Androgen receptor gene polymorphism and prostate cancer in Taiwan.
OBJECTIVE
The length of polymorphic CAG trinucleotide repeats in the polyglutamine region of the androgen receptor (AR) gene has been suggested to be inversely correlated with the transactivation function of the AR. An increase in androgen activity may be associated with prostate cancer, and ethnic variations in CAG repeat length may contribute to varying prostate cancer risks in different populations. This case-control study investigated the potential role of AR polymorphism in prostate cancer risk in Taiwanese.


METHODS
Sixty six pathologically-confirmed prostate cancer patients and 104 controls were studied. CAG repeat polymorphism was genotyped by a polymerase chain reaction (PCR)-based direct sequencing method. Logistic regression was used to determine the relative risk of AR gene CAG number on prostate cancer risk. The associations of AR-CAG polymorphism with disease stage, pathologic grade, and age at diagnosis were assessed. AR-CAG repeat number was first treated as a continuous variable, then was divided into short and long groups (n < 23 vs n > or = 23) for categorical analysis. The extreme groups of AR-CAG distribution were also analyzed for these associations (n < or = 20 vs n > or = 26 and n = 21-25 vs n > or = 26).


RESULTS
The mean number of CAG repeats in patients and controls was similar: 23.2 +/- 3.0 (range, 15 to 31) and 22.9 +/- 3.1 (range, 15 to 31), respectively. No association was found between AR-CAG repeat polymorphism and disease stage (p = 0.30), histological grade (p = 0.49), or age at diagnosis (p = 0.51). After adjusting for other covariates (age, body mass index, education level, smoking, and alcohol status), the number of AR-CAG repeats was not significantly associated with prostate cancer risk [odds ratio (OR) = 0.97, 95% confidence interval (95% CI) = 0.72 to 1.31; p = 0.84]. In categorical analysis, men with short CAG repeats (n < 23) did not have increased risk for prostate cancer (OR = 0.45, 95% CI = 0.29 to 1.05) compared to those with long CAG repeats (n > or = 23). Non-significant differences in prostate cancer risk were also found when comparing the extreme short group (n < or = 20) and the intermediate group (n = 21-25) to the extreme long group (n > or = 26) [n < or = 20 vs n > or = 26: OR = 1.00, 95% CI = 0.34 to 3.00; n = 21-25 vs n > or = 26: OR = 0.82, 95% CI = 0.37 to 1.81].


CONCLUSIONS
The results of this study do not support an important effect of AR-CAG repeat polymorphism on prostate cancer risk. A large-scale study is needed to clarify genetic components of prostate cancer risk in the Taiwanese population.
Huang
Shu-Pin
SP
Department of Urology, Kaohsiung Medical University, Kaohsiung, Taiwan.
Chou
Yii-Her
YH
Chang
Wun-Shaing Wayne
WS
Wu
Ming-Tsang
MT
Yu
Chia-Cheng
CC
Wu
TonyT
T
Lee
Ying-Huei
YH
Huang
Jong-Khing
JK
Wu
Wen-Jeng
WJ
Huang
Chun-Hsiung
CH
D000368:Aged; D016022:Case-Control Studies; D006801:Humans; D008297:Male; D011110:Polymorphism, Genetic; D011471:Prostatic Neoplasms / Q000453:epidemiology / Q000235:genetics*; D011944:Receptors, Androgen / Q000235:genetics*; D013624:Taiwan / Q000453:epidemiology; D018911:Trinucleotide Repeats
D011944:Receptors, Androgen