| Project/Area Number |
04454401
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Urology
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| Research Institution | Mie university |
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Principal Investigator |
KAWAMURA Juichi Mie University・Faculty of Medicine, Professor., 医学部, 教授 (70026839)
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| Co-Investigator(Kenkyū-buntansha) |
ARIMA Kiminobu Mie University, University Hospital, Assistant., 医学部・附属病院, 助手 (10175995)
KINBARA Hiroyuki Mie University, University Hospital, Assistant., 医学部・附属病院, 助手 (40225123)
HAYASHI Norio Mie University・Faculty of Medicine, Assistant., 医学部, 助手 (70198852)
杉村 芳樹 医学部附属病院, 講師 (90179151)
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| Project Period (FY) |
1992 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥7,300,000 (Direct Cost: ¥7,300,000)
Fiscal Year 1994: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1993: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1992: ¥5,300,000 (Direct Cost: ¥5,300,000)
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| Keywords | Epithelial-mesenchymal interaction / Recombination / Urogenital sinus mesenchyme / Cell growth / Secretory protein / Dunning rat tumor / Organ culture / Keratinocyte Growth Factor / 上皮-間質相互作用 / 合成エストロゲン / 異常前立腺腺管 / テストステロン代謝 |
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| Research Abstract |
(1) The fetal urogenital sinus mesenchyme induced all prostatic secretory proteins product as well as the prostatic epithelial growth on any adult rodent prostatic lobes via epithelial-mesenchymal interaction. We examined the role of Keratinocyte growth factor (KGF) for prostatic development with mouse prostatic organ culture system using the serum free conditioning medium. That results suggested the role of KGF as a paracrine mediator for epithelial cells, which was produced by mesenchymal cells.
(2) Neonatal seminal vesicle mesenchyme elicited the reduction of growth rate and the changes of epithelial morphology, secretory protein molecular weight and testosterone metabolic pattern on Dunning rat prostatic carcinoma. Such like induced characteristics were similar to those of normal prostate or seminal vesicle. These findings demonstrate that the connective tissue environment can have profound regulative effects on both normal and neoplastic epithelial cells. The paracrine mediators like a KGF might certainly augment our knowledge of the carcinogenic process and lead to new therapeutic strategies.
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