Meta-analysis reveals a lack of association between UGT2B17 deletion polymorphism and tumor susceptibility.
meta_analysis · Level I
Where this comes from
- Record sourced from PubMed, PMID 24802609.
- Also identified by DOI 10.1371/journal.pone.0096812 and PMC identifier 4011861.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
UGT2B17 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. A 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. Conclusively, 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. These results suggest that the UGT2B17 deletion polymorphism is not associated with tumor risks.
Medical subject headings
- Glucuronosyltransferase
- Neoplasms