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AIM:To evaluate the association between CYP1A1 andGSTs genetic polymorphisms and susceptibility toesophageal squamous cell carcinoma(SCC)and esophagealadenocarcinoma(ADC)in a high risk area of northwest ofFrance.METHODS:A case-control study was conducted toinvestigate the genetic polymorphisms of these enzymes(CYPIAI*2C and GSTP1 exon 7 Val alleles,GSTMI*2/*2and GSTTl *2/*2 null genotypes).A total of 79 esophagealcancer cases and 130 controls were recruited.RESULTS:GSTMI*2/*2 and CYPIAI*IA/*2C genotypefrequencies were higher among squamous cell carcinomasat a level dose to statistical significance(OR =1.83,95% CI0.88-3.83,P=0.11;OR=3.03,95% CI 0.93-9.90,P=0.07,respectively).For GSTP1 polymorphism,no difference wasfound between controls and cases,whatever their histologicalstatus.Lower frequency of GSTT1 deletion was observed inADC group compared to controls with a statistically significantdifference(OR=13.31,95% CI 1.66-106.92,P<0.01).CONCLUSION:In SCC,our results are consistent with thestrong association of this kind of tumour with tobaccoexposure.In ADC,our results suggest 3 distinct hypotheses:(1)activation of exogenous procarcinogens,such as smallhalogenated compounds by GSTT1;(2)contribution ofGSTT1 to the inflammatory response of esophagealmucosa,which is known to be a strong risk factor for ADC,possibly through leukotriene synthesis;(3)higher sensitivityto the inflammatory process associated with intracellulardepletion of glutathione.
AIM: To evaluate the association between CYP1A1 and GSTs genetic polymorphisms and susceptibility to esophageal squamous cell carcinoma (SCC) and esophagealadenocarcinoma (ADC) in a high risk area of northwest of France. METHODS: A case-control study was studied to investigate the genetic polymorphisms of these enzymes (CYPIAI * 2C and GSTP1 exon 7 Val alleles, GSTMI * 2 / * 2 and GSTTl * 2 / * 2 null genotypes). A total of 79 esophagealcancer cases and 130 controls were recruited.RESULTS: GSTMI * 2 / * 2 and CYPIAI * IA / * 2C genotypefrequencies were higher among squamous cell carcinomasat a level dose to statistical significance (OR = 1.83, 95% CI 0.88-3.83, P = 0.11; OR = 3.03, 95% CI 0.93-9.90, P = 0.07, ). For GSTP1 polymorphism, no difference was found between controls and cases, whatever their histological status. Lower frequency of GSTT1 deletion was observed in ADC group compared to controls with a significant significant (OR = 13.31, 95% CI 1.66-106.92, P <0.01) .CONCLUSION: In SCC, our results are consistent with t hestrong association of this kind of tumor with tobacco exposition. ADC, our results suggest 3 distinct hypotheses: (1) activation of exogenous procarcinogens, such as small halogenated compounds by GSTT1; (2) contribution of GSTT1 to the inflammatory response of esophageal mucosa, which is known to be a strong risk factor for ADC, possibly through leukotriene synthesis; (3) higher sensitivity to the inflammatory process associated with intracellular depletion of glutathione.