Analysis of the PI3K pathway in colon cancer and new strategy of Molecular target-based drugs.

Research Project

Project/Area Number	21591721
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Single-year Grants
Section	一般
Research Field	Digestive surgery
Research Institution	The University of Tokyo
Principal Investigator	SUNAMI Eiji 東京大学, 医学部附属病院, 講師 (70345205)
Co-Investigator(Kenkyū-buntansha)	KITAYAMA Joji 東京大学, 医学部附属病院, 准教授 (20251308)
Project Period (FY)	2009 – 2011
Project Status	Completed (Fiscal Year 2011)
Budget Amount *help	¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000) Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000) Fiscal Year 2010: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000) Fiscal Year 2009: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Keywords	大腸癌 / 化学療法 / mTOR / Rapamycin / 多剤併用療法 / 癌 / シグナル伝達 / PI3K-Akt経路 / MAPキナーゼ経路
Research Abstract	We demonstrated that Tesirolimus cause G1 cell cycle arrest in colon cancer cell lines with inhibition of cyclin D1 protein production. Furthermore, we also indicated that Tesirolimus inhibits production of Hypoxia-inducible factor-alpha protein of colon cancer cell lines under the environment of hypoxia. Those explications of the mechanisms of Tesirolimus against cancer proliferation may play an important role in the selection of anticancer agents for colon cancer.

Report

(4 results)