| Project/Area Number |
16K20161
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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 |
Urology
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| Research Institution | Keio University |
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Principal Investigator |
Ezaki Taisuke 慶應義塾大学, 医学部(信濃町), 助教 (50598422)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 前立腺癌 / 去勢抵抗性前立腺癌 / CDK4 / CDK4阻害剤 / 去勢抵抗性前立腺癌(CRPC) / アンドロゲン・アンドロゲンレセプター軸 |
|---|
| Outline of Final Research Achievements |
Although androgen / androgen receptor axis plays a key role in progression of castration-resistant prostate cancer (CRPC), mutation or alteration involving other signaling pathways are also enriched in CRPC. We focused on CDK4, cell cycle regulator, and investigated the therapeutic effect of CDK4 inhibitor, using the human prostate cancer cell line, the human CRPC cell line, and the docetaxel-resistant CRPC cell line. It was found that anti-cancer effect of CDK4 inhibitor was exhibited regardless of the sensitivity to hormone or docetaxel of the cell lines. We also showed that AR expression was not affected by CDK4 inhibitor. These results implied that alteration of cell cycle control plays some important role in CRPC progression and CDK4 inhibitor might be effective in the treatment of CRPC.
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