Explication of mechanism in hormone refractory status in prostate cancer, Analysis of androgen receptor and related factors
Project/Area Number |
17591663
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Urology
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Research Institution | Chiba Cancer Center (Research Institute) |
Principal Investigator |
UEDA Takeshi Chiba Cancer Center (Research Institute), Division of Biochemistry, additional post researcher (10223463)
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Project Period (FY) |
2005 – 2007
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Project Status |
Completed (Fiscal Year 2007)
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Budget Amount *help |
¥3,870,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥270,000)
Fiscal Year 2007: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2006: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2005: ¥1,500,000 (Direct Cost: ¥1,500,000)
|
Keywords | prostate cancer / androgen receptor / relapse / proteome analysis / interleukin-10 / プロテオーム / サイトカイン |
Research Abstract |
The results which I was able to analyze in this period were as follows. Loss of heterozygosity (LOH) were present at least one locus on chromosome 2 of prostate cancer patients. LOH on 2p was observed more frequently in cancer death cases than in organ confined and regional diseases. These results suggest that inactivation of putative tumor suppressor genes on chromosome 2 that may play an important role in the progression of Japanese patients with PCa. I have demonstrated that serum levels of IL-4 are increased in hormone refractory PCa and IL-4 enhanced PSA reporter gene activity by the activation of ARNTD in human LNCaP cells. These results suggest that the AR can be activated by cytokines and this mechanism may play an important role in the transition from androgen-dependent to androgen-independent prostate cancer after patients receive androgen ablation therapy. Serum chromogranin A and NSE related to neuroendocrine differentiation reported it as prognostic factor of hormonotherapy for prostate cancer patients. I analyzed the influence that IL -10 gave to an androgen receptor. IL -10 also activated androgen receptor in in the same way as IL -6, and IL -4 in prostate cancer cells. I analyzed serum proteins obtained from prostatic cancer patients treating by the hormone therapy by means of 2 dimensions of electrophoresis. I already published one part of above-mentioned results of research, and the main papers were shown in this report. From this study, I was able to analyze about androgen refractory molecular biologic mechanism of hormone refractory prostate from the various aspects.
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Report
(4 results)
Research Products
(19 results)
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[Journal Article] Transrectal high-ingh-intensity focused ultrasound in the patient of localized prostate cancer : A multicenter study.2005
Author(s)
Uchida T, Baba S, Irie A, Soh S, Masumori N, Tsukamoto T, Nakatsu H, Fujimoto H, Kakizoe T, Ueda T, Ichikawa T, Ohta N, Kitamura T, Sumitomo M, Hayakawa M, Aoyagi T, Tachibana M, Ikeda R, Suzuki K, Tsuru N, Suzuki K, Ozono S, Fujimoto K, Hirao Y, Monden K, Nasu Y, Kumon H, Nishi K, Ueda S, Koga H, Naitoh S
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Journal Title
Acta Urol Jpn 51
Pages: 651-658
Description
「研究成果報告書概要(欧文)」より
Related Report
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