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Pancreatic Neoplasms: HELP
Articles by Takuto Yoshioka
Based on 2 articles published since 2010
(Why 2 articles?)
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Between 2010 and 2020, Takuto Yoshioka wrote the following 2 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 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.

2 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.