Carcinogenesis Advance Access originally published online on November 23, 2005
Carcinogenesis 2006 27(5):997-1007; doi:10.1093/carcin/bgi280
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DNA repair polymorphisms and cancer risk in non-smokers in a cohort study
1 ISI Foundation and Department of Genetics, Biology and Biochemistry, University of Turin, Turin, Italy, 2 Department of Oncology, Strangeways Research Laboratory, University of Cambridge, Cambridge, UK, 3 Genetics Research Institute, Milan, Italy, 4 Department of Environmental and Occupational Medicine, University of Aarhus, Aarhus, Denmark, 5 International Agency for Research on Cancer, Lyon, France, 6 Cancer Risk Factor Branch, Molecular Biology Laboratory, CSPO-Scientific Institute of Tuscany, Florence, Italy, 7 Istituto Mario Negri, Milan, Italy, 8 Department of Environmental and Occupational Health, Utrecht University, Utrecht, Netherlands, 9 World Health Organization, European Centre for Environment and Health, Bonn, Germany, 10 Department of Epidemiology and Social Medicine, University of Aarhus, Aarhus, Denmark, 11 Institute of Cancer Epidemiology, Danish Cancer Society, Copenhagen, Denmark, 12 INSERM U521, Institut Gustave Roussy, Villejuif, France, 13 Division of Clinical Epidemiology, Deutsches Krebsforschungszentrum, Heidelberg, Germany, 14 German Institute of Human Nutrition, Potsdam-Rehbücke, Germany, 15 Department of Hygiene and Epidemiology, Medical School, University of Athens, Greece, 16 Molecular and Nutritional Epidemiology Unit, CSPO-Scientific Institute of Tuscany, Florence, Italy, 17 Department of Epidemiology, National Cancer Istitute, Milan, Italy, 18 Cancer Registry, Azienda Ospedaliera ‘Civile MP Arezzo’, Ragusa, Italy, 19 Dipartimento di Medicina Clinica e Sperimentale, Università Federico II, Naples, Italy, 20 Centre for Nutrition and Health, National Institute for Public Health and the Environment, Bilthoven, Netherlands, 21 Julius Center for Health Sciences and Primary Care, University Medical Center, Utrecht, Netherlands, 22 Institute of Community Medicine, University of Tromso, Norway, 23 Department of Epidemiology, Catalan Institute of Oncology Barcelona, Spain, 24 Andalusian School of Public Health, Granada, Spain, 25 Department of Public Health of Guipuzkoa, San Sebastian, Spain, 26 Public Health Institute, Navarra, Spain, 27 Consejería de Sanidad y Consumo, Murcia, Spain, 28 Dirección General de Salud Pública, Consejería de Salud y Servicios Sanitarios Asturias, Oviedo, Spain, 29 MRC Dunn Human Nutrition Unit, Cambridge, UK, 30 Cancer Research UK Epidemiology Unit, University of Oxford, UK, 31 Imperial College London, London UK and University of Torino, Italy
* To whom correspondence should be addressed at: Section of Epidemiology, I.S.I Foundation (Institute for Scientific Interchange), Viale Settimio Severo, 65, 10133 Torino, Italy; E-mail: matullo{at}isiosf.isi.it
Environmental carcinogens contained in air pollution, such as polycyclic aromatic hydrocarbons, aromatic amines or N-nitroso compounds, predominantly form DNA adducts but can also generate interstrand cross-links and reactive oxygen species. If unrepaired, such lesions increase the risk of somatic mutations and cancer. Our study investigated the relationships between 22 polymorphisms (and their haplotypes) in 16 DNA repair genes belonging to different repair pathways in 1094 controls and 567 cancer cases (bladder cancer, 131; lung cancer, 134; oral–pharyngeal cancer, 41; laryngeal cancer, 47; leukaemia, 179; death from emphysema and chronic obstructive pulmonary disease, 84). The design was a case–control study nested within a prospective investigation. Among the many comparisons, few polymorphisms were associated with the diseases at the univariate analysis: XRCC1-399 Gln/Gln variant homozygotes [odds ratios (OR) = 2.20, 95% confidence intervals (CI) = 1.16–4.17] and XRCC3-241 Met/Met homozygotes (OR = 0.51, 95% CI = 0.27–0.96) and leukaemia. The recessive model in the stepwise multivariate analysis revealed a possible protective effect of XRCC1-399Gln/Gln in lung cancer (OR = 0.22, 95% CI = 0.05–0.98), and confirmed an opposite effect (OR = 2.47, 95% CI = 1.02–6.02) in the leukaemia group. Our results also suggest that the XPD/ERCC1-GAT haplotype may modulate leukaemia (OR = 1.28, 95% CI = 1.02–1.61), bladder cancer (OR = 1.38, 95% CI = 1.06–1.79) and possibly other cancer risks. Further investigations of the combined effects of polymorphisms within these DNA repair genes, smoking and other risk factors may help to clarify the influence of genetic variation in the carcinogenic process.
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