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Sunlight causes various kinds of DNA damage, including oxidative lesions that are removed effectively by the base excision repair (BER) pathway, in whichADPRT,XRCC1andAPE1play a key role. However, genetic variation in these genes may alter their functions. We hypothesized thatADPRT,XRCC1andAPE1polymorphisms are associated with risk of cutaneous melanoma (CM). In a hospital-based case–control study of 602 CM patients and 603 cancer-free control subjects frequency matched on age, sex and ethnicity, we genotyped for three non-synonymous single nucleotide polymorphisms (SNPs) (i.e. theADPRT Val762Ala,XRCC1 Arg399GlnandAPE1Asp148Glu) and assessed their associations with risk of CM. We found no significant difference in the allele frequencies between cases and controls for any of these three SNPs. However, we found that, compared with theAPE1 Asp/Aspgenotype, a significantly decreased risk of CM was associated with theAPE1 Asp/Glu[adjusted odds ratio (OR), 0.60; 95% confidence interval (CI), 0.41–0.86],Glu/Glu(OR, 0.58; 95% CI, 0.38–0.88) and combinedAPE1 Asp/Glu+Glu/Glu(OR, 0.59; 95% CI, 0.42–0.83) genotypes, but not for otherXRCC1variant genotypes. Moreover, there was evidence for a possible gene–gene interaction betweenXRCC1andAPE1variants in the association with risk of CM (P= 0.030). We conclude that theAPE1 Gluvariant may have an effect or interact withXRCC1in the etiology of CM or in linkage disequilibrium with other untyped protective alleles. Larger studies with more SNPs in the BER genes are needed to verify these findings.

Genetic variants of the ADPRT, XRCC1 and APE1 genes and risk of cutaneous melanoma