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Carcinogenesis Advance Access published online on October 29, 2005
Carcinogenesis, doi:10.1093/carcin/bgi252
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© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received July 12, 2005
Revised October 19, 2005
Accepted October 26, 2005

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

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

Robert C. Millikan 1*, Amanda Hummer 2, Colin Begg 2, Jon Player 1, Allan René de Cotret 1, Scott Winkel 1, Harvey Mohreweiser 3, Nancy Thomas 1, 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 Rebbeck 10, Klaus Busam 2, Lynn From 11, Urvi Mujumdar 2, Marianne Berwick 12, and for the GEM Study Group

1 University of North Carolina, Chapel Hill, NC
2 Memorial Sloan-Kettering Cancer Center, New York, NY
3 University of California, Irvine, CA
4 University of Sydney, Sydney, New South Wales, Australia
5 Cancercare Ontario, Toronto, Ontario, Canada
6 University of Michigan, Ann Arbor, MI
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
11 Women's College Hospital, Toronto, Ontario, Canada
12 University of New Mexico, Albuquerque, NM

* To whom correspondence should be addressed.
Robert C. Millikan, E-mail: millikan{at}email.unc.edu


  Abstract

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. Odds ratios 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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