Carcinogenesis, Vol. 23, No. 8, 1343-1350,
August 2002
© 2002 Oxford University Press
MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION |
Meta- and pooled analyses of the effects of glutathione S-transferase M1 polymorphisms and smoking on lung cancer risk
1 INSERM U521, EMI 00–06, Evry, France,
2 International Agency for Cancer Research, Lyon, France,
3 Karolinska Institutet and National Institute for Working Life, Stockholm, Sweden,
4 Geneva Cancer Registry, Switzerland,
5 Centre of Oncology, Gliwice, Poland,
6 Georg-August-University, Göttingen, Germany,
7 Fox Chase Cancer Center, Philadelphia, Pennsylvania, USA,
8 University of Newcastle, UK,
9 University of Ljubljana, Slovenia,
10 Columbia College of Physicians and Surgeons, New York, USA,
11 Ospedale Maggiore IRCCS, Milan, Italy,
12 National Institute of Occupational Health, Oslo, Norway,
13 Finnish Institute of Occupational Health, Helsinki, Finland,
14 P.J. Safarik University, Kosice, Slovakia,
15 Kyoto University School of Public Health, Kyoto, Japan,
16 Institut de Pathologie, Liège, Belgium,
17 University of Hawaii, Honolulu, Hawaii USA,
18 National Institute for Environmental Health Sciences, Research Triangle Park, North Carolina, USA,
19 Oregon Health Sciences University, Oregon, USA,
20 Nagasaki University Graduate School of Medicine, Nagasaki, Japan,
21 University of Pittsburgh, Pennsylvania, USA,
22 Lund University, Lund, Sweden,
23 Georgetown University Medical Center, Washington, DC, USA,
24 Keele University, Staffordshire, UK,
25 INSERM U170, Villejuif, France and
26 Hospital Clinic Provincial, Barcelona, Spain
Susceptibility to lung cancer may in part be attributable to inter-individual variability in metabolic activation or detoxification of tobacco carcinogens. The glutathione S-transferase M1 (GSTM1) genetic polymorphism has been extensively studied in this context; two recent meta-analyses of case-control studies suggested an association between GSTM1 deletion and lung cancer. At least 15 studies have been published after these overviews. We undertook a new meta-analysis to summarize the results of 43 published case-control studies including >18 000 individuals. A slight excess of risk of lung cancer for individuals with the GSTM1 null genotype was found (odds ratio (OR) = 1.17, 95% confidence interval (CI) 1.07–1.27). No evidence of publication bias was found (P = 0.4), however, it is not easy to estimate the extent of such bias and we cannot rule out some degree of publication bias in our results. A pooled analysis of the original data of about 9500 subjects involved in 21 case-control studies from the International Collaborative Study on Genetic Susceptibility to Environmental Carcinogens (GSEC) data set was performed to assess the role of GSTM1 genotype as a modifier of the effect of smoking on lung cancer risk with adequate power. Analyses revealed no evidence of increased risk of lung cancer among carriers of the GSTM1 null genotype (age-, gender- and center-adjusted OR = 1.08, 95% CI 0.98–1.18) and no evidence of interaction between GSTM1 genotype and either smoking status or cumulative tobacco consumption.
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