Meta- and pooled analyses of the effects of glutathione S-transferase M1 polymorphisms and smoking on lung cancer risk
(2002) In Carcinogenesis 23(8). p.1343-1350- Abstract
- 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... (More)
- 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. (Less)
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- author
- organization
- publishing date
- 2002
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Carcinogenesis
- volume
- 23
- issue
- 8
- pages
- 1343 - 1350
- publisher
- Oxford University Press
- external identifiers
-
- pmid:12151353
- wos:000177231000012
- scopus:0036048429
- ISSN
- 0143-3334
- DOI
- 10.1093/carcin/23.8.1343
- language
- English
- LU publication?
- yes
- id
- d7558ce7-158b-47b7-987e-9732bd749528 (old id 332121)
- date added to LUP
- 2016-04-01 12:14:46
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- 2022-04-13 08:16:38
@article{d7558ce7-158b-47b7-987e-9732bd749528,
abstract = {{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.}},
author = {{Benhamou, S and Lee, WJ and Alexandrie, AK and Boffetta, P and Bouchardy, C and Butkiewicz, D and Brockmoller, J and Clapper, ML and Daly, A and Dolzan, V and Ford, J and Gaspari, L and Haugen, A and Hirvonen, A and Husgafvel-Pursiainen, K and Ingelman-Sundberg, M and Kalina, I and Kihara, M and Kremers, P and Le Marchand, L and London, SJ and Nazar-Stewart, V and Onon-Kihara, M and Rannug, A and Romkes, M and Ryberg, D and Seidegård, Janeric and Shields, P and Strange, RC and Stucker, I and To-Figueras, J and Brennan, P and Taioli, E}},
issn = {{0143-3334}},
language = {{eng}},
number = {{8}},
pages = {{1343--1350}},
publisher = {{Oxford University Press}},
series = {{Carcinogenesis}},
title = {{Meta- and pooled analyses of the effects of glutathione S-transferase M1 polymorphisms and smoking on lung cancer risk}},
url = {{http://dx.doi.org/10.1093/carcin/23.8.1343}},
doi = {{10.1093/carcin/23.8.1343}},
volume = {{23}},
year = {{2002}},
}