The exploration of therapeutic target against colon cancer with KRAS mutation
| Project/Area Number |
26830090
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor biology
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| Research Institution | Aichi Cancer Center Research Institute |
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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)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | マウスモデル / 大腸がん |
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| 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.
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Report
(3 results)
Research Products
(12 results)
