Pick Topic
Review Topic
List Experts
Examine Expert
Save Expert
  Site Guide ··   
Pancreatic Neoplasms: HELP
Articles by Norihiro Goto
Based on 3 articles published since 2010
(Why 3 articles?)
||||

Between 2010 and 2020, Norihiro Goto wrote the following 3 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 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.

2 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.

3 Article Intraductal papillary-mucinous neoplasm of the pancreas penetrating to the stomach and the common bile duct. 2012

Goto, Norihiro / Yoshioka, Masahiro / Hayashi, Motohito / Itani, Toshinao / Mimura, Jun / Hashimoto, Kimio. ·Department of Gastroenterology, Nishi-Kobe Medical Center, Kobe, Hyogo 651-2273, Japan. marshall_prs@nmc-kobe.org ·JOP · Pubmed #22233949.

ABSTRACT: CONTEXT: Intraductal papillary mucinous neoplasm (IPMN) of the pancreas occasionally penetrates to others organs. We present a case of IPMN penetrating to the stomach and the common bile duct. CASE REPORT: A 75-year-old man was admitted to the hospital because of epigastric pain. Computed tomography (CT) showed a papillary tumor protruding into the markedly dilated main pancreatic duct and splenic vein obstruction. The tumor was diagnosed as IPMN arising in the main duct, but he rejected surgery and he was followed without treatment. One year later, gastroduodenoscopy revealed gastropancreatic fistula and we were able to pass an endoscope through the fistula and directly examine the lumen of the main pancreatic duct and the papillary tumor adjacent to the fistula. Absence of malignant cells on histopathology suggested mechanical penetration rather than invasive penetration. CT showed splenic vein reperfusion due to decreased inner pressure of the main pancreatic duct. Two and a half years later, CT revealed biliopancreatic fistula formation. Endoscope biliary drainage was performed but failed. Despite jaundice, he is still ambulatory and seen in the clinic three years after the first admission. CONCLUSIONS: We have experienced a case of IPMN penetrating to the stomach and the common bile duct that has taken a slow course. It represents the importance of distinguishing mechanical penetration from invasive penetration as well as mechanical splenic vein obstruction from splenic vein invasion.