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©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastrointest Pathophysiol. Feb 15, 2016; 7(1): 131-137
Published online Feb 15, 2016. doi: 10.4291/wjgp.v7.i1.131
Published online Feb 15, 2016. doi: 10.4291/wjgp.v7.i1.131
Role of nitric oxide in the pathogenesis of Barrett’s-associated carcinogenesis
Gen Kusaka, Kaname Uno, Katsunori Iijima, Tooru Shimosegawa, Division of Gastroenterology, Tohoku University Hospital, Sendai, Miyagi 981-8574, Japan
Author contributions: All authors contributed to this paper.
Conflict-of-interest statement: None.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Gen Kusaka, MD, PhD, Division of Gastroenterology, Tohoku University Hospital, 1-1 Seiryo-cho, Aoba-ku, Sendai, Miyagi 981-8574, Japan. gkusaka@med.tohoku.ac.jp
Telephone: +81-22-7177171 Fax: +81-22-7177174
Received: June 25, 2015
Peer-review started: June 28, 2015
First decision: August 26, 2015
Revised: October 17, 2015
Accepted: November 10, 2015
Article in press: November 11, 2015
Published online: February 15, 2016
Processing time: 220 Days and 1.9 Hours
Peer-review started: June 28, 2015
First decision: August 26, 2015
Revised: October 17, 2015
Accepted: November 10, 2015
Article in press: November 11, 2015
Published online: February 15, 2016
Processing time: 220 Days and 1.9 Hours
Core Tip
Core tip: Barrett’s carcinogenesis is closely associated with chronic inflammation caused by gastro-esophageal reflux of gastric acid, bile acid and intraluminal microorganisms. Caudal type homeobox 2 (CDX2) is a crucial biomarker of Barrett’s esophagus. We previously demonstrated that a high amount of nitric oxide (NO) at the gastro-esophageal junction (GEJ) might directly induce CDX2 through phosphorylation of epidermal growth factor receptor (EGFR) in a ligand-independent manner. Together with a possible effect of anti-EGFR-targeting drugs in inhibiting Barrett’s adenocarcinoma, future research for controlling NO production around the GEJ might provide a new insight for developing a management strategy of Barrett’s carcinogenesis.