AIM:To characterize cytochrome P4501A1 (CYPIA1),glutathione S-transferases (GSTs) and microsomal epoxidehydrolase (mEH) polymorphisms in Chinese esophagealcancer patients.METHODS:Multiplex polymerase chain reaction (PCR) andPCR based restriction fragment length polymorphisms (PCR-RFLP) were used to detect polymorphism changes of CYP,GSTs and mEH on esophageal cancerous and precancerouslesions as well as in case control group.All the examinationsamples were obtained from Linzhou (formerly Linxian),Henan Province,the highest incidence area for esophagealcancer.RESULTS:The frequency of CYP1A1 3’ polymorphism incase control group (26/38,68%) was significantly higherthan in esophageal squamous cell carcinoma group (ESCC)(29/62,47%) (P<0.05).A significant difference in theincidence of mEH slow allele variant was observed betweencase control group (15/38,39%) and esophageal dysplasiagroup (22/32,69%) or ESCC group (39/62,63%) (P<0.05).However,no significant difference was observed amongdifferent groups in the polymorphisms of CYP1A1 exon 7,GSTM1,GSTT1,GSTP1 and mEH fast allele.CONCLUSION:The present results suggest that CYP1A13’ polymorphism may be one of the promising protectivefactors and its wild gene type may be an indicator for highersusceptibility to esophageal cancer,mEH slow allele variant,associated with the progression of esophageal precancerouslesions,may contribute to the high susceptibility to esophagealcarcinoma. AIM: To characterize cytochrome P4501A1 (CYPIA1), glutathione S-transferases (GSTs) and microsomal epoxidehydrolase (mEH) polymorphisms in Chinese esophageal cancer patients.METHODS: Multiplex polymerase chain reaction (PCR) and PCR based restriction fragment length polymorphisms used to detect polymorphism changes of CYP, GSTs and mEH on esophageal cancerous and precancerous lesions as as as in case control group. All the examinationsamples were obtained from Linzhou (formerly Linxian), Henan Province, the highest incidence area for esophageal cancer .RESULTS: The frequency of CYP1A1 3 ’polymorphism incase control group (26/38, 68%) was significantly higherthan in esophageal squamous cell carcinoma group (ESCC) (29/62, 47%) (P <0.05) allele variant was observed betweencase control group (15 / 38,39%) and esophageal dysplasiagroup (22 / 32,69%) or ESCC group (39 / 62,63%) amongdiffer ent groups in the polymorphisms of CYP1A1 exon 7, GSTM1, GSTT1, GSTP1 and mEH fast allele. CONCLUSION: The present results suggest that CYP1A13 ’polymorphism may one of the promising protective factors and its wild gene type may be an indicator for highers susceptibility to esophageal cancer, mEH slow allele variant, associated with the progression of esophageal precancerous lesions, may contribute to the high susceptibility to esophageal carcinoma.