| Project/Area Number |
25893229
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | The University of Tokyo (2014)
Saitama Medical University (2013) |
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Principal Investigator |
IKEDA Yuji 東京大学, 医学部附属病院, 助教 (80713453)
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| Project Period (FY) |
2013-08-30 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | CDK4/6 / 子宮体癌 / PI3K経路 / TP53 / 放射線治療 / CDK4/6阻害薬 / PI3K/ｍTOR阻害薬 |
|---|
| Outline of Final Research Achievements |
The result of combination both CDK4/6 activity/expression and Ki67 expression was significantly correlated with the prognosis in patients with low risk endometrial cancer. However, the efficacy of CDK4/6 inhibitor to the endometrial cancer celllines was inferior to the other cancer types. Because not only CDK4/6 is suppressed by TP53 via p21, but also TP53 is related with apoptosis, we focused on TP53 and irradiation in endometrial cancer. Our result indicated mutation of TP53 could serve a biomarker to predict radioresistance, a dual PI3K/mTOR inhibitor sensitized cells to irradiation, and suppression of HIF1alpha, which was regulated at least in part by the PI3K/mTOR pathway, enhanced the cytotoxic effect of irradiation.
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