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Bile acid and inflammation activate gastric cardia stem cells in a mouse model of barrett-like metaplasia
Authors
Julian A. Abrams
Samuel Asfaha
+15 more
Govind Bhagat
Zinaida Dubeykovskaya
Jose Luiz Figueiredo
Richard Friedman
Pamela Good
Jan Kitajewski
Michele D. Lee
Yoomi Lee
Charles J. Lightdale
Umar Mahmood
Frederic Marache
Michael Quante
Anil K. Rustgi
Carrie Shawber
Timothy C. Wang
Publication date
17 January 2012
Publisher
Scholarship@Western
Abstract
Esophageal adenocarcinoma (EAC) arises from Barrett esophagus (BE), intestinal-like columnar metaplasia linked to reflux esophagitis. In a transgenic mouse model of BE, esophageal overexpression of interleukin-1β phenocopies human pathology with evolution of esophagitis, Barrett-like metaplasia and EAC. Histopathology and gene signatures closely resembled human BE, with upregulation of TFF2, Bmp4, Cdx2, Notch1, and IL-6. The development of BE and EAC was accelerated by exposure to bile acids and/or nitrosamines, and inhibited by IL-6 deficiency. Lgr5+ gastric cardia stem cells present in BE were able to lineage trace the early BE lesion. Our data suggest that BE and EAC arise from gastric progenitors due to a tumor-promoting IL-1β-IL-6 signaling cascade and Dll1-dependent Notch signaling. © 2012 Elsevier Inc
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oai:ir.lib.uwo.ca:paedpub-1721
Last time updated on 08/10/2022