@article{3094467,
    title = "DNA repair polymorphisms and cancer risk in non-smokers in a cohort study",
    author = "Matullo, G. and Dunning, A.M. and Guarrera, S. and Baynes, C. and Polidoro, S. and Garte, S. and Autrup, H. and Malaveille, C. and Peluso, M. and Airoldi, L. and Veglia, F. and Gormally, E. and Hoek, G. and Krzyzanowski, M. and Overvad, K. and Raaschou-Nielsen, O. and Clavel-Chapelon, F. and Linseisen, J. and Boeing, H. and Trichopoulou, A. and Palli, D. and Krogh, V. and Tumino, R. and Panico, S. and Bueno-De-Mesquita, H.B. and Peeters, P.H. and Lund, E. and Pera, G. and Martinez, C. and Dorronsoro, M. and Barricarte, A. and Tormo, M.J. and Quiros, J.R. and Day, N.E. and Key, T.J. and Saracci, R. and Kaaks, R. and Riboli, E. and Vineis, P.",
    journal = "Journal of Carcinogenesis",
    year = "2006",
    volume = "27",
    number = "5",
    pages = "997-1007",
    issn = "1477-3163",
    doi = "10.1093/carcin/bgi280",
    keywords = "esterase;  excision repair cross complementing protein 1;  glutamine;  methionine;  unclassified drug;  X ray repair cross complementing protein 1, adult;  aged;  article;  bladder cancer;  cancer risk;  carcinogenesis;  case control study;  chronic obstructive lung disease;  cohort analysis;  confidence interval;  controlled study;  DNA polymorphism;  DNA repair;  female;  genetic association;  genetic risk;  genetic variability;  haplotype;  homozygote;  human;  larynx cancer;  leukemia;  lung cancer;  lung emphysema;  major clinical study;  male;  multivariate analysis;  oropharynx cancer;  priority journal;  prospective study;  risk factor;  smoking;  univariate analysis, Adult;  Aged;  Case-Control Studies;  Cohort Studies;  DNA Repair;  False Positive Reactions;  Female;  Humans;  Male;  Middle Aged;  Multivariate Analysis;  Neoplasms;  Odds Ratio;  Polymorphism, Genetic;  Prospective Studies;  Risk;  Smoking",
    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 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. © 2006 Oxford University Press."
}