Esophageal Adenocarcinoma—Is Barrett's Truly to Blame?

Aiming to support the hypothesis that Barrett’s esophagus is the precursor of most adenocarcinomas of the esophagus and cardia, the authors determined a biochemical profile typical of Barrett’s esophagus and esophageal adenocarcinoma. They evaluated the expression of the small intestinal proteins sucrase-isomaltase (SI) and crypt cell antigen (CCAg) in Barrett’s esophagus, in its putative precursor tissues, and in esophageal-cardial adenocarcinomas without Barrett’s esophagus. Tissue samples were obtained by endoscopic biopsy or from surgical resected specimens. Five normal stomach samples were used for negative controls and five jejunum specimens for positive controls. Furthermore, five samples of peptic esophagitis and squamous cell carcinoma were analyzed. All specimens were stained with hematoxylin and eosin and Barrett’s esophagus was classified according to the presence of dysplasia and the type of metaplasia (cardiac and intestinal). Adenocarcinomas of the esophagus were classified using the Siewert-classification. For detection of the two intestinal proteins the authors used an indirect immunofluorescence technique with mouse monoclonal antibodies. The sections were analyzed with laser confocal microscopy imaging. Of the Barrett’s mucosa specimens, 93% showed a positive staining for SI and 89% for CCAg regardless of the type of metaplasia present. The expression of SI and CCAg was also independent of the coexistence of dysplasia or the presence of associated adenocarcinoma. Furthermore there was no statistical difference in SI and CCAg expression between specimens from adenocarcinoma with or without Barrett’s tissue and between tumors located in the esophagus and cardia. In peptic esophagitis or squamous cell carcinoma no expression of SI or CCAg was detected. The authors conclude that Barrett’s esophagus and adenocarcinoma of the esophagus have a similar biochemical phenotype and that these esophageal injuries probably originate from pre-existing Barrett’s esophagus, and furthermore that these data support the concept of a pluripotent stem cell for the development of Barrett’s esophagus and subsequently for adenocarcinoma of the esophagus and cardia. (Am J Gastroenterol 1999;94:1103–1104. © 1999 by Am. Coll. of Gastroenterology)