SRD5A2 Gene Polymorphisms and the Risk of Benign Prostatic Hyperplasia but not Prostate Cancer

Abstract

<b>Background:</b> Testosterone, a primary androgen in males, is converted into its most active form,dihydrotestosterone (DHT), by 5α-reductase type 2 (encoded by the SRD5A2 gene) in the prostate. DHT isnecessary for prostatic growth and has five times higher binding affinity than testosterone for androgen receptors.We hypothesized that polymorphic variations in the SRD5A2 gene may affect the risk of benign prostatichyperplasia and prostate cancer. Materials and <br/><b>Methods</b>: We analyzed SRD5A2 gene polymorphisms in 217 BPHpatients, 192 PCa cases, and 171 controls. Genotyping was undertaken using direct DNA sequencing. Genotypedata were compared between cases and controls using a Chi square statistical tool. <br/><b>Results</b>: We found that theA49T locus was monomorphic with ‘AA’ genotype in all subjects. At V89L locus, the presence of ‘VV’ showeda marginally significant correlation with increased BPH risk (p=0.047). At the (TA)n locus, longer TA repeatswere found to be protective against BPH (p=0.003). However, neither of these polymoprhisms correlated withthe risk of PCa. <br/><b>Conclusions</b>: We conclude that A49T is monomorphic in the study population, VV marginallycorrelates with BPH risk, and longer (TA)n repeats are protective against BPH. None of these polymorphismsaffect the risk of PCa.