Abstract
To investigate the role of microsomal epoxide hydrolase (mEH) polymorphisms in the aetiology of lung cancer and to assess the interaction between mEH polymorphisms and smoking, we performed a meta-analysis of seven published studies, which included 2078 cases and 3081 controls, and a pooled analysis of eight studies (four published and four unpublished at that time) with a total of 986 cases and 1633 controls. The combined meta-analysis odds ratios (ORs) were 0.98 (95% confidence interval [CI] = 0.72-1.35) for polymorphism at amino acid 113 in exon 3 (His/His versus Tyr/Tyr genotype) and 1.00 (95% CI = 0.71-1.41) for polymorphism at amino acid 139 in exon 4 (Arg/Arg versus His/His genotype). In the pooled analysis, we observed a significant decrease in lung cancer risk (OR = 0.70, 95% CI = 0.51-0.96) for exon 3 His/His genotype after adjustment for age, sex, smoking and centre. The protective effect of exon 3 polymorphism seems stronger for adenocarcinoma of the lung than for other histological types. The OR for high predicted mEH activity, compared with low activity, was 1.54 (95% CI = 0.77-3.07) in the meta analysis and 1.18 (95% CI = 0.92-1.52) in the pooled analysis. We did not find a consistent modification of the carcinogenic effect of smoking according to mEH polymorphism, although the risk of lung cancer decreased among never smokers with high mEH activity and among heavy smokers with the exon 3 His/His genotype. In conclusion, this study suggests a possible effect of mEH polymorphisms at exon 3 in modulating lung cancer. If present, this effect may vary among different populations, possibly because of interaction with genetic or environmental factors.
| Original language | English |
|---|---|
| Pages (from-to) | 230-241 |
| Number of pages | 12 |
| Journal | Biomarkers |
| Volume | 7 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 2002 Jul 4 |
| Externally published | Yes |
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Keywords
- Lung cancer
- Microsomal epoxide hydrolase
- Polymorphism
- Smoking
ASJC Scopus subject areas
- Biochemistry
- Clinical Biochemistry
- Health, Toxicology and Mutagenesis
Cite this
Microsomal epoxide hydrolase polymorphisms and lung cancer risk : A quantitative review. / Lee, Won Jin; Brennan, Paul; Boffetta, Paolo; London, Stephanie J.; Benhamou, Simone; Rannug, Agneta; To-Figueras, Jordi; Ingelman-Sundberg, Magnus; Shields, Peter; Gaspari, Laura; Taioli, Emanuela.
In: Biomarkers, Vol. 7, No. 3, 04.07.2002, p. 230-241.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Microsomal epoxide hydrolase polymorphisms and lung cancer risk
T2 - A quantitative review
AU - Lee, Won Jin
AU - Brennan, Paul
AU - Boffetta, Paolo
AU - London, Stephanie J.
AU - Benhamou, Simone
AU - Rannug, Agneta
AU - To-Figueras, Jordi
AU - Ingelman-Sundberg, Magnus
AU - Shields, Peter
AU - Gaspari, Laura
AU - Taioli, Emanuela
PY - 2002/7/4
Y1 - 2002/7/4
N2 - To investigate the role of microsomal epoxide hydrolase (mEH) polymorphisms in the aetiology of lung cancer and to assess the interaction between mEH polymorphisms and smoking, we performed a meta-analysis of seven published studies, which included 2078 cases and 3081 controls, and a pooled analysis of eight studies (four published and four unpublished at that time) with a total of 986 cases and 1633 controls. The combined meta-analysis odds ratios (ORs) were 0.98 (95% confidence interval [CI] = 0.72-1.35) for polymorphism at amino acid 113 in exon 3 (His/His versus Tyr/Tyr genotype) and 1.00 (95% CI = 0.71-1.41) for polymorphism at amino acid 139 in exon 4 (Arg/Arg versus His/His genotype). In the pooled analysis, we observed a significant decrease in lung cancer risk (OR = 0.70, 95% CI = 0.51-0.96) for exon 3 His/His genotype after adjustment for age, sex, smoking and centre. The protective effect of exon 3 polymorphism seems stronger for adenocarcinoma of the lung than for other histological types. The OR for high predicted mEH activity, compared with low activity, was 1.54 (95% CI = 0.77-3.07) in the meta analysis and 1.18 (95% CI = 0.92-1.52) in the pooled analysis. We did not find a consistent modification of the carcinogenic effect of smoking according to mEH polymorphism, although the risk of lung cancer decreased among never smokers with high mEH activity and among heavy smokers with the exon 3 His/His genotype. In conclusion, this study suggests a possible effect of mEH polymorphisms at exon 3 in modulating lung cancer. If present, this effect may vary among different populations, possibly because of interaction with genetic or environmental factors.
AB - To investigate the role of microsomal epoxide hydrolase (mEH) polymorphisms in the aetiology of lung cancer and to assess the interaction between mEH polymorphisms and smoking, we performed a meta-analysis of seven published studies, which included 2078 cases and 3081 controls, and a pooled analysis of eight studies (four published and four unpublished at that time) with a total of 986 cases and 1633 controls. The combined meta-analysis odds ratios (ORs) were 0.98 (95% confidence interval [CI] = 0.72-1.35) for polymorphism at amino acid 113 in exon 3 (His/His versus Tyr/Tyr genotype) and 1.00 (95% CI = 0.71-1.41) for polymorphism at amino acid 139 in exon 4 (Arg/Arg versus His/His genotype). In the pooled analysis, we observed a significant decrease in lung cancer risk (OR = 0.70, 95% CI = 0.51-0.96) for exon 3 His/His genotype after adjustment for age, sex, smoking and centre. The protective effect of exon 3 polymorphism seems stronger for adenocarcinoma of the lung than for other histological types. The OR for high predicted mEH activity, compared with low activity, was 1.54 (95% CI = 0.77-3.07) in the meta analysis and 1.18 (95% CI = 0.92-1.52) in the pooled analysis. We did not find a consistent modification of the carcinogenic effect of smoking according to mEH polymorphism, although the risk of lung cancer decreased among never smokers with high mEH activity and among heavy smokers with the exon 3 His/His genotype. In conclusion, this study suggests a possible effect of mEH polymorphisms at exon 3 in modulating lung cancer. If present, this effect may vary among different populations, possibly because of interaction with genetic or environmental factors.
KW - Lung cancer
KW - Microsomal epoxide hydrolase
KW - Polymorphism
KW - Smoking
UR - http://www.scopus.com/inward/record.url?scp=0035992103&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0035992103&partnerID=8YFLogxK
U2 - 10.1080/13547500210121882
DO - 10.1080/13547500210121882
M3 - Review article
VL - 7
SP - 230
EP - 241
JO - Biomarkers
JF - Biomarkers
SN - 1354-750X
IS - 3
ER -