Mechanisms of pancreatic beta-cell tumorigenesis by tumor suppressor function failure of tumor suppressor gene MEN1.

2016 Fiscal Year Final Research Report

• Project/Area Number: 26461374
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Endocrinology
• Research Institution: Gunma University
• Principal Investigator: OZAWA ATSUSHI 群馬大学, 大学院医学系研究科, 助教 (10573496)
• Co-Investigator(Renkei-kenkyūsha): YAMADA Masanobu 群馬大学, 大学院・医学系研究科, 教授 (90261833)
• Research Collaborator: WATANABE Takuya
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 遺伝子 / 内分泌腫瘍

Outline of Final Research Achievements

The mechanisms of tumorigenesis of pancreatic-neuroendocrine tumor (p-NET) is still unclear. Several genes were reported to be involved in the tumorigensis pathway of p-NET. Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominantly inherited syndrome characterized by the occurrence of tumors in pituitary, parathyroid and enteropancreatic neuroendocrine glands. It is known that JunD is one of the main binding partners of menin encoded by MEN1 gene. We generated and analyzed the transgenic mice that over-expressed mutant JunD. We investigated that this mouse cold be the model of insulinoma. The mechanisms underlying the tumorigensis of this mouse was different from the previous reports revealing the p-NET tumorigensis.

Free Research Field

内分泌代謝