ABSTRACT
PURPOSE: We investigated the association between the length of the polymorphic trinucleotide CAG microsatellite repeats in exon 1 of the AR gene and the risk of prostate cancer. MATERIALS AND METHODS: This is a nested case-control study of 1,159 cases and 1,353 controls from the Prostate Cancer Prevention Trial, a randomized, placebo controlled trial testing whether the 5α-reductase inhibitor finasteride could decrease the 7-year prevalence of prostate cancer. During the course of the trial men underwent annual digital rectal examination and prostate specific antigen measurement. Prostate biopsy was recommended in all men with abnormal digital rectal examination or finasteride adjusted prostate specific antigen greater than 4.0 ng/ml. Cases were drawn from men with biopsy determined prostate cancer identified by for cause or end of study biopsy. Controls were selected from men who completed the end of study biopsy. RESULTS: Mean CAG repeat length did not differ between cases and controls. The frequency distribution of cases and controls for the AR CAG repeat length was similar. There were no significant associations of CAG repeat length with prostate cancer risk when stratified by treatment arm (finasteride or placebo), or when combined. There was also no significant association between CAG repeat length and the risk of low or high grade prostate cancer. CONCLUSIONS: There is no association of AR CAG repeat length with prostate cancer risk. Knowledge of AR CAG repeat length provides no clinically useful information to predict prostate cancer risk.
Subject(s)
Prostatic Neoplasms/genetics , Receptors, Androgen/genetics , Aged , Case-Control Studies , Exons/genetics , Humans , Male , Microsatellite Repeats/genetics , Middle Aged , Prostatic Neoplasms/prevention & control , Randomized Controlled Trials as Topic , Risk FactorsABSTRACT
BACKGROUND: To examine whether androgen receptor (AR) CAG repeat length was associated with the risk of incident benign prostatic hyperplasia (BPH). METHODS: A nested case-control study of 416 BPH cases and 527 controls drawn from Prostate Cancer Prevention Trial placebo-arm participants who were free of BPH at baseline. BPH was assessed over 7 years and was defined as receipt of medical or surgical treatment, two scores > 14 on the International Prostate Symptom Score (IPSS), or two increases in IPSS > or = 5 with at least one score > or = 12. RESULTS: Compared to men with AR repeat length < or = 19, the covariate-adjusted odds ratios [95% CI] were 1.07 [0.73, 1.57] and 0.90 [0.55, 1.45]) for repeat length 20-24 and > or =25, respectively. There was a weak association of AR repeat length with baseline serum testosterone (T) (Spearman r = 0.09, p < 0.02); however, control for or stratification by T did not change study results. Further, results did not differ when stratified by body mass index or baseline concentration of 3alpha-diol glucoronide, and were similar for all BPH definitions. CONCLUSIONS: There were no associations of AR CAG repeat length and BPH risk. Knowledge of AR CAG repeat length provides no clinical useful information for the prevention of symptomatic BPH.
