| Project/Area Number |
16390467
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Nagasaki University |
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Principal Investigator |
KANETAKE Hiroshi Nagasaki University, Graduate School of Biomedical Sciences, Professor, 大学院医歯薬学総合研究科, 教授 (50100839)
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| Co-Investigator(Kenkyū-buntansha) |
SAKAI Hideki Nagasaki University, Hospital of Medicine and Dentistry, Assistant Professor, 医学部・歯学部附属病院, 講師 (40235122)
IGAWA Tsukasa Nagasaki University, Graduate School of Biomedical Sciences, Assistant Professor, 大学院医歯薬学総合研究科, 助手 (40295069)
MIYATA Yasuyoshi Nagasaki University, Hospital of Medicine and Dentistry, Resident, 医学部・歯学部附属病院, 医員 (60380888)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥13,100,000 (Direct Cost: ¥13,100,000)
Fiscal Year 2005: ¥5,200,000 (Direct Cost: ¥5,200,000)
Fiscal Year 2004: ¥7,900,000 (Direct Cost: ¥7,900,000)
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| Keywords | EP receptors / prostate cancer / TNM stage / cell proliferation / transgenic mouse / プロスタグランジンE2 / 予後 / 免疫組織学 / 移行上皮癌 / 前立腺肥大症 |
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| Research Abstract |
We examined the expression of each EP receptor in 122 prostate cancer tissues by immunohistochemistry. We also investigated the relationship between EP receptors and cancer cell proliferation. The rate of immunopositivity for EP1R in cancer cells (36.3±14.3%, mean ± SD) was significantly higher (P<0.01) than in non-tumoral glands (7.1±4.8%), and positively correlated with Gleason's score (P<0.01), T classification (P <0.01), N classification (P=0.03), M classification (P<0.01), and cancer cell proliferation (r =0.35, P<0.01). EP2R expression in cancer cells (38.9± 11.6%) was significantly higher (P<0.01) than in non-tumoral glands (30.6 ±8.6%), and correlated with cancer cell proliferation (P<0.01). EP4R expression in cancer cells was also significantly higher (P<0.01) than in non-tumoral glands. However, the expression of EP2R and EP4R did not correlate with clinicopathological features and EP3R expression was not associated with any parameters. Our results indicate that EP1R, EP2R, and EP4R are associated with prostate carcinogenesis. In particular, EP1 receptor seems to play an important role in malignant aggressiveness and tumor development in patients with prostate cancer.
In addition to such expressions in cancer cells, many infiltrating cells with EP2 receptor were detected in peri-tumoral tissues. We are investigating the clinical and pathological roles of these cells.
Our final goal is to examine the anti-tumoral effect of inhibitors of EP receptors in prostate cancer. So we are investigating them in transgenic mouse model of prostate cancer.
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