Premium
CAG repeat within the androgen receptor gene and incidence of surgery for benign prostatic hyperplasia in U.S. physicians
Author(s) -
Giovannucci Edward,
Stampfer Meir J.,
Chan Andrew,
Krithivas Krishna,
Gann Peter H.,
Hennekens Charles H.,
Kantoff Philip W.
Publication year - 1999
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/(sici)1097-0045(19990501)39:2<130::aid-pros8>3.0.co;2-#
Subject(s) - androgen receptor , transactivation , prostate cancer , medicine , hyperplasia , odds ratio , androgen , exon , prostate , incidence (geometry) , confidence interval , urology , endocrinology , gene , gynecology , cancer , biology , gene expression , genetics , hormone , physics , optics
BACKGROUND CAG repeat length in exon 1 of the androgen receptor (AR) gene correlates inversely with transcriptional transactivation activity of the AR. Men with shorter AR CAG repeat lengths are at higher risk of prostate cancer. Because benign prostatic hyperplasia (BPH) is an androgen‐dependent condition, we examined the hypothesis that a shorter AR gene CAG repeat length increases the risk of developing of BPH. METHODS Among 14,916 men of the Physicians' Health Study who had provided a blood sample in 1982, we measured AR gene CAG repeat lengths for 310 men who had surgery for BPH up to 7.5 years of follow‐up and 1,041 controls. RESULTS Risk of surgery for BPH increased linearly with decreasing AR CAG repeat length ( P (trend) = 0.03). Relative to men with a CAG repeat length ⩾25, men with a repeat length ⩽19 had an odds ratio of BPH surgery of 1.76 (95% confidence interval, 1.16–2.65). CONCLUSIONS Variability in the AR gene CAG repeat influences the development of symptomatic BPH. Prostate 39:130–134, 1999. © 1999 Wiley‐Liss, Inc.