Publication Name	World Journal of Gastrointestinal Pathophysiology
Manuscript ID	20895
Country	Japan

Received	2015-06-25 17:32
Peer-Review Started	2015-06-28 11:07
To Make the First Decision	2015-08-16 17:33
Return for Revision	2015-08-26 09:03
Revised	2015-09-01 06:57
Second Decision	2015-11-02 14:19
Accepted by Journal Editor-in-Chief
Accepted by Executive Editor-in-Chief	2015-11-11 18:00
Articles in Press	2015-11-11 18:00
Publication Fee Transferred
Edit the Manuscript by Language Editor
Typeset the Manuscript	2016-01-20 19:43
Publish the Manuscript Online	2016-01-31 16:11

ISSN	2150-5330 (online)
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/
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Category	Gastroenterology & Hepatology
Manuscript Type	Minireviews
Article Title	Role of nitric oxide in the pathogenesis of Barrett’s-associated carcinogenesis
Manuscript Source	Invited Manuscript
All Author List	Gen Kusaka, Kaname Uno, Katsunori Iijima and Tooru Shimosegawa
Funding Agency and Grant Number
Corresponding Author	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
Key Words	Barrett’s esophagus; Nitric oxide; Epithelial growth factor receptor; Caudal type homeobox 2; Microbiome
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.
Publish Date	2016-01-31 16:11
Citation	Kusaka G, Uno K, Iijima K, Shimosegawa T. Role of nitric oxide in the pathogenesis of Barrett’s-associated carcinogenesis. World J Gastrointest Pathophysiol 2016; 7(1): 131-137
URL	http://www.wjgnet.com/2150-5330/full/v7/i1/131.htm
DOI	http://dx.doi.org/10.4291/wjgp.v7.i1.131

Full Article (PDF)	WJGP-7-131.pdf
Full Article (Word)	WJGP-7-131.doc
Manuscript File	20895-Review.docx
Answering Reviewers	20895-Answering reviewers.pdf
Audio Core Tip	20895-Audio core tip.mp3
Conflict-of-Interest Disclosure Form	20895-Conflict-of-interest statement.pdf
Copyright License Agreement	20895-Copyright assignment.pdf
Non-Native Speakers of English Editing Certificate	20895-Language certificate.pdf
Peer-review Report	20895-Peer-review(s).pdf
Scientific Misconduct Check	20895-Scientific misconduct check.pdf
Scientific Editor Work List	20895-Scientific editor work list.pdf