Contribution of glucocorticoid receptor in the mechanism of castration resistancy of prostate cancers
| Project/Area Number |
25460426
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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 |
Human pathology
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| Research Institution | National Cancer Center Japan |
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Principal Investigator |
Kuwata Takeshi 国立研究開発法人国立がん研究センター, 東病院, 科長 (00327321)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 前立腺癌 / 抗アンドロゲン療法 / アンドロゲン受容体 / グルココルチコイド受容体 / アンドロゲン |
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| Outline of Final Research Achievements |
In this study, the role of glucocorticoid receptor (GR) in castration resistancy of androgen-receptor(AR)-positive prostate cancer. In a human prostate cancer cell line, LNCap, expresses GR in addition to AR. Dexamethasone could activate androgen-receptor-respose-element and induces PSA in LNCap-GR, constitutively expressing GR. LNCap-GR could also subcutaneous-transplantable in SICD mice, while parental LNCap could not.
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Report
(4 results)
Research Products
(3 results)
