| Project/Area Number |
23592328
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Urology
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KITAGAWA Yasuhide 金沢大学, 大学病院, 講師 (00452102)
KADONO Yoshifumi 金沢大学, 大学病院, 助教 (10397218)
KYO Satoru 金沢大学, 医学系, 准教授 (50272969)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
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| Keywords | 去勢抵抗性前立腺癌 / 核内受容体 / NF-κB / クロストーク / アンドロゲン受容体 / エストロゲン受容体 / グルココルチコイド受容体 / シグナル伝達 / AR / GR / ER / 転写活性 / NF-kB |
|---|
| Research Abstract |
Elucidating a comprehensive mechanism through which most patients with advanced prostate cancer have an initial response to androgen deprivation therapy, but eventually progress to a castration-resistant state is critical to establish a novel treatment strategy for castration refractory prostate cancer (CRPC). We investigate the mechanism of CRPC from the perspective of some cross-talks in signal transduction pathway between NF-kB and an intranuclear steroid receptor superfamily containing androgen receptor, glucocorticoid receptor, and estrogen receptor. Also we target the cross-talk with various methods of inhibiting the signaling transduction pathway and established the integrated treatment strategy of CRPC. Consequently, our study made it clear that cross-talk between NF-kB and an intranuclear steroid receptor superfamily might existence, and also suggested inhibiting the cross-talk of signaling pathway network might be novel therapeutics for the management of CRPC.
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