Meta-Analysis:
Lack of association between NAT2 polymorphism and prostate cancer risk: a meta-analysis and trial sequential analysis
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Abstract
Feng Wang1,*, Zhiqiang Qin2,*, Shuhui Si3,*, Jingyuan Tang2, Lingyan Xu4, Haoxiang Xu2, Ran Li2, Peng Han2 and Haiwei Yang1,2
1Department of Radiation Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210009, China
2State Key Laboratory of Reproductive Medicine, Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China
3Research Division of Clinical Pharmacology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210009, China
4Department of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210009, China
*These authors contributed equally to this work
Correspondence to:
Haiwei Yang, email: [email protected]
Keywords: NAT2*4, gene polymorphism, prostate cancer, meta-analysis
Received: March 29, 2017 Accepted: June 17, 2017 Published: July 05, 2017
ABSTRACT
Previous studies have investigated the association between NAT2 polymorphism and the risk of prostate cancer (PCa). However, the findings from these studies remained inconsistent. Hence, we performed a meta-analysis to provide a more reliable conclusion about such associations. In the present meta-analysis, 13 independent case-control studies were included with a total of 14,469 PCa patients and 10,689 controls. All relevant studies published were searched in the databates PubMed, EMBASE, and Web of Science, till March 1st, 2017. We used the pooled odds ratios (ORs) with 95% confidence intervals (CIs) to evaluate the strength of the association between NAT2*4 allele and susceptibility to PCa. Subgroup analysis was carried out by ethnicity, source of controls and genotyping method. What’s more, we also performed trial sequential analysis (TSA) to reduce the risk of type I error and evaluate whether the evidence of the results was firm. Firstly, our results indicated that NAT2*4 allele was not associated with PCa susceptibility (OR = 1.00, 95% CI= 0.95–1.05; P = 0.100). However, after excluding two studies for its heterogeneity and publication bias, no significant relationship was also detected between NAT2*4 allele and the increased risk of PCa, in fixed-effect model (OR = 0.99, 95% CI= 0.94–1.04; P = 0.451). Meanwhile, no significant increased risk of PCa was found in the subgroup analyses by ethnicity, source of controls and genotyping method. Moreover, TSA demonstrated that such association was confirmed in the present study. Therefore, this meta-analysis suggested that no significant association between NAT2 polymorphism and the risk of PCa was found.
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