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2015 Fiscal Year Final Research Report

The exploration of therapeutic target against colon cancer with KRAS mutation

Research Project

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Project/Area Number 26830090
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Tumor biology
Research InstitutionAichi Cancer Center Research Institute

Principal Investigator

Fujishita Teruaki  愛知県がんセンター(研究所), 分子病態学部, 主任研究員 (50511870)

Project Period (FY) 2014-04-01 – 2016-03-31
Keywordsマウスモデル / 大腸がん
Outline of Final Research Achievements

Activating mutations in KRAS gene are found in about 40% of colon cancer patients, and effective treatment for these patients with KRAS mutation is yet to be established. This study determined whether the MEK/ERK signaling, a downstream pathway of KRAS, would be a therapeutic target for colon cancer. The MEK/ERK signaling was activated in the stroma of intestinal polyps of a mouse model for familial adenomatous polyposis, and was responsible for promoting intestinal polyp expansion through stimulation of COX2 expression and angiogenesis. Treatment with a MEK inhibitor blocked intestinal adenocarcinoma formation in a mouse model for Kras mutant colorectal cancer. These results suggest that the MEK/ERK signaling may be an attractive therapeutic target for colon cancer regardless of the KRAS mutation status.

Free Research Field

総合生物

URL: 

Published: 2017-05-10  

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