The sequential model of Barrett's esophagus and adenocarcinoma induced by duodeno-esophageal reflux without exogenous carcinogens

• Published in: Anticancer research Vol. 22; no. 1A; p. 39
• Main Authors: Sato, Takahiro, Miwa, Koichi, Sahara, Hiroyuki, Segawa, Masataka, Hattori, Takanori
• Format: Journal Article
• Language: English
• Published: Greece 01.01.2002
• Subjects: Adenocarcinoma - etiology; Adenocarcinoma - pathology; Animals; Barrett Esophagus - etiology; Barrett Esophagus - pathology; Disease Models, Animal; Duodenogastric Reflux - complications; Duodenogastric Reflux - pathology; Duodenum - surgery; Esophageal Neoplasms - etiology; Esophageal Neoplasms - pathology; Esophagus - surgery; Gastrectomy; Male; Rats
• ISSN: 0250-7005

The experiment was designed to sequentially examine the histogenesis of Barrett's esophagus and esophageal adenocarcinoma induced by duodenal reflux without exogenous carcinogens. Wistar male rats, 200 in all, each weighing approximately 250 g were used. The totally gastrectomized animals were reconstructed by Schlatter's method to produce duodeno-esophageal reflux (n = 100), for comparison with no reflux, Roux-en-Y reconstruction (n = 100). The excised esophagus was histopathologically examined every 10 weeks after surgery until 50 weeks. Among the animals with reflux, Barrett's epithelium developed near esophago-jejunostoma 10 weeks after surgery and subsequently spread upward. Columnar dysplasia was first identified in the zone of Barrett's epithelium at 20 weeks, simultaneously with adenocarcinoma. As the incidence of Barrett's esophagus increased over time, the incidence of both dysplasia and adenocarcinoma also increased. Adenocarcinoma developed in the area of columnar dysplasia. The temporal progression from Barrett's esophagus to columnar dysplasia and adenocarcinoma is induced by duodeno-esophageal reflux. Columnar dysplasia is a morphological marker for adenocarcinogenesis.