E-CADHERIN EXPRESSION IN GASTROESOPHAGEAL REFLUX DISEASE, BARRETTS-ESOPHAGUS, AND ESOPHAGEAL ADENOCARCINOMA - AN IMMUNOHISTOCHEMICAL AND IMMUNOBLOT STUDY

Background/Aims: Cadherins are cell adhesion molecules that are though t to play a vital role in cell-cell adhesion; loss or down-regulation of their expression has been implicated in neoplasia. Barrett's esopha geal columnar metaplasia (BE) is a premalignant lesion for esophageal adenocarcinoma with clinical symptoms similar to those of gastroesopha geal reflux disease and esophagitis. In this study, we investigated th e potential relationship between E-cadherin expression and inflammatio n, metaplasia, and carcinogenesis in esophagitis, BE, and esophageal a denocarcinoma. Methods: Endoscopically obtained mucosal biopsy specime ns of esophagitis (n = 6), BE with or without dysplasia (n = 16), and esophageal adenocarcinoma (n = 6) were analyzed for the expression of E-cadherin by both Western analysis and immunoperoxidase staining. Res ults: Densitometric analysis of Western blots revealed the expression of E-cadherin to be significantly lower in patients with BE compared w ith normal esophageal epithelium, regardless of the presence or absenc e of dysplasia (p < 0.03). No significant differences were noticed bet ween the normal esophagus and the esophagitis groups. In the adenocarc inoma group, one patient showed complete loss of E-cadherin expression , and the other five patients showed significantly reduced expression that was even lower than that in BE (p < 0.01). Immunoperoxidase stain ing matched the Western analysis results. Conclusions: We conclude tha t loss of or reduced E-cadherin expression may play a role in the prog ression of BE to adenocarcinoma.