| 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)
|
|---|
| 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.
|
