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Carcinogenesis Advance Access originally published online on October 29, 2005
Carcinogenesis 2006 27(3):610-618; doi:10.1093/carcin/bgi252
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Carcinogenesis vol.27 no.3 © Oxford University Press 2005; all rights reserved.

Polymorphisms in nucleotide excision repair genes and risk of multiple primary melanoma: the Genes Environment and Melanoma Study

Robert C. Millikan *, Amanda Hummer 1, Colin Begg 1, Jon Player, Allan René de Cotret, Scott Winkel, Harvey Mohrenweiser 3, Nancy Thomas, Bruce Armstrong 4, Anne Kricker 4, Loraine D. Marrett 5, Stephen B. Gruber 6, Hoda Anton Culver 3, Roberto Zanetti 7, Richard P. Gallagher 8, Terence Dwyer 9, Timothy R. Rebbeck 10, Klaus Busam 1, Lynn From 11, Urvi Mujumdar 1, Marianne Berwick 2 for the GEM Study Group

Department of Epidemiology, CB #7435, School of Public Health, University of North Carolina, Chapel Hill, NC 27599, USA, 1 Memorial Sloan-Kettering, Cancer Center, New York, NY, USA, 2 University of New Mexico, Albuquerque, NM, USA, 3 University of California, Irvine; CA, USA, 4 University of Sydney, Sydney, New South, Wales, Australia, 5 Cancercare Ontario, Toronto, Ontario, Canada, 6 University of Michigan, Ann Arbor, MI, USA, 7 Centro per la Prevenzione Oncologia, Torino, Piemonte, Italy, 8 British Columbia Cancer Agency, Vancouver, BC, Canada, 9 Royal Children's Hospital, Parkville, Victoria, Australia, 10 University of Pennsylvania, Philadelphia, PA, USA and 11 Women's College Hospital, Toronto, Ontario, Canada

* To whom correspondence should be addressed. Tel: +919 966 7437; Fax: +919 966 2089; Email: millikan{at}email.unc.edu

Polymorphisms in six genes involved in nucleotide excision repair of DNA were examined in a large population-based case–control study of melanoma. Genotyping was conducted for 2485 patients with a single primary melanoma (controls) and 1238 patients with second or higher order primary melanomas (cases). Patients were ascertained from nine geographic regions in Australia, Canada, Italy and the United States. Positive associations were observed for XPD 312 Asn/Asn versus Asp/Asp [odds ratio (OR) = 1.5, 95% confidence interval (CI) 1.2–1.9] and XPD 751 Gln/Gln versus Lys/Lys (OR = 1.4, 95% CI 1.1–1.7) genotypes and melanoma. The combined XPD Asn (A) 312 + Gln (C) 751 haplotype was significantly more frequent in cases (32%) compared with controls (29%) (P = 0.003) and risk of melanoma increased significantly with one and two copies of the haplotype (ORs 1.2, 95% CI 1.0–1.4, and 1.6, 95% CI 1.2–2.0, trend P = 0.002). No significant associations were observed for HR23B codon 249, XPG codon 1104, XPC codon 939, XPF codon 415, XPF nt 2063, ERCC6 codon 1213 or ERCC6 codon 1230. ORs for XPD and XPC genotypes were stronger for melanoma diagnosed at an early age, but tests for interaction were not statistically significant. The results provide further evidence for a role of XPD in the etiology of melanoma.


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