| Project/Area Number |
13671635
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Urology
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| Research Institution | CHIBA UNIVERSITY |
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Principal Investigator |
SUZUKI Hiroyoshi Chiba University, Graduate School of Medicine, Assistant, 大学院・医学研究院, 助手 (60301818)
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| Project Period (FY) |
2001 – 2002
|
| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 2002: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 2001: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | prostate cancer / hormonal therapy / hormone-independency / androgen receptor / testosterone / p51 gene / neuroendocrine differentiation / chromogrnine A / 前平腺癌 / ホルモン依存性腫瘍 / 内分泌療法 / CD44 / KAI1 / retinoic acid receptor β / p51 |
|---|
| Research Abstract |
(1) Neuroendocrine differentiation (NED) is thought to be one of important mechanisms involved in hormone-refractory process in prostate cancer. I found that serum NED markers (i.e., chromogrnine A and neuro-specific enolase) could be prognostic markers for matastatic prostate cancer patients treated by hormonal therapy.
(2) I found that serum testosterone level and/or CAG polymorphic lengths of androgen receptor gene could be prognostic markers for matastatic prostate cancer patients treated by hormonal therapy.
(3) I investigated expression and structural abnormalities of p51 gene, a homologue of p53 tumor suppressor gene, and found that this gene is related to prostate cancer progression.
These results made clear hormone-refractory processes of prostate cancer. To clarify more detail of molecular mechanism of prostate cancer, further studies should be performed.
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