Summary
Barrett’s esophagus (BE) is a premalignant condition with increased risk for the development of esophageal adenocarcinoma (EAC). Surveillance relies on regular endoscopy with biopsies to detect dysplasia (disordered cellular growth) and diagnose cancer at an early, treatable stage. BE is a metaplastic response at the gastroesophageal boundary to chronic tissue injury by acid reflux. Metaplasia is the transformation of one differentiated cell type to another differentiated cell type: BE is characterized by replacement of normal squamous epithelium by columnar epithelium with gastric and intestinal features. The origin of metaplastic columnar cells is unclear, and different candidate precursor cells have been suggested. Better knowledge about the pathogenesis of BE may lead to better diagnosis, stratification, and treatment, and might help to develop targeted chemopreventive strategies in the future. On page 760 of this issue, Nowicki-Osuch et al. (1) find good evidence to support gastric cells as the origin of BE.
