| Research Abstract |
Prostate cancer is one of the most common neoplasms in Western countries, and while it has been infrequent in Japan, its incidence has recently been increasisng. Epidemiological and pathological studies indicate that human cancer development is a multistep process. Recent application of molecular biological techniques has pointed to the involvement of many oncogenes and tumor suppressor genes in carcinogenesis.
In this study, to clanify the role of accumulation of genetic alterations on prostate cancer development, we performed mutational analyzes of the p 53 gene and examined alllelie loss in loci containing unidentifiedor the known tumor supressor genes in Japanese prostate cancers.
Of the 90 cases examined, eleven cases had mutations in exons 2-11 of the p53 gene and we found that the proportion of transvertions in Japanse is higher than that previously reported in American and European cases, suggesting that there are different factors responsible for carcinogenesis of the prostate glands.
A seires of 25 primary prostate cancers were screened for loss of heterozygosity (LOH) using microsatellite markers containing AFC,DCC,TF53, BRCA1 and BRCA2. Frequent LOH was observed for D8S201 (48%), LPL (48%) and DCC (26%). In contrast, the incidence did not exceed 15% at BRCA1 and BRCA2 loci. These data suggest that LOH on chromosome 8p may be involved in carcinogenesis of the prostate, howener, BRCA1 and BRCA2 may not be largely involved in the development of prostate cencerin the Japanese population.
Our study partially clarified the involvement of oncogenes and tumor suppressor genes in prostate cancer development, however, further study is needed.
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