The Colorectal Cancer Risk of Meat Intake, Smoking, and CYP2E1 Polymorphisms: The Comparison of Colorectal Cancer Patients with Controls

ABSTRACT

PURPOSE: Genetic susceptibility for colorectal cancer is explained by polymorphisms of the drug-metabolizing enzymes. CYP2E1 activate the procarcinogens and they are involved in carcinogenesis. We analyzed the polymorphisms of CYP2E1 in colorectal cancer patients and the controls, and we examined the interaction between meat intake, smoking and CYP2E1 polymorphisms in colorectal cancer. METHODS: Polymerase chain reaction was performed for 96- bp insertion polymorphisms in 113 colorectal cancer patients and 110 controls. 80 cancer patients and 75 controls were interviewed for determining their meat intake and smoking behavior. We analyzed the clinical characteristics and the combined effect of meat intake, smoking and CYP2E1 polymorphisms on the susceptibility to colorectal cancer. RESULTS: The insert 0, insert 1 and insert 2 subtypes for the 96-bp insertion polymorphism were seen in 75 (66.4%), 35 (31.0%) and 3 (2.7%) cases, respectively, and in 82 (74.5%), 26 (23.6%) and 2 (1.8%), respectively. CYP2E1 polymorphisms didn't increase the colorectal cancer risk (OR 1.5, 95% CI 0.3~10.1) in the insert 1 group and the insert 2 group. The combined effects of CYP2E1 polymorphisms, meat intake and smoking were not significant, (OR 1.6, 95% CI 0.4~4.7) in the low-meat intake group, the high-meat intake group, (OR 0.4, 95% CI 0.1~2.5) and in the smokers and ex-smokers (OR 0.8, 95% CI 0.3~2.3). CONCLUSION: The CYP2E1 polymorphisms, alone or combined with meat intake or smoking, did not increase the risk of colorectal cancer. Further well designed large scaled studies will be needed to determine the effects of CYP2E1 polymorphisms on colorectal cancer.