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World J Gastroenterol. May 14, 2013; 19(18): 2736-2739
Published online May 14, 2013. doi: 10.3748/wjg.v19.i18.2736
Relationships of CDXs and apical sodium-dependent bile acid transporter in Barrett’s esophagus
Jingbo Zhao, Hans Gregersen
Jingbo Zhao, Mech-Sense, Department of Gastroenterology and Surgery, Aalborg University Hospital, DK-9000 Aalborg, Denmark
Jingbo Zhao, Hans Gregersen, College of Bioengineering, Chongqing University, Chongqing 400044, China
Hans Gregersen, the Giome Institute, DK-8000 Aarhus, Denmark
Author contributions: Zhao J designed and drafted the manuscript; Gregersen H edited English language and grammar; Zhao J and Gregersen H revised and finally approved this paper.
Correspondence to: Jingbo Zhao, MD, PhD, Mech-Sense, Department of Gastroenterology and Surgery, Aalborg University Hospital, Sdr. Skovvej 15, DK-9000 Aalborg, Denmark. jz@rn.dk
Telephone: +45-9-9326907 Fax: +45-9-9326801
Received: April 2, 2013
Revised: May 2, 2013
Accepted: May 7, 2013
Published online: May 14, 2013
Processing time: 42 Days and 12 Hours
Core Tip

Core tip: Aberrant co-expression of Caudal-related homeodomain transcription factors (CDXs) and apical sodium-dependent bile acid transporter (ASBT) in the epithelium of Barrett’s esophagus (BE) indicates association among these factors. Acid and bile reflux induce CDXs gene expression and can lead to formation of BE. CDX-mediated promoter activation can lead to aberrant expression of ASBT. The BE phenotype may be better than squamous epithelium to protect against refluxed acid and bile. On the other hand the BE phenotype is associated with increased risk of esophageal adenocarcinoma (EAC). Furthermore, the decreased expressions of CDXs and ASBT in high-grade esophageal dysplasia indicate that CDXs and ASBT are inhibitory factors to the progression of EAC.