1Department of Preventive Medicine, Seoul National University College of Medicine, Korea. 2Department of Internal Medicine, Hallym University College of Medicine, Korea. 3Department of Preventive Medicine, Dogguk University College of Medicine, Korea. 4Institute of Environmental Medicine, Seoul National University Medical Research Center, Korea. 5Department of Urology, Seoul National University College of Medicine, Seoul, Korea. 6Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea.
ABSTRACT
PURPOSE: The interactive effects of genetic polymorphisms of cytochrome P4502E1 (CYP2E1) & N-acetyltransferase 1 (NAT1) and smoking on lung cancer development were evaluated in hospital based case-control study.
MATERIALS AND METHODS: Male lung cancer patients (N= 157) and the male patients with no present or previous history of systemic illnesses who visited the urology department (N=138) were recruited (1998-1999). CYP2E1 & NAT1 genotypes were determined by PCR-RFLP method using RsaI and MboII digestion, respectively.
RESULTS: CYP2E1 c2 or NAT1 *10 allele did not increased the risk of lung cancer. Heavy smokers (35<PY) with CYP2E1 c2 or NAT1 *10 allele were at the higher risk compared with light smokers (0<PY< or =35) with othergenotypes (OR=2.6, 95% CI=1.0-6.5; OR=4.2, 95% CI=1.5 -11.6, repectively).
Interactive effects of CYP2E1 or NAT1 genotypes and smoking were observed (p-for interaction= 0.003; <0.001 respectively). Heavy smokers with both c2 and *10 allele were at the higher risk compared with light smokers with other combined genotypes (OR=3.5, 95% CI=1.4-9.5) and interactive effect with smoking was observed (p-for interaction=0.003).
CONCLUSION: These results suggest the gene-environment interaction between genetic polymorphisms of CYP2E1 & NAT1 and smoking in lung cancer development.
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