From genetics to signaling pathways: molecular pathogenesis of esophageal adenocarcinoma

Publication date: Available online 30 May 2019Source: Biochimica et Biophysica Acta (BBA) - Reviews on CancerAuthor(s): Ravindran Caspa Gokulan, Monica T. Garcia-Buitrago, Alexander I. ZaikaAbstractEsophageal adenocarcinoma (EAC) has one of the fastest rising incidence rates in the U.S. and many other Western countries. One of the unique risk factors for EAC is gastroesophageal reflux disease (GERD), a chronic digestive condition in which acidic contents from the stomach, frequently mixed with duodenal bile, enter the esophagus resulting in esophageal tissue injury. At the cellular level, progression to EAC is underlined by continuous DNA damage caused by reflux and chronic inflammatory factors that increase the mutation rate and promote genomic instability. Despite recent successes in cancer diagnostics and treatment, EAC remains a poorly treatable disease. Recent research has shed new light on molecular alterations underlying progression to EAC and revealed novel treatment options. This review focuses on the genetic and molecular studies of EAC. The molecular changes that occur during the transformation of normal Barrett’s esophagus to esophageal adenocarcinoma are also discussed.
Source: Biochimica et Biophysica Acta (BBA) Reviews on Cancer - Category: Cancer & Oncology Source Type: research