Abstract
A full understanding of the etiology of prostate cancer is a goal we have yet to attain. Until recently, epidemiologists have focused mainly on possible environmental risk factors. After several decades of studies, no clear, single strong environmental risk factor has emerged, and this work has not led to a clear pathogenic pathway involving environmental influences (39). The opportunities created by evolving molecular technology in recent years have led to an increasing emphasis on determining the possible genetic influences on risk. As prostate cancer is a highly familial disease, recent studies have attempted to exploit this powerful risk factor by conducting genetic linkage studies in large multiplex prostate cancer families searching for one or several single locus, high-penetrance susceptibility genes. Although this work has revealed several suggestive loci on several chromosomes (41,49), confirmatory work for each of these to date has been largely inconclusive. Cloning of such a susceptibility gene for prostate cancer, a gene comparable in penetrance to the BRCA1 and BRCA2 loci for breast and ovarian cancer, remains elusive and is not likely to occur in the very near future. The alternative molecular epidemiologic focus in prostate cancer etiology has been on lowpenetrance candidate genes, which are significant not only to familial prostate cancer, but even more so to the sporadic forms of the disease—because the products of these genes serve functions along plausible biologic pathways of prostate carcinogenesis.
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Ross, R.K., Reichardt, J.K.V., Ingles, S.A., Coetzee, G.A. (2001). The Genetic Epidemiology of Prostate Cancer. In: Chung, L.W.K., Isaacs, W.B., Simons, J.W. (eds) Prostate Cancer. Contemporary Cancer Research. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-009-4_7
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DOI: https://doi.org/10.1007/978-1-59259-009-4_7
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