AIM: To elucidate the role of tobacco smoking and polymorphisms of carcinogen metabolism genes in cervical carcinogenesis. METHODS: We analyzed genotypes of nine genes, 11 polymorphisms encoding carcinogen metabolizing enzymes, information on smoking, and the presence of human papillomavirus in 124 Japanese cervical cancer patients and 125 healthy controls. RESULTS: The incidence of human papillomavirus infection (95.5% vs 9.9%; P < 0.001; odds ratio (OR), 231.98; 95% confidence interval [CI], 57.17-941.22), and smoking (41.1% vs 18.4%; P < 0.001; OR, 3.40; 95% CI, 1.88-6.17) were both significantly higher in patients than in controls. The genotype distributions of CYP1A1, CYP2E1, CYP2A6, NQO1, NAT2, mEH, MPO and GSTT1 genes were not statistically different; however, the ratio of the GSTM1 null genotype was significantly higher in patients than in controls (62.1% vs 47.2%; P = 0.019; OR, 1.83; 95% CI, 1.11-3.04). The incidence of GSTM1 null was significantly higher in the non-smoking group (63.0% vs 47.1%; P = 0.038; OR, 1.92; 95% CI, 1.04-3.54), and not in the smoking group (60.8% vs 47.8%; P = 0.300; OR, 1.69; 95% CI, 0.63-4.56). CONCLUSIONS: In the current study, risk factors for developing cervical cancer were tobacco smoking and GSTM1 null; however, no association was observed between these two factors. We could not prove that smoking-GSTM1 null interaction was responsible for the increase in cervical cancer among young Japanese, and further studies with more detailed smoking status, not only active but passive smoking, will be required.
AIM: To elucidate the role of tobacco smoking and polymorphisms of carcinogen metabolism genes in cervical carcinogenesis. METHODS: We analyzed genotypes of nine genes, 11 polymorphisms encoding carcinogen metabolizing enzymes, information on smoking, and the presence of human papillomavirus in 124 Japanese cervical cancerpatients and 125 healthy controls. RESULTS: The incidence of human papillomavirus infection (95.5% vs 9.9%; P < 0.001; odds ratio (OR), 231.98; 95% confidence interval [CI], 57.17-941.22), and smoking (41.1% vs 18.4%; P < 0.001; OR, 3.40; 95% CI, 1.88-6.17) were both significantly higher in patients than in controls. The genotype distributions of CYP1A1, CYP2E1, CYP2A6, NQO1, NAT2, mEH, MPO and GSTT1 genes were not statistically different; however, the ratio of the GSTM1 null genotype was significantly higher in patients than in controls (62.1% vs 47.2%; P = 0.019; OR, 1.83; 95% CI, 1.11-3.04). The incidence of GSTM1 null was significantly higher in the non-smoking group (63.0% vs 47.1%; P = 0.038; OR, 1.92; 95% CI, 1.04-3.54), and not in the smoking group (60.8% vs 47.8%; P = 0.300; OR, 1.69; 95% CI, 0.63-4.56). CONCLUSIONS: In the current study, risk factors for developing cervical cancer were tobacco smoking and GSTM1 null; however, no association was observed between these two factors. We could not prove that smoking-GSTM1 null interaction was responsible for the increase in cervical cancer among young Japanese, and further studies with more detailed smoking status, not only active but passive smoking, will be required.
Authors: Jacqueline M Vink; Folkert J van Kemenade; Chris J L M Meijer; Mariel K Casparie; Gerrit A Meijer; Dorret I Boomsma Journal: Eur J Hum Genet Date: 2010-08-18 Impact factor: 4.246