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RNASEL Gene Polymorphisms and the Risk of Prostate Cancer: a Meta-analysis

Authors' Affiliations: ¹ Biostatistics Unit, Division of Clinical Trials and Epidemiological Sciences, National Cancer Centre and ² Centre for Molecular Epidemiology and Department of Community, Occupational and Family Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore

Requests for reprints: Huihua Li, Division of Clinical Trials and Epidemiological Sciences, National Cancer Centre, 11 Hospital Drive, Singapore, Singapore 169610. Phone: 65-62369451; Fax: 65-65365503; E-mail: ctelhh{at}nccs.com.sg.

Purpose: Studies revealing conflicting results on the role of RNASEL polymorphisms Glu265X, Arg462Gln, and Asp541Glu on prostate cancer risk led us to perform a meta-analysis to investigate the association of these polymorphisms and prostate cancer risk.

Experimental Design: Relevant studies were selected by searching PubMed from January 1996 to August 2005 using keywords "RNASEL gene AND prostate cancer." For each study, odds ratio (OR) with 95% confidence interval (95% CI) was calculated to estimate the gene effect. Pooled estimates of the OR were computed using the random effects model.

Results: Ten studies were included in the meta-analysis. The overall results suggested no major influence of these variants on prostate cancer risk. However, analysis of the Asp541Glu polymorphism by ethnic populations showed that Asp/Glu (familial cases versus control: OR, 1.38; 95% CI, 1.04-1.82; sporadic cases versus control: OR, 1.26; 95% CI, 1.07-1.48; prostate cancer versus control: OR, 1.29; 95% CI, 1.12-1.48) and Asp/Glu + Glu/Glu (familial cases versus control: OR, 1.37; 95% CI, 1.10-1.70; sporadic cases versus control: OR, 1.24; 95% CI, 1.07-1.44; prostate cancer versus control: OR, 1.27; 95% CI, 1.13-1.44) increased prostate cancer risk in Caucasians, thus suggesting a dominant model for the Glu variant.

Conclusions: Compared with the genotype Asp/Asp, the Glu variant at the Asp541Glu polymorphism increases prostate cancer risk by <2-fold in Caucasians, regardless of family history of the disease. This suggests that genuine genetic effects of this polymorphism may account for only a part of prostate cancer in the Caucasian population.

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