| Project/Area Number |
08671841
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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 | KITASATO UNIVERSITY |
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Principal Investigator |
EGAWA Shin Kitasato Univ.School of Medicine, Dept.Urology, Assistant Professor, 医学部, 講師 (60160347)
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| Co-Investigator(Kenkyū-buntansha) |
KOSHIBA Ken Kitasato Univ.School of Medicine, Depat.fUrology, Professor, 医学部, 教授 (40050380)
KUWANO Sadahito Kitasato Univ.School of Medicine, Dept.Urology, Associate Professor, 医学部, 助教授 (70137925)
UCHIDA Toyoaki Kitasato Univ.School of Medicine, Dept.Urology, Assistant Professor, 医学部, 講師 (70146489)
IWAMURA Masatsugu Kitasato Univ.School of Medicine, Dept.Urology, Assistant Professor, 医学部, 講師 (20176564)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1997: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1996: ¥600,000 (Direct Cost: ¥600,000)
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| Keywords | Prostate cancer / competitive PCR / molecular marker / racial difference / point mutation / 点突然変異定性 / 生物学的活性 / genomic instability / DNA ploidy / TGF-beta1 |
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| Research Abstract |
Prostate cancer is unique among potentially lethal human malignancies in terms of striking differences in the mortality rate and incidence according to country. Environmental factors and differences in the probability of occurrence in genetic events essential for tumor progression may possibly be factors responsible for cancer cell proliferation. However, molecular mechanisms for prostate carcinogenesis is very little understood despite these considerations. The PCR-based microsatellite instability assay was used to screen 66 patients with prostatic adenocarcinoma for possible mutator phenotype at 8 microsatellite marker loci on 5 chromosomes in our previous study. Unstable microsatellites was detected in 13 of the 66 (19.7%) patients. Somatic instability may be related to a phenotype with the ability to invade outside the confines of the prostate gland. We could not find any distinct differences in volume, distribution or DNA ploidy status of a tumor from western counterpart. Examination was made of structural abnormality of the androgen receptor (AR) gene in 29 human prostate cancer. A point mutation was found in the exon D hormone-binding domain of AR leading to substitution of glutamine (CAG) for wild-type arginine (CGG) at codon 629 in 1 (3.4%) hormone-independent stage D2 patient. Microsatellite instability was detected in 5 of the 27 (18.5%)patients, 1 of 6 (16.7%) hormon independent stage D2 and 4 of 2l (19.0%) hormdne-dependent and non-treated prostate cancer patients. Competitive PCR method was employed to further investigate the pattern of expression of kai-1, bcl2, TGFbeta and PTHrP in human prostate cancer. No specific pattern of expression was determined.
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