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World J Gastroenterol. Apr 21, 2013; 19(15): 2307-2312
Published online Apr 21, 2013. doi: 10.3748/wjg.v19.i15.2307
Role of interleukin-6 in Barrett’s esophagus pathogenesis
Katerina Dvorak, Bohuslav Dvorak
Katerina Dvorak, Department of Cellular and Moleculart Medicine, The University of Arizona, Tucson, AZ 85724, United States
Bohuslav Dvorak, Department of Pediatrics and Steele Children’s Research Center, The University of Arizona, Tucson, AZ 85724, United States
Author contributions: Dvorak K and Dvorak B solely contributed to this paper.
Supported by GI SPORE Grant p50 CA95060 from the National Cancer Institute, to Dvorak K
Correspondence to: Katerina Dvorak, PhD, Associate Professor, Department of Cellular and Moleculart Medicine, The University of Arizona, Tucson, AZ 85724, United States. kdvorak@email.arizona.edu
Telephone: +1-520-9710255 Fax: +1-520-6265009
Received: August 16, 2012
Revised: October 31, 2012
Accepted: November 14, 2012
Published online: April 21, 2013
Abstract

Barrett’s esophagus (BE) is a metaplastic lesion of the distal esophagus arising as a consequence of chronic gastroesophageal reflux disease. Multiple studies show that BE is associated with increased risk of esophageal adenocarcinoma (EAC). Epidemiological studies and animal models demonstrate that chronic inflammation triggered by repeated exposure to refluxate predisposes to the development of BE and EAC. The chronic inflammation is associated with cytokine alterations. Interleukin 6 (IL-6) is a cytokine that stimulates cell proliferation and apoptosis resistance is frequently increased in different cancers. Importantly, IL-6 and transcriptional factor signal transducer and activator of transcription 3 (STAT3) that is activated by IL-6 are also increased in BE and EAC. This review critically appraises the role of IL-6/STAT3 pathway in progression of BE to EAC from the published evidence currently available.

Keywords: Barrett’s esophagus, Interleukin 6, Bile acids, Inflammation, Apoptosis