Carcinogenesis Advance Access originally published online on March 28, 2003
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Carcinogenesis, Vol. 24, No. 5, 875-882,
May 2003
© 2003 Oxford University Press
MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION |
CYP1A1 and GSTM1 genetic polymorphisms and lung cancer risk in Caucasian non-smokers: a pooled analysis
1 Unit of Environmental Cancer Epidemiology, International Agency for Research on Cancer, 150 Cours Albert-Thomas, F-69372 Lyon Cedex 08, France
2 Department of Epidemiology, School of Public Health, University of California at Los Angeles, Los Angeles, CA, USA
3 Institute of Clinical Pharmacology, Georg August University Goettingen, Germany
4 Department of Tumor Biology, Centre of Oncology, Gliwice, Poland
5 Institute of Pharmacology, Ernst Moritz Arndt University Greifswald, Germany
6 Divisions of Population Science and Medical Science, Fox Chase Cancer Center, Philadelphia, PA, USA
7 Genetics Research Institute ONLUS, Milan, Italy
8 Department of Toxicology, National Institute of Occupational Health, Oslo, Norway
9 Finnish Institute of Occupational Health, Helsinki, Finland
10 Department of Medical Biology, School of Medicine, P.J.Safárik University, Kosice, Slovakia
11 Cancer Research Center of Hawaii, University of Hawaii, Honolulu, HI, USA
12 Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA
13 Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
14 Environmental and Occupational Health, Center for Clinical Pharmacology, University of Pittsburgh, Pittsburgh, PA, USA
15 Department of Biochemistry, National Institute of Environmental Health, Budapest, Hungary
16 Department of Environmental Medicine, IRCCS University of Milano, Milan, Italy
17 To whom correspondence should be addressed Email: boffetta{at}iarc.fr
Polymorphisms for genes encoding the metabolic enzymes cytochrome P450 1A1 (CYP1A1) and glutathione S-transferase M1 (GSTM1) might contribute to the variability in individual susceptibility to lung cancer. The role of CYP1A1 and GSTM1 in lung carcinogenesis might be more important at low levels of exposure to carcinogens. Non-smokers represent a population at low exposure, however, they are often overlooked because of the small number of cases. We therefore conducted a pooled analysis of 14 case–control studies on lung cancer in Caucasian non-smokers with comparable information on genetic polymorphisms included in the International Collaborative Study on Genetic Susceptibility to Environmental Carcinogens. We pooled the raw data from a total of 302 cases and 1631 controls with random effects models. We also evaluated the possibility of inclusion bias and conducted influence analyses. The odds ratio (OR) of lung cancer for the variant CYP1A1 Ile462Val polymorphism (Ile/Val, Val/Val) was 2.99 [95% confidence interval (95%CI) 1.51–5.91]; this effect was stronger on lung adenocarcinoma (OR 4.85, 95%CI 2.03–11.6). After excluding outlying or imprecise studies, we did not observe a significant effect of the CYP1A1 MspI (T3801C) polymorphism or GSTM1 null genotype (OR 1.20, 95%CI 0.89–1.63). Furthermore, our analyses suggested a combined effect of the CYP1A1 Ile462Val polymorphism and GSTM1 null genotype. The OR for the combination of the CYP1A1 Ile462Val variant and GSTM1 null genotype was 4.67 (95%CI 2.00–10.9) compared with the concurrent presence of the CYP1A1 wild-type and GSTM1 non-null genotype. We did not observe a modification of the effect of the GSTM1 null genotype according to exposure to environmental tobacco smoke and urban/rural residence. Our study therefore suggests that the CYP1A1 Ile462Val variant allele might play a role in lung carcinogenesis among non-smokers, possibly in combination with the GSTM1 null genotype.
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