Objective: The aim of this study was to investigate the characteristics of gene changes from Barrett’s esophagus (BE) to esophageal adenocarcinoma by cDNA microarray. Methods: The cDNA retro-transcribed from equal quantity mRNA from esophageal carcinoma and BE tissues as well as control normal epithelium of esophagus which were from one patient with esophageal adenocarcinoma were labeled with Cy5 and Cy3 fluorescence as probes. The mixed probes were hybridized with two pieces gene chip respectively. It was scanned by laser scanner Scan Array 4000. The acquired images were analyzed by software GenePix Pro 3.0. Results: A total of 214 genes were screened out which expression levels were more than 2 times in hybridization of esophageal adenocarcinoma vs normal epithelium of esophagus, whereas 90 genes in hybridization of BE vs normal epithelium. A parallel comparison among these two gene profiles showed that a total of 45 genes with 24 downregulation and 21 up-regulation which expression levels were more than 2 times between the BE and the esophageal adenocarcinoma. Among these, there were 27 genes with 18 downregulation and 9 up-regulation which implicated the tendencies progressing from BE to esophageal adenocarcinoma. Conclusion: These genes or their products which implicate the tendencies can be chosen as indicators of carcinogenesis with high risk index for BE. Objective: The aim of this study was to investigate the characteristics of gene changes from Barrett’s esophagus (BE) to esophageal adenocarcinoma by cDNA microarray. Methods: The cDNA retro-transcribed from equal quantities mRNA from esophageal carcinoma and BE tissues as well as control normal epithelium of esophagus which were from one patient with esophageal adenocarcinoma were labeled with Cy5 and Cy3 fluorescence as probes. The mixed probes were hybridized with two pieces gene chip respectively. It was scanned by laser scanner Scan Array 4000. The acquired images were analyzed by software GenePix Pro 3.0. Results: A total of 214 genes were screened out which expression levels were more than 2 times in hybridization of esophageal adenocarcinoma vs normal epithelium of esophagus, while 90 genes in hybridization of BE vs normal epithelium. A parallel comparison among these two gene profiles showed that a total of 45 genes with 24 downregulation and 21 up-regulation which expressio n levels were more than 2 times between the BE and the esophageal adenocarcinoma. Among these, there were 27 genes with 18 downregulation and 9 up-regulation which implicated the tendencies progressing from BE to esophageal adenocarcinoma. Conclusion: These genes or their products which implicate the tendencies can be chosen as indicators of carcinogenesis with high risk index for BE.