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Androgen receptor gene polymorphism and prostate cancer in Taiwan.
J Formos Med Assoc. 2003 Oct; 102(10):680-6.JF

Abstract

BACKGROUND AND PURPOSE

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.

Authors+Show Affiliations

Department of Urology, Kaohsiung Medical University, Kaohsiung, Taiwan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

14691592

Citation

Huang, Shu-Pin, et al. "Androgen Receptor Gene Polymorphism and Prostate Cancer in Taiwan." Journal of the Formosan Medical Association = Taiwan Yi Zhi, vol. 102, no. 10, 2003, pp. 680-6.
Huang SP, Chou YH, Chang WS, et al. Androgen receptor gene polymorphism and prostate cancer in Taiwan. J Formos Med Assoc. 2003;102(10):680-6.
Huang, S. P., Chou, Y. H., Chang, W. S., Wu, M. T., Yu, C. C., Wu, T., Lee, Y. H., Huang, J. K., Wu, W. J., & Huang, C. H. (2003). Androgen receptor gene polymorphism and prostate cancer in Taiwan. Journal of the Formosan Medical Association = Taiwan Yi Zhi, 102(10), 680-6.
Huang SP, et al. Androgen Receptor Gene Polymorphism and Prostate Cancer in Taiwan. J Formos Med Assoc. 2003;102(10):680-6. PubMed PMID: 14691592.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Androgen receptor gene polymorphism and prostate cancer in Taiwan. AU - Huang,Shu-Pin, AU - Chou,Yii-Her, AU - Chang,Wun-Shaing Wayne, AU - Wu,Ming-Tsang, AU - Yu,Chia-Cheng, AU - Wu,TonyT, AU - Lee,Ying-Huei, AU - Huang,Jong-Khing, AU - Wu,Wen-Jeng, AU - Huang,Chun-Hsiung, PY - 2003/12/24/pubmed PY - 2004/3/16/medline PY - 2003/12/24/entrez SP - 680 EP - 6 JF - Journal of the Formosan Medical Association = Taiwan yi zhi JO - J. Formos. Med. Assoc. VL - 102 IS - 10 N2 - BACKGROUND AND PURPOSE: 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. SN - 0929-6646 UR - https://www.unboundmedicine.com/medline/citation/14691592/Androgen_receptor_gene_polymorphism_and_prostate_cancer_in_Taiwan_ L2 - http://www.diseaseinfosearch.org/result/9175 DB - PRIME DP - Unbound Medicine ER -