Abstract
PurposeUGT2B17 is a vital member of the UGT2 family and functions as a detoxification enzyme which catalyzes the glucuronidation of lipophilic compounds. Accumulating evidences implicates that it may contribute to the susceptibility of tumor risk. Identification of a UGT2B17 deletion polymorphism has attracted studies to evaluate the association between the UGT2B17 deletion polymorphism and tumor risk in diverse populations. However, the available results are conflicting.MethodsA meta-analysis based on 14 studies from 10 publications including 5,732 cases and 5,112 controls was performed. Published literature from PubMed, EMBASE and Web of Science was pooled and the crude odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to estimate the strength of the associations.ResultsConclusively, our results indicate that individuals with a UGT2B17 deletion polymorphism were associated with tumor risks (OR = 1.29, 95% CI = 1.03–1.63, P<0.001) in a recessive model. However, after excluding two studies for their heterogeneity, the result then demonstrated that the UGT2B17 deletion polymorphism was not associated with tumor risks (OR = 1.118, 95%CI = 0.938–1.332, P>0.1). A subgroup analysis based on tumor type, sex or race did not show significant results.ConclusionThese results suggest that the UGT2B17 deletion polymorphism is not associated with tumor risks.
Highlights
Tumors are a multifactorial disease and have become a major global public health burden in recent years
Conclusively, our results indicate that individuals with a UGT2B17 deletion polymorphism were associated with tumor risks (OR = 1.29, 95% confidence intervals (CIs) = 1.03–1.63, P,0.001) in a recessive model
After excluding two studies for their heterogeneity, the result demonstrated that the UGT2B17 deletion polymorphism was not associated with tumor risks (OR = 1.118, 95%CI = 0.938–1.332, P.0.1)
Summary
Tumors are a multifactorial disease and have become a major global public health burden in recent years. Studies have demonstrated that tumors are a result of the intricate interactions between interior and environmental factors [1], such as race, age, family history, obesity, red and processed meat consumption, smoking and steroid hormone levels [2]. It has been demonstrated that enzymes may play an important role in the sensitivity to tumor risk through their functions of detoxifying carcinogenic substances and DNA synthesis [3,4]. UDP-glucuronosyltransferases (UGTs) are a family of phase II detoxification enzymes which catalyze the glucuronidation of lipophilic compounds like drugs, dietary substances, tobacco toxins and environmental xenobiotics [5,6,7]. UGTs function to glucuronidate endogenous and exogenous estrogens and androgens and transfer them to less active compounds which might reduce the risk of sex-related tumors, such as prostate and breast tumor
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