Androgen receptor CAG polymorphism and the risk of benign prostatic hyperplasia in a Brazilian population

Vanderlei Biolchi,Walter Koff,Ilma Simoni Brum,Brasil Silva Neto

doi:10.1590/s1677-55382012000300010

Abstract

Benign prostatic hyperplasia (BPH) is a very frequent age-related proliferative abnormality in men. Polymorphic CAG repeat in the androgen receptor (AR) can alter transactivation of androgen-responsive genes and potentially influence BPH risk. We investigated the association between CAG repeat length and risk of BPH in a case-control study of a Brazilian population. We evaluated 214 patients; 126 with BPH and 88 healthy controls. DNA was extracted from peripheral leucocytes and the AR gene was analyzed using fragment analysis. Hazard ratio (HR) and 95% confidence interval were estimated using logistic regression models. Mean CAG length was not different between patients with BPH and controls. The CAG repeat length was examined as a categorical variable (CAG ≤ 21 vs. CAG > 21 and CAG ≤ 22 vs. CAG > 22) and did not differ between the control vs. the BPH group. We found no evidence for an association between AR CAG repeat length in BPH risk in a population-based sample of Brazilians.

Highlights

Benign prostatic hyperplasia (BPH) is a very frequent age-related proliferative abnormality in men
Prostatic volume was higher in the BPH group than in the control group (p < 0.001)
Our results showed no association between androgen receptor (AR) CAG allele length and risk of developing BPH

Summary

Introduction

Benign prostatic hyperplasia (BPH) is a very frequent age-related proliferative abnormality in men. Polymorphic CAG repeat in the androgen receptor (AR) can alter transactivation of androgen-responsive genes and potentially influence BPH risk. We investigated the association between CAG repeat length and risk of BPH in a case-control study of a Brazilian population. Mean CAG length was not different between patients with BPH and controls. We found no evidence for an association between AR CAG repeat length in BPH risk in a population-based sample of Brazilians. Androgen binding promotes the activation of the androgen receptor (AR) and recruitment of co-factors, leading to the transcription of hormone-dependent target genes [6,7,8,9]. In vitro studies have shown a negative correlation between the number of CAG repeats and the transcriptional activity of the AR. The increased number of these repeats reduces transcriptional activity in the AR, whereas a reduction to zero induces increased AR [11,14,15]

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