Mechanism of Gastric Carcinogenesis in the progression to mucosal atrophy and intestinal metaplasia through Notch1 signaling

Research Project

Project/Area Number	23590910
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Research Field	Gastroenterology
Research Institution	Tohoku University
Principal Investigator	IMATANI AKIRA 東北大学, 医学(系)研究科(研究院), 教授 (30333876)
Project Period (FY)	2011 – 2013
Project Status	Completed (Fiscal Year 2013)
Budget Amount *help	¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000) Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000) Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000) Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Keywords	胃 / Helicobacter pylori / 癌抑制遺伝子 / 分化制御 / 分化 / 発現制御 / 癌幹細胞 / マイクロアレイ
Research Abstract	H.pylori infection causes the precancerous gastric mucosal atrophy. A transmembrane receptor Notch1 promotes differentiation and maintenance of stem cells. In vitro and in vivo analyses in this study revealed that H.pylori infection triggered Notch1 suppression, leading to the gastric mucosal atrophy through the down-regulation of Sox2. In addition, loss-of-function of Notch1 signaling may contribute to gastric carcinogenesis.

Report

(4 results)