| Project/Area Number |
10671474
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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 | Hiroshima University |
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Principal Investigator |
MATSUBARA Akio (1999) HIROSHIMA UNIVERSITY, MEDICAL HOSPITAL UROLOGY, RESEARCH ASSOCIATE, 医学部・附属病院, 助手 (10239064)
中原 満 (1998) 広島大学, 医学部, 助教授 (70155802)
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| Co-Investigator(Kenkyū-buntansha) |
MITA Kouji HIROSHIMA UNIVERSITY, FACULTY OF MEDICINE UROLOGY, RESEARCH ASSOCIATE, 医学部, 助手 (70304425)
松原 昭郎 広島大学, 医学部・附属病院, 助手
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 1999: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1998: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | FGF / PROSTATE CANCER / GENE THERAPY / 成長因子 |
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| Research Abstract |
We have been investigating the potential roles of fibroblast growth factor receptors (FGFRs) in growth control of prostate tumors. Consequently we have recently found that hormone-dependent prostate tumor cells express FGFR2IIIb which mediates response to stromal-derived growth regulator FGF-7, while they lose the expression of FGFR2IIIb during progression from hormone-dependent to hormone-independent and escape the growth regulation by FGF-7. Instead the hormone-independent prostate tumor cells express FGFR1 and acquire autonomy. The results indicate that both restoration of FGFR2IIIb and deactivation of FGFR1 may result in a treatment of hormone-refractory prostate cancer. Thus, we induced the expression of FGFR2IIIb in hormone-independent rat prostate tumor cells by transfection. As a result, the transfected cells regained communication with stroma and not only showed reduced population growth rates, but also recovered cytokeratin expression and gland-like morphology specific to hormone-dependent tumors. We also transfected hormone-independent rat prostate tumor cells with kinase-defective FGFR1 to deactivate the endogenous FGFR1 by dominant-negative effect. As a result, in vivo growth of the transfected cells was similar to that of FGFR2IIIb-introduced cells.
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