| Project/Area Number |
15K20109
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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 |
Hongo Hiroshi 慶應義塾大学, 医学部(信濃町), 特任助教 (10626675)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 去勢抵抗性前立腺癌 / ドセタキセル耐性 / 相互依存的シグナル / アンドロゲン受容体 / 抗癌剤耐性 / 相互依存的シグナルネットワーク / 相互依存的シグナル機構 |
|---|
| Outline of Final Research Achievements |
We evaluated the therapeutic potential of targeting STAT5 signaling. We used two human prostate cancer cell lines: LNCaP, a androgen-dependent prostate cancer cell line; and C4-2AT6, a castration-resistant prostate cancer cell line. C4-2AT6 had docetaxel resistance. Western blotting showed higher expression of pAKT and pSTAT5 in C4-2AT6. We identified a novel stat5 inhibitor, ME001. ME001 had anti-tumor effect for C4-2AT6 in vitro and in vivo.
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