Prostate cancer is the most common cancer diagnosed in men and is the second most common cause of cancer death. Despite its prevalence, determinants of prostate cancer risk remain largely unidentified. Previously, our laboratory has demonstrated an association between a silent Taq I polymorphism in exon 9 of the vitamin D receptor (VDR) and increased prostate cancer risk. Subsequently, another group demonstrated an association between a poly-A length polymorphism in the 3? untranslated region (3?UTR) of the VDR and increased prostate cancer risk. We hypothesized that the poly-A polymorphism, a homopolymeric run of adenines that varies in length from 14 to 22, was a more likely candidate polymorphism in the VDR to have functional significance. We developed a method to genotype DNA samples for the poly-A polymorphism and then analyzed a case group of 108 men who underwent radical prostatectomy at UNC Hospitals and a control group of 170 noncancer patients from the Urology clinics at Duke University Medical Center. These samples were previously genotyped for the VDR polymorphism in exon 9. We are currently analyzing these data and are genotyping another group of prostate cancer cases and controls from Bowman Gray Medical Center. By genotyping the cases and controls from the UNC/Duke and Bowman Gray studies for the TaqI and poly-A polymorphisms , we hope to better characterize the association of genetic polymorphisms in the VDR and the development of prostate cancer that has previously been described. In addition, these results may help direct efforts to locate the DNA sequence polymorphism that has functional significance in the VDR gene.
