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AIM:To analyze the association of tobacco smoking,polymorphism of CYP1A1(7~(th)exon)and GSTMI genotypeand esophageal cancer(EC)in Xi’an.METHODS:A hospital based case-control study,withmolecular epidemiological method,was carried out.Polymorphism of CYP1At and GSTM1 of samples from 127EC cases and 101 controls were detected by PCR method:RESULTS:There were no significant difference of age andgender between cases and controls.Tobacco smokingwas the main risk factor(OR=1.97;95% Cl=1.12-3.48)for EC in Xi’an.The proportions of CYP1A1 Ile/Ile,Ile/Val and Val/Val gene types in cases and controls was19.7%,45.7%,34.6% and 30.7%,47.5%,21.8%respectively(P=0.049).Individuals with CYP1 A1 Val/Valgenotype compared to those with CYPIA1 Ile/Ilegenotype had higher risk for EC increased(OR=2.48,95%Cl=1,12-5.54).The proportions of GSTM1 deletiongenotype in cases and controls were 58,3% and 43.6%(OR=1.81,95%CI=1.03-3.18,P=0.028).Analysis ofgene-environment interaction showed that tobaccosmoking and CYP1AI Val/Val genotype;tobacco smokingand GSTM1 deletion genotype had synergism interactionrespectively.Analysis of gene-gene interaction did notfind synergistic interaction between these two genes.Butin GSTMI deletion group,there was significant differenceof distribution of CYP1A1 genotype between cases andcontrols(P=0.011).CONCLUSION:CYP1A1 Val/Val and GSTM1 deletiongenotypes are genetic susceptibility biomarkers for EC.Therisk increases,when person with CYP1A1 Val/Val and/orGSTMI deletion genotype.And these two-metabolic enzymesseem to have interactions with tobacco smoking,in which themechanism still needs further study.
AIM: To analyze the association of tobacco smoking, polymorphism of CYP1A1 (7 th (ex)) and GSTMI genotype and esophageal cancer (EC) in Xi’an. METHHODS: A hospital based case-control study, with molecular epidemiological method, was carried out. Polymorphism of CYP1At and GSTM1 of samples from 127EC cases and 101 controls were detected by PCR method: RESULTS: There were no significant difference of age and gender between cases and controls. Tobacco smoking was the main risk factor (OR = 1.97; 95% Cl = 1.12-3.48) for EC in Xi’an. Proportions of CYP1A1 Ile / Ile, Ile / Val and Val / Val gene types in cases and controls was 19.7%, 45.7%, 34.6% and 30.7%, 47.5% 21.8% respectively (P = 0.049) .Individuals with CYP1 A1 Val / Valgenotype compared to those with CYPIA1 Ile / Ilegenotype had higher risk for EC increased (OR = 2.48,95% Cl = 1,12-5.54). These proportions of GSTM1 environment of interaction-showed interaction between tobaccosmoking and CYP1AI (OR = 1.81, 95% CI = 1.03-3.18, P = 0.028) Val / Val genotype; tobacco smoking and GSTM1 deletion genotype had synergism interactionrespectively. Analysis of gene-gene interaction did not find synergistic interaction between these two genes. Butin GSTMI deletion group, there was a significant difference of distribution of CYP1A1 genotype between cases and controls (P = 0.011) .CONCLUSION: CYP1A1 Val / Val and GSTM1 deletion genotypes are genetic susceptibility biomarkers for EC.Therb increases, when person with CYP1A1 Val / Val and / or GSTMI deletion genotype. These two-metabolic enzymes see have the interaction with tobacco smoking, in which themechanism still needs further study.