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Carcinogenesis Advance Access originally published online on April 18, 2006
Carcinogenesis 2006 27(9):1894-1901; doi:10.1093/carcin/bgl042
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© The Author 2006. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
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Genetic variants of the ADPRT, XRCC1 and APE1 genes and risk of cutaneous melanoma

Chunying Li1, Zhensheng Liu1, Li-E Wang1, Sara S. Strom1, Jeffrey E. Lee2, Jeffrey E. Gershenwald2, Merrick I. Ross2, Paul F. Mansfield2, Janice N. Cormier2, Victor G. Prieto3, Madeleine Duvic4, Elizabeth A. Grimm5 and Qingyi Wei*

1Department of Epidemiology, The University of Texas M. D. Anderson Cancer Center Houston, TX, USA
2 Department of Surgical Oncology, The University of Texas M. D. Anderson Cancer Center Houston, TX, USA
3 Department of Pathology, The University of Texas M. D. Anderson Cancer Center Houston, TX, USA
4 Department of Dermatology, The University of Texas M. D. Anderson Cancer Center Houston, TX, USA
5 Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center Houston, TX, USA

*To whom correspondence should be addressed at: Department of Epidemiology, Unit 1365, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA. Tel: +1 713 792 3020; Fax: +1 713 563 0999; Email: qwei{at}mdanderson.org.

Sunlight causes various kinds of DNA damage, including oxidative lesions that are removed effectively by the base excision repair (BER) pathway, in which ADPRT, XRCC1 and APE1 play a key role. However, genetic variation in these genes may alter their functions. We hypothesized that ADPRT, XRCC1 and APE1 polymorphisms 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. the ADPRT Val762Ala, XRCC1 Arg399Gln and APE1Asp148Glu) 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 the APE1 Asp/Asp genotype, a significantly decreased risk of CM was associated with the APE1 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 combined APE1 Asp/Glu+Glu/Glu (OR, 0.59; 95% CI, 0.42–0.83) genotypes, but not for other XRCC1 variant genotypes. Moreover, there was evidence for a possible gene–gene interaction between XRCC1 and APE1 variants in the association with risk of CM (P = 0.030). We conclude that the APE1 Glu variant may have an effect or interact with XRCC1 in 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.


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