摘要
Increasing epidemiological studies were recently performed to assess the relationship of NAD(P)H: quinine oxidoreductase 1 (NQO1) Pro187Ser polymorphism and the risk of prostate cancer (PCa) to yield inconsistent results. In this study, we aimed to generate large-scale evidence on whether NQO1 Pro187Ser polymorphism conferred to the susceptibility of PCa. The database of PubMed was comprehensively reviewed until September 12th, 2013, without any linguistic limitation. Meta-analysis was complied in the codominant, dominant, recessive and allele models by either fixed or random effect models. Odds ratios (OR) and 95% confidence intervals (95%CI) were calculated to evaluate the strength of the association between the two. Finally, six eligible studies with 717 cases and 1764 controls were included. In overall analyses, significant associations were found in the dominant (OR = 1.26, 95%CI = 1.04 - 1.52, P = 0.02), allele (OR = 1.20, 95%CI = 1.03 - 1.40, P = 0.02) and the heterozygous codominant (OR = 1.24, 95%CI = 1.02 - 1.52, P = 0.03) models. Also, significant results were found in the stratified analyses by Hardy-Weinberg equilibrium (HWE). Still, subgroup analysis showed an increased risk of PCa in Asian rather than Caucasian population. Besides, NQO Pro187Ser polymorphism correlated with a heightened risk of PCa in the hospital-based studies. Our study indicated that NQO1 functional Pro187Ser polymorphism could be a potentially genetic biomarker for the risk of PCa, especially in Asian population.
Increasing epidemiological studies were recently performed to assess the relationship of NAD(P)H: quinine oxidoreductase 1 (NQO1) Pro187Ser polymorphism and the risk of prostate cancer (PCa) to yield inconsistent results. In this study, we aimed to generate large-scale evidence on whether NQO1 Pro187Ser polymorphism conferred to the susceptibility of PCa. The database of PubMed was comprehensively reviewed until September 12th, 2013, without any linguistic limitation. Meta-analysis was complied in the codominant, dominant, recessive and allele models by either fixed or random effect models. Odds ratios (OR) and 95% confidence intervals (95%CI) were calculated to evaluate the strength of the association between the two. Finally, six eligible studies with 717 cases and 1764 controls were included. In overall analyses, significant associations were found in the dominant (OR = 1.26, 95%CI = 1.04 - 1.52, P = 0.02), allele (OR = 1.20, 95%CI = 1.03 - 1.40, P = 0.02) and the heterozygous codominant (OR = 1.24, 95%CI = 1.02 - 1.52, P = 0.03) models. Also, significant results were found in the stratified analyses by Hardy-Weinberg equilibrium (HWE). Still, subgroup analysis showed an increased risk of PCa in Asian rather than Caucasian population. Besides, NQO Pro187Ser polymorphism correlated with a heightened risk of PCa in the hospital-based studies. Our study indicated that NQO1 functional Pro187Ser polymorphism could be a potentially genetic biomarker for the risk of PCa, especially in Asian population.
