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Human Molecular Genetics Advance Access published online on November 29, 2007
Human Molecular Genetics, doi:10.1093/hmg/ddm351
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© The Author 2007. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Comprehensive analysis of the role of DNA repair gene polymorphisms on risk of glioma

Lara Bethke1, Emily Webb1, Anne Murray1, Minouk Schoemaker2, Christoffer Johansen3, Helle Collatz Christensen3, Kenneth Muir4, Patricia McKinney5, Sarah Hepworth5, Polyxeni Dimitropoulou4, Artitaya Lophatananon4, Maria Feychting6, Stefan Lönn7, Anders Ahlbom6, Beatrice Malmer8, Roger Henriksson8, Anssi Auvinen9,10, Anne Kiuru10, Tiina Salminen9,10, Anthony Swerdlow2 and Richard Houlston1,*

1 Section of Cancer Genetics, Institute of Cancer Research, Sutton, UK 2 Section of Epidemiology, Institute of Cancer Research, Sutton, UK 3 Institute of Cancer Epidemiology, Danish Cancer Society, Copenhagen, Denmark 4 Division of Epidemiology and Public Health, University of Nottingham Medical School Queen's Medical Centre, Nottingham, UK 5 Centre for Epidemiology and Biostatistics, University of Leeds, UK 6 Division of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden 7 Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden 8 Department of Radiation Sciences, Oncology Umeå University, Sweden 9 Department of Epidemiology, Tampere School of Public Health, University of Tampere, Finland 10 Department of Research and Environmental Surveillance, Radiation and Nuclear Safety Authority, STUK, Helsinki, Finland

* Correspondence should be addressed to: Richard Houlston Institute of Cancer Research, 15 Cotswold Rd, Sutton, Surrey SM2 5NG, UK, Tel: +44-(0)-208-722-4175, Fax: +44-(0)-208-722-4059, e-mail: richard.houlston{at}icr.ac.uk

Received October 16, 2007; Revised November 28, 2007; Accepted November 28, 2007

Much of the variation in inherited risk of glioma is likely to be explained by combinations of common low risk variants. The established relationship between glioma risk and exposure to ionising radiation led us to examine whether variants in the DNA repair genes contribute to disease susceptibility. We evaluated 1,127 haplotype-tagging single nucleotide polymorphisms (SNPs) supplemented with 388 putative functional SNPs to capture most of the common variation in 136 DNA repair genes, in five unique case-control series from four different countries (1,013 cases, 1,016 controls). We identified 16 SNPs associated with glioma risk at the 1% significance level. The highest association observed across the five independent case-control datasets involved rs243356, which maps to intron 3 of CHAF1A (trend odds ratio, 1.32; 95% confidence interval, 1.14-1.54; P = 0.0002; false positive report probability = 0.055, based on a prior probability of 0.01). Our results provide additional support for the hypothesis that low penetrance variants contribute to the risk of developing glioma and suggest that a genetic variant located in or around the CHAF1A gene contributes to disease risk.


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