Wiseman EF, Ang YS. Risk factors for neoplastic progression in Barrett’s esophagus. World J Gastroenterol 2011; 17(32): 3672-3683 [PMID: 21990948 DOI: 10.3748/wjg.v17.i32.3672]
Corresponding Author of This Article
Yeng S Ang, MD, FRCP, FRCPI, FEBG, Consultant Gastroenterologist/Honorary Senior Lecturer, Department of Gastroenterology, Royal Albert Edward Infirmary, Wigan Lane, Wigan, Greater Manchester, WN1 2NN, United Kingdom. yeng.ang@wwl.nhs.uk
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World J Gastroenterol. Aug 28, 2011; 17(32): 3672-3683 Published online Aug 28, 2011. doi: 10.3748/wjg.v17.i32.3672
Risk factors for neoplastic progression in Barrett’s esophagus
Elizabeth F Wiseman, Yeng S Ang
Elizabeth F Wiseman, Yeng S Ang, Department of Gastroenterology, Royal Albert Edward Infirmary, Wigan Lane, Wigan, Greater Manchester, WN1 2NN, United Kingdom
Yeng S Ang, Faculty of Medical and Human Sciences, School of Translational Medicine, The University of Manchester, Oxford Road, Manchester, M13 9PL, United Kingdom
Author contributions: Wiseman EF performed the literature review and prepared the manuscript; Ang YS conceived the article; Wiseman EF and Ang YS contributed to revision of the original manuscript; all authors read and approved the final manuscript.
Correspondence to: Yeng S Ang, MD, FRCP, FRCPI, FEBG, Consultant Gastroenterologist/Honorary Senior Lecturer, Department of Gastroenterology, Royal Albert Edward Infirmary, Wigan Lane, Wigan, Greater Manchester, WN1 2NN, United Kingdom. yeng.ang@wwl.nhs.uk
Telephone: +44-1942-773119 Fax: +44-1942-822340
Received: July 21, 2010 Revised: October 11, 2010 Accepted: October 18, 2010 Published online: August 28, 2011
Abstract
Barrett’s esophagus (BE) confers a significant increased risk for development of esophageal adenocarcinoma (EAC), with the pathogenesis appearing to progress through a “metaplasia-dysplasia-carcinoma” (MDC) sequence. Many of the genetic insults driving this MDC sequence have recently been characterized, providing targets for candidate biomarkers with potential clinical utility to stratify risk in individual patients. Many clinical risk factors have been investigated, and associations with a variety of genetic, specific gastrointestinal and other modifiable factors have been proposed in the literature. This review summarizes the current understanding of the mechanisms involved in neoplastic progression of BE to EAC and critically appraises the relative roles and contributions of these putative risk factors from the published evidence currently available.
