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Pancreatic Neoplasms: HELP
Articles by Motoyuki Tsuda
Based on 5 articles published since 2010
(Why 5 articles?)
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Between 2010 and 2020, Motoyuki Tsuda wrote the following 5 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Hes1 plays an essential role in Kras-driven pancreatic tumorigenesis. 2019

Nishikawa, Yoshihiro / Kodama, Yuzo / Shiokawa, Masahiro / Matsumori, Tomoaki / Marui, Saiko / Kuriyama, Katsutoshi / Kuwada, Takeshi / Sogabe, Yuko / Kakiuchi, Nobuyuki / Tomono, Teruko / Mima, Atsushi / Morita, Toshihiro / Ueda, Tatsuki / Tsuda, Motoyuki / Yamauchi, Yuki / Sakuma, Yojiro / Ota, Yuji / Maruno, Takahisa / Uza, Norimitsu / Uesugi, Motonari / Kageyama, Ryoichiro / Chiba, Tsutomu / Seno, Hiroshi. ·Department of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, 54 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto, 606-8507, Japan. · Department of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, 54 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto, 606-8507, Japan. kodamayu@kuhp.kyoto-u.ac.jp. · Department of Gastroenterology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, Hyogo, 650-0017, Japan. kodamayu@kuhp.kyoto-u.ac.jp. · Institute for Chemical Research, Kyoto University, Uji, Kyoto, 611-0011, Japan. · Institute for Integrated Cell-Material Sciences (iCeMS), Kyoto University, Uji, Kyoto, 611-0011, Japan. · Institute for Frontier Life and Medical Sciences, Kyoto University, Shogoin-Kawahara, Sakyo-ku, Kyoto, 606-8507, Japan. · Kansai Electric Power Hospital, 2-1-7 Fukushima, Fukushima-ku, Osaka, 553-0003, Japan. ·Oncogene · Pubmed #30705405.

ABSTRACT: Most pancreatic ductal adenocarcinoma (PDAC) develops from pancreatic epithelial cells bearing activating mutant KRAS genes through precancerous lesions, i.e. acinar-to-ductal metaplasia (ADM) and pancreatic intraepithelial neoplasia (PanIN). During pancreatic tumorigenesis, Hes1 expression starts with the transition from acinar cells to ADM, and continues during PanIN and PDAC formation, but the role of Hes1 in pancreatic tumorigenesis is not fully elucidated. Here we show that Hes1 plays an essential role in the initiation and progression of KRAS-driven pancreatic tumorigenesis. In vitro, activation of MAPK signaling due to EGF or mutant KRAS activation induced sustained Hes1 expression in pancreatic acinar cells. In vivo, acinar cell-specific activation of mutant KRAS by Elastase1-CreERT2;Kras

2 Article Nardilysin inhibits pancreatitis and suppresses pancreatic ductal adenocarcinoma initiation in mice. 2019

Ikuta, Kozo / Fukuda, Akihisa / Ogawa, Satoshi / Masuo, Kenji / Goto, Norihiro / Hiramatsu, Yukiko / Tsuda, Motoyuki / Kimura, Yoshito / Matsumoto, Yoshihide / Kimura, Yuto / Maruno, Takahisa / Kanda, Keitaro / Nishi, Kiyoto / Takaori, Kyoichi / Uemoto, Shinji / Takaishi, Shigeo / Chiba, Tsutomu / Nishi, Eiichiro / Seno, Hiroshi. ·Department of Gastoenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan. · Cardiovascular Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan. · Division of Hepato-Biliary-Pancreatic Surgery and Transplantation, Department of Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan. · Laboratory for Malignancy Control Research (DSK project), Medical Innovation Center, Kyoto University Graduate School of Medicine, Kyoto, Japan. · Kansai Electric Power Hospital, Osaka, Japan. · Department of Pharmacology, Shiga University of Medical Science, Shiga, Japan. ·Gut · Pubmed #29798841.

ABSTRACT: OBJECTIVE: Nardilysin (NRDC), a zinc peptidase, exhibits multiple localisation-dependent functions including as an enhancer of ectodomain shedding in the extracellular space and a transcriptional coregulator in the nucleus. In this study, we investigated its functional role in exocrine pancreatic development, homeostasis and the formation of pancreatic ductal adenocarcinoma (PDA). DESIGN: We analysed RESULTS: We found that pancreatic deletion of CONCLUSION: Nrdc inhibits pancreatitis and suppresses PDA initiation in mice.

3 Article Analysis of Prognostic Factors in Pancreatic Metastases: A Multicenter Retrospective Analysis. 2018

Ito, Takashi / Takada, Ryoji / Omoto, Shunsuke / Tsuda, Motoyuki / Masuda, Daisuke / Kato, Hironari / Matsumoto, Toshihiko / Moriyama, Ichiro / Okabe, Yoshinobu / Shiomi, Hideyuki / Ishida, Etsuji / Hatamaru, Keiichi / Hashimoto, Shinichi / Tanaka, Kiyohito / Kawamoto, Hirofumi / Yanagisawa, Akio / Katayama, Toshiro / Yazumi, Shujiro / Anonymous2350956. ·Department of Hepatobiliary and Pancreatic Oncology, Osaka International Cancer Institute, Osaka, Japan. · Department of Gastroenterology and Hepatology, Kindai University Faculty Medicine, Osaka-Sayama, Japan. · Department of Gastroenterology and Hepatology, Graduate School of Medicine Kyoto University, Kyoto, Japan. · 2nd Department of Internal Medicine, Osaka Medical College, Takatsuki, Japan. · Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan. · Department of Gastroenterology, National Hospital Organization Shikoku Cancer Center, Matsuyama, Japan. · Department of Hematology/Oncology, Shimane University Hospital, Shimane, Japan. · Division of Gastroenterology, Department of Medicine, Kurume University School of Medicine, Kurume, Japan. · Division of Gastroenterology, Department of Internal Medicine, Graduate School of Medicine, Kobe University, Kobe, Japan. · Department of Gastroenterology and Hepatology, Kurashiki Central Hospital, Okayama, Japan. · Department of Gastroenterology and Hepatology, Japanese Red Cross Society, Wakayama Medical Center, Wakayama, Japan. · Digestive and Lifestyle Diseases, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan. · Department of Gastroenterology, Kyoto Second Red Cross Hospital, Kyoto, Japan. · Department of Internal Medicine, Kawasaki Medical School General Medical Center, Okayama, Japan. · Department of Surgical Pathology, Japanese Red Cross Kyoto Daiichi Hospital, Kyoto, Japan. · Faculty of Medical Engineering, Himeji Dokkyo University School of Health Care Sciences, Himeji, Japan. ·Pancreas · Pubmed #30048381.

ABSTRACT: OBJECTIVES: Pancreatic metastases (PMs) account for 1% to 2% of pancreatic tumors, and their prognostic significance is poorly defined. We evaluated the incidence and clinical characteristics of primary tumors and defined prognostic factors. METHODS: This retrospective study of 39 Japanese tertiary referral hospitals (January 2005 to August 2015) analyzed patient and tumor characteristics and survival time. Kaplan-Meier analysis and Cox proportional hazards models were applied to evaluate overall survival and prognostic factors, respectively. RESULTS: We enrolled 159 patients with a pathologic diagnosis of PM. The most common primary tumor was renal cell carcinoma (38.4%), followed by lung cancer (24.5%), colorectal cancer (11.3%), and sarcoma (6.3%). Eight patients were lost during follow-up, and 151 patients were included for statistical analysis. Median overall survival was 43.0 months, and the 5-year survival rate was 42.6%. Multivariate analysis identified 3 independent prognostic factors: extrapancreatic metastasis (hazard ratio, 2.13; 95% confidence interval, 1.11-4.07; P = 0.02), tumor-related symptoms at diagnosis (hazard ratio, 5.39; 95% confidence interval, 2.92-9.91; P < 0.001), and pathologic diagnosis of primary tumors (P < 0.001). CONCLUSIONS: Treatment strategies and prognoses for PMs completely differ according to the primary tumor type. A definitive pathologic diagnosis of PMs is essential for selecting the appropriate treatment.

4 Article The BRG1/SOX9 axis is critical for acinar cell-derived pancreatic tumorigenesis. 2018

Tsuda, Motoyuki / Fukuda, Akihisa / Roy, Nilotpal / Hiramatsu, Yukiko / Leonhardt, Laura / Kakiuchi, Nobuyuki / Hoyer, Kaja / Ogawa, Satoshi / Goto, Norihiro / Ikuta, Kozo / Kimura, Yoshito / Matsumoto, Yoshihide / Takada, Yutaka / Yoshioka, Takuto / Maruno, Takahisa / Yamaga, Yuichi / Kim, Grace E / Akiyama, Haruhiko / Ogawa, Seishi / Wright, Christopher V / Saur, Dieter / Takaori, Kyoichi / Uemoto, Shinji / Hebrok, Matthias / Chiba, Tsutomu / Seno, Hiroshi. ·Department of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan. · Diabetes Center, Department of Medicine, UCSF, San Francisco, California, USA. · Department of Pathology and Tumor Biology, Kyoto University Graduate School of Medicine, Kyoto, Japan. · Hematology, Oncology and Tumorimmunology, Charite-Universitätsmedizin Berlin, Berlin, Germany. · Department of Pathology, UCSF, San Francisco, California, USA. · Department of Orthopaedics, Gifu University, Gifu, Japan. · Program in Developmental Biology and Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA. · Department of Internal Medicine II, Klinikum Rechts der Isar, Technische Universität München, Munich, Germany. · Division of Hepatobiliary-Pancreatic Surgery and Transplantation, Department of Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan. · Kansai Electric Power Hospital, Osaka, Japan. ·J Clin Invest · Pubmed #30010625.

ABSTRACT: Chromatin remodeler Brahma related gene 1 (BRG1) is silenced in approximately 10% of human pancreatic ductal adenocarcinomas (PDAs). We previously showed that BRG1 inhibits the formation of intraductal pancreatic mucinous neoplasm (IPMN) and that IPMN-derived PDA originated from ductal cells. However, the role of BRG1 in pancreatic intraepithelial neoplasia-derived (PanIN-derived) PDA that originated from acinar cells remains elusive. Here, we found that exclusive elimination of Brg1 in acinar cells of Ptf1a-CreER; KrasG12D; Brg1fl/fl mice impaired the formation of acinar-to-ductal metaplasia (ADM) and PanIN independently of p53 mutation, while PDA formation was inhibited in the presence of p53 mutation. BRG1 bound to regions of the Sox9 promoter to regulate its expression and was critical for recruitment of upstream regulators, including PDX1, to the Sox9 promoter and enhancer in acinar cells. SOX9 expression was downregulated in BRG1-depleted ADMs/PanINs. Notably, Sox9 overexpression canceled this PanIN-attenuated phenotype in KBC mice. Furthermore, Brg1 deletion in established PanIN by using a dual recombinase system resulted in regression of the lesions in mice. Finally, BRG1 expression correlated with SOX9 expression in human PDAs. In summary, BRG1 is critical for PanIN initiation and progression through positive regulation of SOX9. Thus, the BRG1/SOX9 axis is a potential target for PanIN-derived PDA.

5 Article ARID1A Maintains Differentiation of Pancreatic Ductal Cells and Inhibits Development of Pancreatic Ductal Adenocarcinoma in Mice. 2018

Kimura, Yoshito / Fukuda, Akihisa / Ogawa, Satoshi / Maruno, Takahisa / Takada, Yutaka / Tsuda, Motoyuki / Hiramatsu, Yukiko / Araki, Osamu / Nagao, Munemasa / Yoshikawa, Takaaki / Ikuta, Kozo / Yoshioka, Takuto / Wang, Zong / Akiyama, Haruhiko / Wright, Christopher V / Takaori, Kyoichi / Uemoto, Shinji / Chiba, Tsutomu / Seno, Hiroshi. ·Department of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan. · Department of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan. Electronic address: fukuda26@kuhp.kyoto-u.ac.jp. · Department of Cardiac Surgery, Cardiovascular Research Center, University of Michigan, Ann Arbor, Michigan. · Department of Orthopaedics, Gifu University, Gifu City, Japan. · Program in Developmental Biology and Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, Tennessee. · Division of Hepatobiliary-Pancreatic Surgery and Transplantation, Department of Surgery, Kyoto University Graduate School of Medicine, Kyoto Japan. ·Gastroenterology · Pubmed #29604291.

ABSTRACT: BACKGROUND & AIMS: The ARID1A gene encodes a protein that is part of the large adenosine triphosphate (ATP)-dependent chromatin remodeling complex SWI/SNF and is frequently mutated in human pancreatic ductal adenocarcinomas (PDACs). We investigated the functions of ARID1A during formation of PDACs in mice. METHODS: We performed studies with Ptf1a-Cre;Kras RESULTS: Ptf1a-Cre;Kras CONCLUSIONS: ARID1A regulates expression of SOX9, activation of the mTOR pathway, and differentiation of PDCs. ARID1A inhibits formation of PDACs from IPMNs in mice with pancreatic expression of activated KRAS and is down-regulated in IPMN and PDAC tissues from patients.