CDX2 Alone Plays an Important Role in Epithelial Phenotypic Changes in Barrett's Metaplasia in the Esophagus, and Esophageal Submucosal Glands Seem to Be the Predominant Cell of Origin for Barrett’s Esophagus

Abstract

Gastroesophageal Reflux Disease (GERD) is a long-known disorder caused by back flow of acid (also known as acid reflux) from the stomach into the esophagus. A patient with GERD may develop Barrett’s Esophagus and have increased risk of developing esophageal adenocarcinoma, a potentially fatal cancer of the esophagus with a low chance of survival. In esophageal research, there are two fields of study regarding Barrett’s esophagus. There is the field intent on understanding the pathogenesis of the change from the normal squamous lining of the esophagus to Barrett’s esophagus and the second field concerns the transition from Barrett’s esophagus to adenocarcinoma. This thesis explores the first question. Upon evaluation of the current literature, the cell-of-origin and transcription factors involved highly support the hypothesis that a submucosal cell in the esophagus and CDX2 an intestinal transcription factor alone are responsible for Barrett’s disease. CDX2 is normally present in intestinal epithelium that plays a role in maintaining an intestinal epithelial phenotype. By improving treatment options, therapeutic treatments or surveillance for patients (similar to colorectal cancer), we hope to be able to lower the incidence of Barrett’s or adenocarcinoma.