| Project/Area Number |
21592061
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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 | Asahi University (2010-2011)
Kanazawa Medical University (2009) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TANAKA Takuji 金沢医科大学, 医学部, 教授 (40126743)
YASUI Yumiko 金沢医科大学, 医学部, 助教 (90434472)
OYAMA Takeru 金沢医科大学, 医学部, 助教 (00515314)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2009: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 前立腺発がん / 幹細胞 / 去勢 / ラット / PhIP / 前立腺 / 発がん / 炎症 / 前立腺がん |
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| Research Abstract |
In this study, the relation between prostate carcinogenesis and stem cell or inflammation is analyse in animal experimental carcinogenesis model targeted stem cells associated with prostatitis. Any prostate neoplasma were not found in any castrated rats, although prostate neoplasms was observed only in non-castration groups. From these results, the origin of cancer was assumed to be lost by castration. TP had a suppressive effect in PhIP prostate carcinogenesis. he hypothesis which Prostate cancer originated from stem cell. The lobes with inflammation were different the lobes with PIN. The modifying effect of inflammation for prostate carcinogenesis is not clear, yet. Further consideration will be necessary.
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