BACKGROUND/AIMS: Cadherins are cell adhesion molecules that are thought to play a vital role in cell-cell adhesion; loss or down-regulation of their expression has been implicated in neoplasia. Barrett's esophageal columnar metaplasia (BE) is a premalignant lesion for esophageal adenocarcinoma with clinical symptoms similar to those of gastroesophageal reflux disease and esophagitis. In this study, we investigated the potential relationship between E-cadherin expression and inflammation, metaplasia, and carcinogenesis in esophagitis, BE, and esophageal adenocarcinoma. METHODS: Endoscopically obtained mucosal biopsy specimens 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. RESULTS: Densitometric analysis of Western blots revealed the expression of E-cadherin to be significantly lower in patients with BE compared with normal esophageal epithelium, regardless of the presence or absence of dysplasia (p < 0.03). No significant differences were noticed between the normal esophagus and the esophagitis groups. In the adenocarcinoma 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 staining matched the Western analysis results. CONCLUSIONS: We conclude that loss of or reduced E-cadherin expression may play a role in the progression of BE to adenocarcinoma.
BACKGROUND/AIMS: Cadherins are cell adhesion molecules that are thought to play a vital role in cell-cell adhesion; loss or down-regulation of their expression has been implicated in neoplasia. Barrett's esophageal columnar metaplasia (BE) is a premalignant lesion for esophageal adenocarcinoma with clinical symptoms similar to those of gastroesophageal reflux disease and esophagitis. In this study, we investigated the potential relationship between E-cadherin expression and inflammation, metaplasia, and carcinogenesis in esophagitis, BE, and esophageal adenocarcinoma. METHODS: Endoscopically obtained mucosal biopsy specimens 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. RESULTS: Densitometric analysis of Western blots revealed the expression of E-cadherin to be significantly lower in patients with BE compared with normal esophageal epithelium, regardless of the presence or absence of dysplasia (p < 0.03). No significant differences were noticed between the normal esophagus and the esophagitis groups. In the adenocarcinoma 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 staining matched the Western analysis results. CONCLUSIONS: We conclude that loss of or reduced E-cadherin expression may play a role in the progression of BE to adenocarcinoma.
Authors: Paras Jethwa; Mushal Naqvi; Robert G Hardy; Neil-A Hotchin; Sally Roberts; Robert Spychal; Chris Tselepis Journal: World J Gastroenterol Date: 2008-02-21 Impact factor: 5.742
Authors: Michael Herfs; Pascale Hubert; Natalia Kholod; Jean Hubert Caberg; Christine Gilles; Geert Berx; Pierre Savagner; Jacques Boniver; Philippe Delvenne Journal: Am J Pathol Date: 2008-04-01 Impact factor: 4.307