Review Article
Pathogenesis of Barrett s Esophagus
Haoxiang Zhang, Caifei Shen, Pu Wang, Ji Feng, Yin Xu, Jingwen Li, Anran Zhang, Yiju Xia, Wu Yan and Dianchun Fang*
Department of Gastoenterology, Southwest Hospital, Third Military Medical University, Chongqing 400038, China
- Corresponding Author:
- Dianchun Fang
Department of Gastroenterology, Southwest Hospital
Third Military Medical University, Gaotanyan Street 30
Chongqing 400038, China
Tel: 86-023-68754480
E-mail: fangdianchun@hotmail.com
Received Date: March 16, 2016; Accepted Date: April 21, 2016; Published Date: April 27, 2016
Citation: Zhang H, Shen C, Wang P, Feng J, Xu Y, et al. (2016) Pathogenesis of Barrett’s Esophagus. J Gastrointest Dig Syst 6:417. doi:10.4172/2161-069X.1000417
Copyright: © 2016 Zhang H, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Barrett’s esophagus (BE) is characterized as histologic evidence of intestinal metaplasia is present in distal esophageal epithelium and is an important pathology because it is the major risk factor for developing esophageal adenocarcinoma (EAC). It’s well known that chronic gastroesophageal reflux disease (GERD) leads to the development of metaplasia. However, the cellular and molecular mechanism of the replacement of squamous esophageal epithelium with a columnar type is largely unknown. Efforts to understand the pathogenesis of BE and its disposition to EAC have been increasing over the previous 2 decades. This review aims to explore current data on the major risk factors, origin, genetic changes of BE, provide an insight into the molecular biomarkers related with BE and seek for possible development of therapies that could prevent BE from progressing to EAC.
