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Genome-wide association study identifies three new melanoma susceptibility loci.

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Date
2011-10-09
Authors
Barrett, Jennifer H
Iles, Mark M
Harland, Mark
Taylor, John C
Aitken, Joanne F
Andresen, Per Arne
Akslen, Lars A
Armstrong, Bruce K
Avril, Marie-Francoise
Azizi, Esther
Bakker, Bert
Bergman, Wilma
Bianchi-Scarrà, Giovanna
Bressac-de Paillerets, Brigitte
Calista, Donato
Cannon-Albright, Lisa A
Corda, Eve
Cust, Anne E
Dębniak, Tadeusz
Duffy, David
Dunning, Alison M
Easton, Douglas F
Friedman, Eitan
Galan, Pilar
Ghiorzo, Paola
Giles, Graham G
Hansson, Johan
Hocevar, Marko
Höiom, Veronica
Hopper, John L
Ingvar, Christian
Janssen, Bart
Jenkins, Mark A
Jönsson, Göran
Kefford, Richard F
Landi, Giorgio
Landi, Maria Teresa
Lang, Julie
Lubiński, Jan
Mackie, Rona
Malvehy, Josep
Martin, Nicholas G
Molven, Anders
Montgomery, Grant W
van Nieuwpoort, Frans A
Novakovic, Srdjan
Olsson, Håkan
Pastorino, Lorenza
Puig, Susana
Puig-Butille, Joan Anton
Randerson-Moor, Juliette
Snowden, Helen
Tuominen, Rainer
Van Belle, Patricia
van der Stoep, Nienke
Whiteman, David C
Zelenika, Diana
Han, Jiali
Fang, Shenying
Lee, Jeffrey E
Wei, Qingyi
Lathrop, G Mark
Gillanders, Elizabeth M
Brown, Kevin M
Goldstein, Alisa M
Kanetsky, Peter A
Mann, Graham J
Macgregor, Stuart
Elder, David E
Amos, Christopher I
Hayward, Nicholas K
Gruis, Nelleke A
Demenais, Florence
Bishop, Julia A Newton
Bishop, D Timothy
GenoMEL Consortium
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Abstract
We report a genome-wide association study for melanoma that was conducted by the GenoMEL Consortium. Our discovery phase included 2,981 individuals with melanoma and 1,982 study-specific control individuals of European ancestry, as well as an additional 6,426 control subjects from French or British populations, all of whom were genotyped for 317,000 or 610,000 single-nucleotide polymorphisms (SNPs). Our analysis replicated previously known melanoma susceptibility loci. Seven new regions with at least one SNP with P < 10(-5) and further local imputed or genotyped support were selected for replication using two other genome-wide studies (from Australia and Texas, USA). Additional replication came from case-control series from the UK and The Netherlands. Variants at three of the seven loci replicated at P < 10(-3): an SNP in ATM (rs1801516, overall P = 3.4 × 10(-9)), an SNP in MX2 (rs45430, P = 2.9 × 10(-9)) and an SNP adjacent to CASP8 (rs13016963, P = 8.6 × 10(-10)). A fourth locus near CCND1 remains of potential interest, showing suggestive but inconclusive evidence of replication (rs1485993, overall P = 4.6 × 10(-7) under a fixed-effects model and P = 1.2 × 10(-3) under a random-effects model). These newly associated variants showed no association with nevus or pigmentation phenotypes in a large British case-control series.
Type
Journal article
Subject
GenoMEL Consortium
Humans
Melanoma
Skin Neoplasms
Genetic Predisposition to Disease
Case-Control Studies
Polymorphism, Single Nucleotide
Genome-Wide Association Study
Permalink
https://hdl.handle.net/10161/17972
Published Version (Please cite this version)
10.1038/ng.959
Publication Info
Barrett, Jennifer H; Iles, Mark M; Harland, Mark; Taylor, John C; Aitken, Joanne F; Andresen, Per Arne; ... GenoMEL Consortium (2011). Genome-wide association study identifies three new melanoma susceptibility loci. Nature genetics, 43(11). pp. 1108-1113. 10.1038/ng.959. Retrieved from https://hdl.handle.net/10161/17972.
This is constructed from limited available data and may be imprecise. To cite this article, please review & use the official citation provided by the journal.
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Scholars@Duke

Wei

Qingyi Wei

Professor in Population Health Sciences
Qingyi Wei, MD, PhD, Professor in the Department of Medicine, is Associate Director for Cancer Control and Population Sciences, Co-leader of CCPS and Co-leader of Epidemiology and Population Genomics (Focus Area 1). He is a professor of Medicine and an internationally recognized epidemiologist focused on the molecular and genetic epidemiology of head and neck cancers, lung cancer, and melanoma. His research focuses on biomarkers and genetic determinants for the DNA repair deficient phenotype and
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