Mechanism of Gastric Carcinogenesis in the progression to mucosal atrophy and intestinal metaplasia through Notch1 signaling
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)
Research Products
(3 results)