Background: Previous studies suggested that the H63D and C282Y polymorphisms in the HFE genes weresusceptible to many cancer types, nevertheless, the present results were inconclusive. Thus, the present studywas aimed to evaluate the association between the HFE polymorphisms (H63D and C282Y) and cancer riskvia meta-analysis. Materials and
Methods: We retrieved PubMed, Google Scholar, Embase and Web of Sciencedatabases for all eligible studies up to April 1, 2015. All the statistical analysis was conducted by STATA 12.0.
Results: Finally, a total of 20 publications including 24 case-control studies, comprising 6,524 cases and 31,080controls for HFE-C282Y polymorphism and 19 publications including 21 case control studies, comprising 5,648cases and 14,257 controls for HFE-H63D polymorphism were enrolled in our analysis. An increased risk for overallcancer risk was identified in HFE-H63D polymorphism under allele contrast (D vs H: OR=1.153; 95%CI=1.031-1.289, Pheterogeneity=0.002), homozygotes vs wide type (DD vs HH: OR=1.449; 95%CI=1.182-1.777,Pheterogeneity=0.391), dominant model (DD+HD vs HH: OR=1.145; 95%CI=1.007-1.301, Pheterogeneity=0.002)and recessive model (DD vs HD+HH: OR=1.416 ; 95%CI=1.156-1.735, Pheterogeneity=0.549), as well as HFEC282Yunder homozygotes vs wide type (YY vs CC: OR=1.428, 95%CI=1.017-2.006, Pheterogeneity=0.220). Inaddition, in the stratified analysis by cancer type, an increased risk was identified in hepatocellular carcinomaand breast cancer in C282Y polymorphism, as well as pancreatic cancer in H63D polymorphism, whereas adecreased risk of colorectal cancer was identified in C282Y polymorphism.
Conclusions: Present study suggestedthat H63D and C282Y polymorphisms associated with an increased risk of overall cancer. Nevertheless, welldesignedstudy with large sample size will be continued on this issue of interest.