We know that both a positive family history and racial background are among the strongest epidemiological risk factors for prostate cancer.
It is also recognized that the role of candidate genetic markers to prostate cancer is more difficult to identify than the identification of other cancer susceptibility genes. Despite the localization of several susceptibility loci, there has been limited success in identifying high-risk susceptibility genes analogous to BRCA1 or BRCA2 for breast and ovarian cancer.
Despite this there are three strong candidate susceptibility genes, namely ELAC2 (chromosome 17p11/HPC2 region),
2?-5?-oligoadenylate-dependent ribonuclease L (RNASEL), a gene in the HPC1 region, and Macrophage Scavenger Receptor 1 (MSR1), a gene within a region of linkage on chromosome 8p.
We are in desperate need of additional studies using larger sample sizes to fully evaluate the role of these genes in prostate cancer risk and disease progression. Until that happens we will remain in the dark without genetic biomarkers which we so desperately need.
It is also of interest to mention that a significant percentage of men with early-onset (prostate cancer at a younger age) harbor germline mutation in the BRCA2 gene thus confirming its role as a high-risk prostate cancer susceptibility gene.
Although initial analyses supported the hypothesis that a number of rare highly penetrant loci contribute to the Mgenetic inheritance of prostate cancer, current experimental evidence better supports the hypothesis that some of the familial risks may be due to inheritance of multiple moderate-risk genetic variants. In this regard, it is not surprising that analyses of genes encoding key proteins involved in androgen biosynthesis and action led to the observation of a significant association between a susceptibility to prostate cancer and common genetic variants in some of these genes.
Endocrine-Related Cancer (2003) 10 225–259
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