Meta- and pooled analyses of the effects of glutathione S-transferase M1 polymorphisms and smoking on lung cancer risk

Simone Benhamou, Won Jin Lee, Anna Karin Alexandrie, Paolo Boffetta, Christine Bouchardy, Dorota Butkiewicz, Jurgen Brockmöller, Margie L. Clapper, Ann Daly, Vita Dolzan, Jean Ford, Laura Gaspari, Aage Haugen, Ari Hirvonen, Kirsti Husgafvel-Pursiainen, Magnus Ingelman-Sundberg, Ivan Kalina, Masahiro Kihara, Pierre Kremers, Loïc Le MarchandStephanie J. London, Valle Nazar-Stewart, Masako Onon-Kihara, Agneta Rannug, Marjorie Romkes, David Ryberg, Janeric Seidegard, Peter Shields, Richard C. Strange, Isabelle Stücker, Jordi To-Figueras, Paul Brennan, Emanuela Taioli

Research output: Contribution to journalArticle

232 Citations (Scopus)

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 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.

Original languageEnglish
Pages (from-to)1343-1350
Number of pages8
JournalCarcinogenesis
Volume23
Issue number8
Publication statusPublished - 2002 Aug 29
Externally publishedYes

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Meta-Analysis
Lung Neoplasms
Smoking
Genotype
Case-Control Studies
Publication Bias
Odds Ratio
Confidence Intervals
Environmental Carcinogens
Tobacco Use
Genetic Polymorphisms
Genetic Predisposition to Disease
Carcinogens
Tobacco
glutathione S-transferase M1

ASJC Scopus subject areas

  • Cancer Research

Cite this

Benhamou, S., Lee, W. J., Alexandrie, A. K., Boffetta, P., Bouchardy, C., Butkiewicz, D., ... Taioli, E. (2002). Meta- and pooled analyses of the effects of glutathione S-transferase M1 polymorphisms and smoking on lung cancer risk. Carcinogenesis, 23(8), 1343-1350.

Meta- and pooled analyses of the effects of glutathione S-transferase M1 polymorphisms and smoking on lung cancer risk. / Benhamou, Simone; Lee, Won Jin; Alexandrie, Anna Karin; Boffetta, Paolo; Bouchardy, Christine; Butkiewicz, Dorota; Brockmöller, Jurgen; Clapper, Margie L.; Daly, Ann; Dolzan, Vita; Ford, Jean; Gaspari, Laura; Haugen, Aage; Hirvonen, Ari; Husgafvel-Pursiainen, Kirsti; Ingelman-Sundberg, Magnus; Kalina, Ivan; Kihara, Masahiro; Kremers, Pierre; Le Marchand, Loïc; London, Stephanie J.; Nazar-Stewart, Valle; Onon-Kihara, Masako; Rannug, Agneta; Romkes, Marjorie; Ryberg, David; Seidegard, Janeric; Shields, Peter; Strange, Richard C.; Stücker, Isabelle; To-Figueras, Jordi; Brennan, Paul; Taioli, Emanuela.

In: Carcinogenesis, Vol. 23, No. 8, 29.08.2002, p. 1343-1350.

Research output: Contribution to journalArticle

Benhamou, S, Lee, WJ, Alexandrie, AK, Boffetta, P, Bouchardy, C, Butkiewicz, D, Brockmöller, J, Clapper, ML, Daly, A, Dolzan, V, Ford, J, Gaspari, L, Haugen, A, Hirvonen, A, Husgafvel-Pursiainen, K, Ingelman-Sundberg, M, Kalina, I, Kihara, M, Kremers, P, Le Marchand, L, London, SJ, Nazar-Stewart, V, Onon-Kihara, M, Rannug, A, Romkes, M, Ryberg, D, Seidegard, J, Shields, P, Strange, RC, Stücker, I, To-Figueras, J, Brennan, P & Taioli, E 2002, 'Meta- and pooled analyses of the effects of glutathione S-transferase M1 polymorphisms and smoking on lung cancer risk', Carcinogenesis, vol. 23, no. 8, pp. 1343-1350.
Benhamou S, Lee WJ, Alexandrie AK, Boffetta P, Bouchardy C, Butkiewicz D et al. Meta- and pooled analyses of the effects of glutathione S-transferase M1 polymorphisms and smoking on lung cancer risk. Carcinogenesis. 2002 Aug 29;23(8):1343-1350.
Benhamou, Simone ; Lee, Won Jin ; Alexandrie, Anna Karin ; Boffetta, Paolo ; Bouchardy, Christine ; Butkiewicz, Dorota ; Brockmöller, Jurgen ; Clapper, Margie L. ; Daly, Ann ; Dolzan, Vita ; Ford, Jean ; Gaspari, Laura ; Haugen, Aage ; Hirvonen, Ari ; Husgafvel-Pursiainen, Kirsti ; Ingelman-Sundberg, Magnus ; Kalina, Ivan ; Kihara, Masahiro ; Kremers, Pierre ; Le Marchand, Loïc ; London, Stephanie J. ; Nazar-Stewart, Valle ; Onon-Kihara, Masako ; Rannug, Agneta ; Romkes, Marjorie ; Ryberg, David ; Seidegard, Janeric ; Shields, Peter ; Strange, Richard C. ; Stücker, Isabelle ; To-Figueras, Jordi ; Brennan, Paul ; Taioli, Emanuela. / Meta- and pooled analyses of the effects of glutathione S-transferase M1 polymorphisms and smoking on lung cancer risk. In: Carcinogenesis. 2002 ; Vol. 23, No. 8. pp. 1343-1350.
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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 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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T1 - Meta- and pooled analyses of the effects of glutathione S-transferase M1 polymorphisms and smoking on lung cancer risk

AU - Benhamou, Simone

AU - Lee, Won Jin

AU - Alexandrie, Anna Karin

AU - Boffetta, Paolo

AU - Bouchardy, Christine

AU - Butkiewicz, Dorota

AU - Brockmöller, Jurgen

AU - Clapper, Margie L.

AU - Daly, Ann

AU - Dolzan, Vita

AU - Ford, Jean

AU - Gaspari, Laura

AU - Haugen, Aage

AU - Hirvonen, Ari

AU - Husgafvel-Pursiainen, Kirsti

AU - Ingelman-Sundberg, Magnus

AU - Kalina, Ivan

AU - Kihara, Masahiro

AU - Kremers, Pierre

AU - Le Marchand, Loïc

AU - London, Stephanie J.

AU - Nazar-Stewart, Valle

AU - Onon-Kihara, Masako

AU - Rannug, Agneta

AU - Romkes, Marjorie

AU - Ryberg, David

AU - Seidegard, Janeric

AU - Shields, Peter

AU - Strange, Richard C.

AU - Stücker, Isabelle

AU - To-Figueras, Jordi

AU - Brennan, Paul

AU - Taioli, Emanuela

PY - 2002/8/29

Y1 - 2002/8/29

N2 - 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 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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