The exploration of therapeutic target against colon cancer with KRAS mutation

2015 Fiscal Year Final Research Report

• Project/Area Number: 26830090
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Tumor biology
• Research Institution: Aichi 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