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Carcinogenesis Advance Access published online on November 23, 2005
Carcinogenesis, doi:10.1093/carcin/bgi280
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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 29, 2005
Revised November 7, 2005
Accepted November 15, 2005

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

DNA repair polymorphisms and cancer risk in non-smokers in a cohort study

G. Matullo 1 *, A. M. Dunning 2, S. Guarrera 1, C. Baynes 2, S. Polidoro 1, S. Garte 3, H. Autrup 4, C. Malaveille 5, M. Peluso 6, L. Airoldi 7, F. Veglia 1, E. Gormally 5, G. Hoek 8, M. Krzyzanowski 9, K. Overvad 10, O. Raaschou-Nielsen 11, F. Clavel-Chapelon 12, J. Linseisen 13, H. Boeing 14, A. Trichopoulou 15, D. Palli 16, V. Krogh 17, R. Tumino 18, S. Panico 19, H. B. Bueno-De-Mesquita 20, P. H. Peeters 21, E. Lund 22, G. Pera 23, C. Martinez 24, M. Dorronsoro 25, A. Barricarte 26, M. J. Tormo 27, J. R. Quiros 28, N. E. Day 29, T. J. Key 30, R. Saracci 5, R. Kaaks 5, E. Riboli 5, and P. Vineis 31

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, United Kingdom
3 Genetics Research Institute, Milan, Italy
4 Department of Environmental and Occupational Medicine, 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; University of Torino, Italy

* To whom correspondence should be addressed.
G. Matullo, E-mail: matullo{at}isiosf.isi.it


  Abstract

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 inter-strand 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, leukemia 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 (OR = 2.20, 95% CI = 1.16-4.17) and XRCC3-241 Met/Met homozygotes (OR = 0.51, 95% CI = 0.27-0.96) and leukemia. 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 leukemia group. Our results also suggest that the XPD/ERCC1-GAT haplotype may modulate leukaemia (OR = 1.28, 95% CI = 1.02-1.61), bladder (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.

Keywords: DNA repair; lung; bladder; leukemia; air pollution; ETS.
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