuhiko Yoshimoto, Mitsuo Itakura, 重清俊雄, Shiro Saito and 白神あきら : プロトロンビン・トクシマのPCR-SSCP法による遺伝子解析, 第88回日本内科学会総会(京都), Apr. 1991.
320.	長宅芳男, 橋本浩三, 平沢龍登, 鈴木信也, 太田善介, 大橋輝久, 大枝忠史, 大森弘之, 小松原正吉, 村上正和, Katsuhiko Yoshimoto, 脇谷勇夫 and 三宅淳史 : MEN 2A (Sipple症候群)の一例, 第63回日本内分泌学会秋期学術大会(岐阜), Nov. 1990.
321.	横井健治, Katsuhiko Yoshimoto, 鈴木まどか, Hiroshi Bandou, 山崎柳一, Shiro Saito and Toshiaki Sano : 家族性多発性内分泌腫瘍症I型の一家系二症例, 第63回日本内分泌学会秋期学術大会(岐阜), Nov. 1990.
322.	久保克之, Katsuhiko Yoshimoto, 横越浩, Shiro Saito and 露口勝 : 甲状腺腫瘍における対立遺伝子の欠失, 第63回日本内分泌学会秋期学術大会(岐阜), Nov. 1990.
323.	Katsuhiko Yoshimoto, 坂本幸裕, 横井健治, 久保克之, Hiroshi Bandou, 山崎柳一 and Shiro Saito : ソマトスタチン・アナログによりカルシトニン分泌抑制のみられた多発性内分泌腺腫瘍症(MEN)2B型の一例, 第63回日本内分泌学会秋期学術大会(岐阜), Nov. 1990.
324.	河野宗夫, 大下和司, 三木仁司, 井上洋行, 福井康雄, 笹三徳, Yasumasa Monden, Katsuhiko Yoshimoto and Toshiaki Sano : 上皮小体機能亢進症の手術を行ったMEN type1の1家系 (母，娘), 第23回甲状腺外科検討会(前橋), Sep. 1990.
325.	久保克之, 横越浩, Katsuhiko Yoshimoto, Shiro Saito and 露口勝 : 甲状腺腫瘍における遺伝子異常の解析, 第49回日本癌学会総会(東京), Jul. 1990.
326.	坂本幸裕, Katsuhiko Yoshimoto, 横井健治, 久保克之, Hiroshi Bandou, 山崎柳一 and Shiro Saito : 多発性内分泌腺腫瘍症(MEN)2B型の一症例, 第62回日本内科学会四国地方会(徳島), Jun. 1990.
327.	久保克之, 横越浩, Katsuhiko Yoshimoto, Shiro Saito and 露口勝 : 甲状腺腫瘍における遺伝子異常, 第63回日本内分泌学会学術総会, May 1990.
328.	Katsuhiko Yoshimoto : (シンポジウム) 多発性内分泌腺腫瘍症(MEN)の基礎と臨床 1. MEN I型の臨床, 第63回日本内分泌学会学術総会, May 1990.
329.	宇野由佳, 重清俊雄, Katsuhiko Yoshimoto, Shiro Saito and 猪本享司 : 先天性plasminogen欠乏症の1家系におけるplasminogenの性状と遺伝子異常に関する検討, 第52回日本血液学会総会(東京), Mar. 1990.
330.	Katsuhiko Yoshimoto : (ミニシンポジウム)トピックス1 多発性内分泌腺腫瘍症I型における遺伝子異常, 第200回徳島医学会(平成元年度冬期総会), Jan. 1990.
331.	大幸貴美子, Katsuhiko Yoshimoto, 川井尚臣, 淡河洋一, 横田武彦 and Shiro Saito : 血液透析中の患者にみられた筋萎縮性側索硬化症, 第47回日本神経学会中国四国地方会(岡山), Dec. 1989.
332.	岩花弘之, 折田正人, 林健志, 金沢浩, Katsuhiko Yoshimoto, Shiro Saito and 関谷剛男 : HRAS1遺伝子の新しい繰り返し配列多型, 第47回日本癌学会総会(名古屋), Oct. 1989.
333.	井出真, Hiroshi Bandou, 横越浩, 西田善彦, 山崎柳一, Shiro Saito, 片上秀喜 and Katsuhiko Yoshimoto : 肺転移を伴った卵巣類内膜癌によるHumoral Hypercalcemia of Malignancy (HHM) の一例, 第199回徳島医学会 (平成2年度夏期総会), Jul. 1989.
334.	横越浩, 久保克之, Katsuhiko Yoshimoto and Shiro Saito : 褐色細胞腫における腫瘍化機構, 第62回日本内分泌学会学術総会 (東京), Jun. 1989.
335.	久保克之, 高田幸伸, Katsuhiko Yoshimoto, 山崎柳一, 住友正幸, 桧沢一夫, 中村由利子, 右見正夫 and Shiro Saito : 異所性ACTH症候群の一剖検例 -POMC遺伝子の解析-, 第60回日本内科学会四国地方会 (高松), May 1989.
336.	堀内宣昭, 岡川和人, Katsuhiko Yoshimoto, 小阪昌明 and Shiro Saito : MDS症例におけるJH, Tcbeta, c-fms遺伝子による腫瘍細胞クロ-ンの解析, 第51回日本血液学会総会(前橋), Apr. 1989.
337.	横越浩, 久保克之, Katsuhiko Yoshimoto and Shiro Saito : 褐色細胞腫における第11番染色体の対立遺伝子のヘテロ接合性の消失, 第86回日本内科学会講演会(京都), Apr. 1989.
338.	重清俊雄, 宇野由佳, Katsuhiko Yoshimoto, Shiro Saito, 藤野修 and 斎藤誠一郎 : DNAプロ-ブを用いて保因者診断を行った血友病Aの潜在保因者の1例, 第198回徳島医学会(平成2年度冬期総会), Jan. 1989.
339.	溝渕樹, 小島章裕, 近藤由子, 西田善彦, Katsuhiko Yoshimoto, 山崎柳一, Shiro Saito and 三橋信次 : 部分的尿崩症と考えられる2例, 第198回徳島医学会(平成2年度冬期総会), Jan. 1989.
340.	Shuji Ozaki, 中尾克之, 堀内宣昭, 宮本貴由, 高木美穂, Katsuhiko Yoshimoto, 岡川和人, 小阪昌明 and Shiro Saito : RA様症状と高gamma-グロブリン血症を合併し，抗核抗体陽性であったT8-CLL症例の末梢血リンパ球性状の検討, 第30回日本臨床血液学会 (岡山), Nov. 1988.
341.	Katsuhiko Yoshimoto, 岩花弘之, 横越浩, 山崎柳一, 坂井秀樹, 手束卯一郎, 岡川和人, 高橋正倫 and Shiro Saito : 異所性PTH産生により高Ca血症をきたしたと考えられる肺癌の1例, 第61回日本内分泌学会秋期学術大会(大阪), Nov. 1988.
342.	久保克之, Katsuhiko Yoshimoto, 山崎柳一, 住友正幸, 桧沢一夫, 中村由利子, 右見正夫 and Shiro Saito : 糖尿病を合併した異所性ACTH症候群の一剖検例, 第26回日本糖尿病学会中国四国地方会(広島), Oct. 1988.
343.	岩花弘之, 折田正人, 金沢浩, 林健志, Katsuhiko Yoshimoto, Shiro Saito and 関谷剛男 : 一本鎖DNAの電気泳動における移動度の差を利用したDNA多型の検出, 第46回日本癌学会総会(東京), Sep. 1988.
344.	横越浩, Katsuhiko Yoshimoto, 関谷剛男 and Shiro Saito : 褐色細胞腫における遺伝子異常の分析, 第46回日本癌学会総会(東京), Sep. 1988.
345.	宇野由佳, 重清俊雄, Katsuhiko Yoshimoto, 小阪昌明, Shiro Saito and 仁木俊介 : 抗けいれん剤を約20年間服用中にサルコイド-シスを発症した一例, 第197回徳島医学会(平成元年度夏期総会), Jul. 1988.
346.	Katsuhiko Yoshimoto, 横越浩, 山崎柳一 and Shiro Saito : 多発性内分泌腫瘍症(MEN)に発生した腫瘍における遺伝子異常について, 第85回日本内科学会講演会(仙台), Mar. 1988.
347.	松本直也, Katsuhiko Yoshimoto, 岡川和人, 小阪昌明, 川井尚臣 and Shiro Saito : Vindesineにより紅皮症を来したと思われるHodgkin病の一例, 第196回徳島医学会(昭和63年度冬期総会), Jan. 1988.
348.	高木美穂, 西田善彦, 山崎柳一, Katsuhiko Yoshimoto, 川井尚臣 and Shiro Saito : 痴呆を主症状とした multiple endocrine neoplasia (MEN) type 1の一例, 第196回徳島医学会(昭和63年度冬期総会), Jan. 1988.
349.	Katsuhiko Yoshimoto, Shiro Saito, 山崎柳一 and Haruhiko Saito : GHRH産生腫瘍におけるGHRHの性状と遺伝子発現, 厚生省がん研究助成金:腫瘍におけるホルモン産生遺伝子の発現機構と腫瘍細胞の機能分化に関する研究昭和61年度班会議, Dec. 1987.
350.	Hiroshi Bandou, 山崎柳一, 山崎保寛, Katsuhiko Yoshimoto and Shiro Saito : LHRHのパルス投与が有効であった視床下部性性腺機能低下症の一例, 第57回日本内科学会中国四国地方会(出雲), Nov. 1987.
351.	Katsuhiko Yoshimoto, 飯塚真由, 岩花弘之, 山崎柳一, 齋藤晴比彦, 齋藤史郎 and 関谷剛男 : 多発性内分泌腺腫症(MEN) 1型に発生した膵腫瘍での第11番染色体短腕領域での対立遺伝子欠損, 第46回日本癌学会総会(東京), Sep. 1987.
352.	飯塚真由, Katsuhiko Yoshimoto, 大木操, 広橋説雄 and 関谷剛男 : ヒト肺巨細胞癌Lu65におけるc-myc遺伝子5'上流の二重の遺伝子再編成, 第46回日本癌学会総会(東京), Sep. 1987.
353.	Katsuhiko Yoshimoto, 白石昌彦, 飯塚真由, 広橋説雄 and 関谷剛男 : ヒト肺巨細胞がん細胞(Lu65)におけるc-myc遺伝子の再編成とその発現, 第58回日本遺伝学会・第9回日本分子生物学会合同年会(名古屋), Dec. 1986.
354.	Katsuhiko Yoshimoto, 白石昌彦, 関谷剛男, 白石昌彦, 広橋説雄, 下里幸雄, 蒲生忍 and 清水信義 : ヒト肺巨細胞癌細胞(Lu65)におけるc-myc遺伝子の再編成, 第45回日本癌学会総会(札幌), Dec. 1986.
355.	Katsuhiko Yoshimoto, 白石昌彦, 関谷剛男, 広橋説雄, 下里幸雄, 蒲生忍 and 清水信義 : ヒト肺巨細胞癌細胞(Lu65)におけるc-myc遺伝子の再編成, 第45回日本癌学会総会(札幌), Oct. 1986.
356.	Katsuhiko Yoshimoto, 広橋説雄 and 関谷剛男 : ヒト肺がんにおけるc-myc mRNA増大, 第8回日本分子生物学会年会(東京), Dec. 1985.
357.	関谷剛男, 金沢浩, Katsuhiko Yoshimoto, 白石昌彦 and 伏見昌子 : ヒトc-Ha-ras-1遺伝子の発現と細胞のがん化, 第58回日本生化学会大会(仙台), Sep. 1985.
358.	Katsuhiko Yoshimoto, 井口敬一, 星島康男, 齋藤芳国, 小阪昌明, 白神あきら, Shiro Saito, 桑村康子 and Kunio Ii : 自己免疫性溶血性貧血(AIHA)の経過中に発症したマクログロブリン血症の一剖検例, 第51回日本内科学会中国四国地方会(高松), Nov. 1984.
359.	Katsuhiko Yoshimoto, 中村敏一, 新見伸吾 and Akira Ichihara : 成熟ラット初代肝細胞におけるG6PDH mRNAのホルモン調節, 第56回日本生化学会大会(福岡), Sep. 1983.
360.	Katsuhiko Yoshimoto, 田村克也, 小松まち子, 池田峰子, 三橋信次, 伊勢浩, 重清俊雄, 川内茂徳, 白神あきら, Shiro Saito and 吉田全夫 : 血小板減少症を伴った原発性肺高血圧症の一例, 第187回徳島医学会(昭和58年度夏期総会), Jul. 1983.
361.	中村敏一, Katsuhiko Yoshimoto and Akira Ichihara : 初代肝培養細胞を用いた細胞間相互作用の生化学的研究, 第35回日本細胞生物学会(福岡), Nov. 1982.
362.	中村敏一, Katsuhiko Yoshimoto, Yumiko Tomita and Akira Ichihara : 初代肝培養細胞を用いた細胞間相互作用の生化学的研究:肝細胞の細胞密度依存性調節, 第55回日本生化学会大会(豊中), Oct. 1982.
363.	Katsuhiko Yoshimoto, 中村敏一 and Akira Ichihara : 初代肝培養細胞を用いたEGFによるG6PDH誘導と脂質代謝ならびに細胞増殖との関連, 第55回日本生化学会大会(豊中), Oct. 1982.
364.	Katsuhiko Yoshimoto, 中村敏一, 青山和司 and Akira Ichihara : ラット肝初代培養細胞を用いたリポタンパク合成の細胞内脂質による調節について, 第54回日本生化学会大会 (仙台), Sep. 1981.
365.	Katsuhiko Yoshimoto, 中村敏一 and Akira Ichihara : ラット肝初代培養細胞を用いたglucose-6-phosphate脱水素酵素のホルモン調節, 第53回日本生化学会大会(東京), Oct. 1980.

Et cetera, Workshop:

1.	Katsuhiko Yoshimoto : 家族性内分泌腫瘍・下垂体腫瘍Update, 徳島県臨床内科医会会報, No.21, 34-37, Nov. 2016. (Tokushima University Institutional Repository) ● Metadata: 109983 (Tokushima University Institutional Repository: 109983)
2.	Katsuhiko Yoshimoto : 下垂体NETのoverview-分子生物学的視点から, AMED革新的がん医療実用化研究事業領域1 研究課題名:「希少がんである神経内分泌腫瘍の個別化医療開発に向けたがん抑制遺伝子 PHLDA3 の機能解析」第1回班会議, Sep. 2015.
3.	Hisahiro Takeuchi, Toshiyuki Suge, Yukihiro Momota, Kazumi Ozaki, Atsuko Nakamichi, Yoichiro Miyake, Katsuhiko Yoshimoto and Tetsuo Ichikawa : 日本歯科大学臨床実習視察報告, Shikoku Dental Research, Vol.24, No.2, 85-94, Jan. 2012. (Tokushima University Institutional Repository) ● Metadata: 109821 (Tokushima University Institutional Repository: 109821)
4.	Kan Nagao, Tomoko Kimura, Akihiro Yasue, Yoichiro Miyake, Katsuhiko Yoshimoto and Tetsuo Ichikawa : 東京医科歯科大学歯学部歯学科の臨床実習視察報告, Shikoku Dental Research, Vol.24, No.2, 79-84, Jan. 2012. (Tokushima University Institutional Repository) ● Metadata: 109820 (Tokushima University Institutional Repository: 109820)
5.	Katsuhiko Yoshimoto : Multiple Endocrine Neoplasia (MEN) 2型の保因者診断, 平成7年度癌克服10ケ年研究事業分野6 「新しい治療法の開発」指定研究「難治がん治療のための新技術開発」研究班, Multiple Endocrine Neoplasia (MEN) 2型の保因者診断と予防的外科手術に関する検討会, Mar. 1996.

Report:

1.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa, Shozo Yamada and 井下尚子 : 頭蓋咽頭腫の各タイプにおける遺伝子異常, 成長科学協会研究年報, No.40, 163-166, Sep. 2017. (Tokushima University Institutional Repository) ● Metadata: 114139 (Tokushima University Institutional Repository: 114139)
2.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa and Shozo Yamada : cAMP-protein kinase Aシグナル異常によるGH細胞腫瘍化機構, 成長科学協会研究年報, No.39, 157-160, Sep. 2016. (Tokushima University Institutional Repository) ● Metadata: 114138 (Tokushima University Institutional Repository: 114138)
3.	Katsuhiko Yoshimoto : 下垂体腺腫の分子病理学, Pharma Medica, Vol.34, No.6, 113-115, Jun. 2016.
4.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa, Shozo Yamada, 西岡宏 and 井下尚子 : 頭蓋咽頭腫の腫瘍化機構の解析, 成長科学協会研究年報, No.38, 149-152, Aug. 2015. (Tokushima University Institutional Repository) ● Metadata: 114137 (Tokushima University Institutional Repository: 114137)
5.	Takanori Satoh, Masanori Miyata, Kazuhiro Tsutsumi, Steve Toshihisa Fukuda, Takahito Saito, Ray S. Furuya, Katsuhiko Yoshimoto, Norikazu Miyoshi and Hideo Araki : 全学共通教育センター FDの歴史, 徳島大学FDの歴史, Vol.2, 91-111, Tokushima, Dec. 2014.
6.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa, Shinji Ono and Shozo Yamada : 成長ホルモン産生腺腫における14q32.3インプリンティング領域のmiRNA発現増加機構の解析, 成長科学協会研究年報, Vol.37, 177-181, Aug. 2014. (Tokushima University Institutional Repository) ● Metadata: 114136 (Tokushima University Institutional Repository: 114136)
7.	Toshiyuki Suge, Naoto Noguchi, Takashi Matsuo, Katsuhiko Yoshimoto and Tetsuo Ichikawa : 日本大学松戸歯学部臨床実習視察報告, Shikoku Dental Research, Vol.26, No.2, 81-89, Tokushima, Feb. 2014. (Tokushima University Institutional Repository) ● Metadata: 109848 (Tokushima University Institutional Repository: 109848)
8.	Keiji Oishi, 竹内裕久, Takashi Matsuo, Katsuhiko Yoshimoto and Tetsuo Ichikawa : 広島大学歯学部臨床実習視察報告, Shikoku Dental Research, Vol.26, No.2, 71-79, Feb. 2014. (Tokushima University Institutional Repository) ● Metadata: 109847 (Tokushima University Institutional Repository: 109847)
9.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa, Zhi-Rong Qian and Shozo Yamada : 成長ホルモン産生腺腫および血清におけるmiRNAの解析, 成長科学協会研究年報, No.34, 209-215, Aug. 2011. (Tokushima University Institutional Repository) ● Metadata: 114135 (Tokushima University Institutional Repository: 114135)
10.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa, Zhi-Rong Qian, Toshiaki Sano and 山田正三 : 成長ホルモン産生腺腫におけるmiRNAの解析, 成長科学協会研究年報, Vol.33, 191-196, Jul. 2010. (Tokushima University Institutional Repository) ● Metadata: 114134 (Tokushima University Institutional Repository: 114134)
11.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa, Toshiaki Sano and Shozo Yamada : 成長ホルモン産生腺腫におけるp18INK4C遺伝子異常の解析, 成長科学協会研究年報, No.32, 243-247, Aug. 2009. (Summary) ヒトGH産生腺腫におけるp18INK4C遺伝子の関与を検討するために，腺腫におけるp18INK4C遺伝子の発現レベル，体細胞変異，メチル化異常を解析した．散発性GH・プロラクチン産生腺腫1例およびGH産生腺腫14例では，p18INK4C蛋白の発現を免疫組織化学で，p18INK4C遺伝子発現を定量的リアルタイムRT-PCR法で解析した．また，正常下垂体のmRNA量に比べて30 (Keyword) 免疫組織化学 CpG Island DNA変異分析 DNAメチル化プロモーター領域 RT-PCR法 SNPs Cyclin-Dependent Kinase Inhibitor p18 *下垂体腺腫-成長ホルモン産生(遺伝学,診断) ヒト成人(19~44) 中年(45~64) 男女 (Tokushima University Institutional Repository) ● Metadata: 114161 (Tokushima University Institutional Repository: 114161)
12.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa, Toshiaki Sano and 山田正三 : 成長ホルモン(GH)産生腺腫における癌抑制遺伝子異常の解析, 成長科学協会研究年報, No.31, 199-202, 2008. (Summary) 家族性成長ホルモン(GH)産生腺腫家系5家系を対象とてし，癌抑制遺伝子aryl hydrocarbon receptor-interating protein(AIP)異常の解析を行った．いずれの家系においてもカーニー複合体の症候はみられなかった．白血球からゲノムDNAを抽出し，AIP,MEN1,PRKAR1A,p27Kip1遺伝子の塩基配列を同定した．5家系において，API,MEN1,PRKAR1A,p27Kip1遺伝子の胚細胞変異はみられなかった．AIP遺伝子のプロモーター部位遺伝子では1家系においてC-270-269CG>AA及びC.911G>Aの変化がみられ，これは日本人対照78名にはみられなかった．家族性副甲状腺機能亢進症はMEN1の亜型の可能性があるため，9家系についてp27Kip1の遺伝子を解析したが，胚細胞変異はみられなかった．1家系においてc.165A>Gの一塩基多型がみられた．家族性GH産生腺腫発症にはAIP,MRN1,PRKAR1A,p27Kip1以外の遺伝子変化が関与している可能性が高いと考えられた． (Keyword) 血統癌抑制遺伝子多発性内分泌腫瘍1型 Cyclin-Dependent Kinase Inhibitor p27 下垂体腺腫-成長ホルモン産生(遺伝学) Aryl Hydrocarbon Receptor Nuclear Translocator PRKAR1A遺伝子ヒト (Tokushima University Institutional Repository) ● Metadata: 114160 (Tokushima University Institutional Repository: 114160)
13.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa, Toshiaki Sano and 山田正三 : 成長ホルモン (GH) 産生腺腫におけるAIP遺伝子異常の解析, 成長科学協会研究年報, No.30, Jul. 2007. (Tokushima University Institutional Repository) ● Metadata: 114159 (Tokushima University Institutional Repository: 114159)
14.	Katsuhiko Yoshimoto, Qian Rong Zhi, Toshiaki Sano and 山田正三 : 成長ホルモン(GH)産生腺腫におけるDNAメチル化異常の解析, 成長科学協会研究年報, No.29, 279-286, Jul. 2006. (Tokushima University Institutional Repository) ● Metadata: 114158 (Tokushima University Institutional Repository: 114158)
15.	Katsuhiko Yoshimoto, Qian Rong Zhi, Toshiaki Sano and 山田正三 : DNAメチル化による成長ホルモン(GH)産生細胞腫瘍化機構の解析, 成長科学協会研究年報, No.28, 289-295, Jul. 2005. (Tokushima University Institutional Repository) ● Metadata: 114157 (Tokushima University Institutional Repository: 114157)
16.	Katsuhiko Yoshimoto, Toshiaki Sano, 山田正三 and 脇坂晟 : 形態および機能の異なる2種の成長ホルモン産生腺腫の遺伝子発現プロフィルの解析, Annual Research Reports, No.27, 331-336, Tokyo, Jul. 2004. (Tokushima University Institutional Repository) ● Metadata: 114156 (Tokushima University Institutional Repository: 114156)
17.	Katsuhiko Yoshimoto, 山崎弘幸 and Shozo Yamada : cAMP産生異常による成長ホルモン(GH)産生細胞腫瘍化機構の解析, Annual Research Reports, No.26, 391-398, Tokyo, Jul. 2003. (Tokushima University Institutional Repository) ● Metadata: 114155 (Tokushima University Institutional Repository: 114155)
18.	Shiro Saito, 横越浩 and Katsuhiko Yoshimoto : 成長ホルモン分泌下垂体腫瘍における遺伝子異常, 厚生省特定疾患「間脳下垂体機能障害」調査研究班平成4年度総括研究事業報告書, 68-71, Tokyo, Jan. 1993.
19.	Shiro Saito, 横越浩 and Katsuhiko Yoshimoto : 間脳下垂体疾患長期予後調査報告(第二報), 厚生省特定疾患「間脳下垂体機能障害」調査研究班平成2年度総括研究事業報告書, 196-199, Tokyo, Jan. 1991.
20.	Shiro Saito, Katsuhiko Yoshimoto and 横越浩 : MEN 1型の下垂体病変と予後, 厚生省特定疾患「間脳下垂体機能障害」調査研究班平成2年度総括研究事業報告書, 191-195, Tokyo, Jan. 1991.
21.	Shiro Saito, Katsuhiko Yoshimoto, 横越浩, 斎藤晴比古, 広瀬隆則 and Toshiaki Sano : 褐色細胞腫における神経ペプチドの遺伝子発現, 厚生省特定疾患「副腎ホルモン産生異常症」調査研究班昭和62年度研究報告書, 367-377, Tokyo, Jan. 1988.

Patent:

1.	Takeo Iwata, Katsuhiko Yoshimoto, Hisaaki Taniguchi and Masamichi Kuwajima : D-ドーパクロームトートメラーゼを用いた, 脂肪蓄積異常の検出方法と抗肥満物質のスクリーニング方法, 並びに肥満の治療・予防剤, 2008-018866 (Jan. 2008), .
2.	Noriko Mizusawa and Katsuhiko Yoshimoto : GLP-1の発現・分泌を指標としたスクリーニング系, 2008-075833 (Dec. 2007), .

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)

A strategy for the development of anti-obesity drugs related to D-dopachrome tautomerase. (Project/Area Number: 18K09520 )
下垂体腺腫におけるインプリント異常を含むDNAメチル化脱制御の解析 (Project/Area Number: 18K08481 )
miR-1290 promotes cell growth in NS-SV-AC, human submandibular gland cell line (Project/Area Number: 15K11042 )
Mechanisms of adipose tissue-specific expression and action of D-dopachrome tautomrase (Project/Area Number: 15K11040 )
Regulation of miRNAs located within the imprinted DLK1-DIO3 locus at 14q32 in pituitary adenomas (Project/Area Number: 15K09435 )
The elucidation of miRNAs in response to stress stimuli and its secretion into an oral cavity (Project/Area Number: 25670822 )
Salivary miRNA as new cell-to-cell communication molecules (Project/Area Number: 24592800 )
A study of molecular mechanisms by which D-dopachrome tautomerase improves insulin resistance in obesity (Project/Area Number: 24592799 )
Genetic identification and functional analysis in Japanese families with a short stature (Project/Area Number: 24591514 )
Network of microRNA in pituitary adenomas (Project/Area Number: 24591365 )
Analysis of the salivatin function as incretin mimetics (Project/Area Number: 21592363 )
Functional analysis of parafibromin with activities of tumor suppressor and oncogene (Project/Area Number: 21591180 )
Role of the AIP gene in tumorigenesis of growth hormone-producing cells (Project/Area Number: 19591079 )
Function of parafibromin inhibiting parathyroid tumorigenesis (Project/Area Number: 17590963 )
Characterization of β cell-specific gene obtained by large cDNA sequencing. (Project/Area Number: 15590943 )
Molecular basic research for obtaining genes specifying characteristics of pancreatic α and β cells. (Project/Area Number: 12671115 )
Immunosuppressive role of TGF-β1 against autoimmune destruction of islet β cells and a basic study on islet β cells of NOD-RGP-TGF-β1 Tg (Project/Area Number: 11671090 )
Analysis of Tumor Suppressor Genes on Tumorigenesis of Human Pituitary Adenomas (Project/Area Number: 09670188 )
Isolation of genes related to malignant transformation of thyroid tumors and gene therapy for undifferentiated carcinoma of the thyroid (Project/Area Number: 07671143 )
Analysis of Immunological Destruction Mechanism of Pancreatic Islet B Cells Using a Transgenic Mouse Model (Project/Area Number: 05454323 )
Analysis genetic changes in human endocrine tumors (Project/Area Number: 04671484 )
Development of Gene Therapy for Type I Diabetes Using Cytokine Gene and Pancreatic Islet B Cell-Specific Lymphocytes (Project/Area Number: 04557132 )
Molecular Analysis of a Glucose-concentration sensing system which Regulates Insulin Gene Expression (Project/Area Number: 03454518 )
Structure and Mechanism of Signal Transduction of GHRH Receptor,and its Clinical Significance. (Project/Area Number: 02454509 )
Development of the Methods for Regulated Expression of Transduced Gene in Transkaryotic Gene Therapy (Project/Area Number: 01870051 )
本邦初の先天性プロテインS異常症に関する研究 (Project/Area Number: 63570573 )
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Professor Emeritus / Professor : Yoshimoto, Katsuhiko

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Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)