Etiology and Pathophysiology of Barrett's Esophagus/Neoplasia

Abstract

Background: Barrett's esophagus and its malignant progression to Barrett's adenocarcinoma are becoming increasingly prevalent worldwide, yet their underlying mechanisms remain incompletely understood.

Summary: The pathogenesis of Barrett's esophagus and Barrett's adenocarcinoma is multifactorial, involving environmental, genetic, and cellular factors. Chronic acid and bile reflux are well-established contributors, promoting cellular transformation in the esophageal epithelium. Obesity further exacerbates this risk, both indirectly by increasing reflux and directly via proinflammatory adipokines. Recent genetic studies have identified several genetic risk variants, with loss of p53 recognized as critical event in malignant progression. Moreover, the origin of Barrett's esophagus remains under investigation, with proposed sources including cells of esophageal submucosal glands, cells of gastric cardia, and circulating bone marrow-derived cells.

Key messages: The pathophysiological mechanisms underlying Barrett's esophagus and the development of Barrett's adenocarcinoma are still under active investigation. Understanding these mechanisms is essential for developing effective preventive and therapeutic strategies.

Keywords: Barrett’s adenocarcinoma; Esophageal adenocarcinoma; Gastroesophageal reflux disease.