| Project/Area Number |
25860263
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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 |
Human pathology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
TANAKA Mariko 東京大学, 医学(系)研究科(研究院), 助教 (50645710)
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| Research Collaborator |
深山 正久
石川 俊平
砂河 孝行
鈴木 洋
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 膵癌 / 発癌 / 分化異常 / EVI1 / KRAS / microRNA / 膵臓癌 / 胃上皮化生 |
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| Outline of Final Research Achievements |
Pancreatic cancer typically manifests a very poor prognosis. The precise mechanism of pancreatic carcinogensis is still unclear. Although an activating point mutation of KRAS is an early event in pancreatic carcinogenesis, it remains unclear whether KRAS mutation is solely responsible for initiation of pancreatic carcinogenesis. By tracking potential transcriptional regulators of gastric epithelial genes in pancreatic neoplasms, we found that overt expression of ecotropic viral integration site 1 (EVI1) oncoprotein is a hallmark of human pancreatic cancer and its precursors. In pancreatic cancer cells, EVI1 poses the oncogenic role by upregulating KRAS expression through suppression of a potent KRAS suppressor, miR-96. Results suggest that EVI1 oncoprotein and KRAS mutation converge on activation of the KRAS pathway in the early phase of pancreatic carcinogenesis and implicate EVI1 and/or miR-96 as candidate early markers and therapeutic targets in pancreatic cancer.
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