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©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. May 14, 2016; 22(18): 4567-4575
Published online May 14, 2016. doi: 10.3748/wjg.v22.i18.4567
Published online May 14, 2016. doi: 10.3748/wjg.v22.i18.4567
Methylation of DAPK and THBS1 genes in esophageal gastric-type columnar metaplasia
Roberto Herrera-Goepfert, José Luis Mosqueda-Vargas, Department of Pathology, Instituto Nacional de Cancerología (INCan), 10480 México, DF, México
Luis F Oñate-Ocaña, Clinical Research Division, Instituto Nacional de Cancerología (INCan), 10480 México, DF, México
Luis A Herrera, Clementina Castro, Julia Mendoza, Rodrigo González-Barrios, Unidad de Investigación Biomédica en Cáncer, Instituto Nacional de Cancerología (INCan)-Instituto de Investigaciones Biomédicas (IIB), Universidad Nacional Autónoma de México (UNAM), 14080 México, DF, México
Author contributions: Herrera-Goepfert R contributed to study concept and design, acquisition of data, analysis and interpretation of data, drafting of the manuscript, critical revision of the manuscript for important intellectual content, statistical analysis, funding, and study supervision; Mosqueda-Vargas JL, Mendoza J and González-Barrios R contributed to acquisition of data, drafted of the manuscript, and technical support; Herrera LA, Oñate-Ocaña LF and Castro C contributed to analysis and interpretation of data, drafting of the manuscript, critical revision of the manuscript for important intellectual content, statistical analysis, and technical support; all authors have read and approved the final version to be published.
Institutional review board statement: The protocol study was revised and approved by Research and Ethics on Research Committees at the Institute.
Conflict-of-interest statement: The authors declare no conflicts of interest.
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: Roberto Herrera-Goepfert, MD, Department of Pathology, Instituto Nacional de Cancerología (INCan), México, Av. San Fernando 22, Colonia Sección XVI, Delegación Tlalpan, 10480 México, DF, México. rhgoepfert@gmail.com
Telephone: +52-55-47471020-11069
Received: December 2, 2015
Peer-review started: December 4, 2015
First decision: December 31, 2015
Revised: January 19, 2016
Accepted: January 30, 2016
Article in press: January 30, 2016
Published online: May 14, 2016
Processing time: 154 Days and 5.3 Hours
Peer-review started: December 4, 2015
First decision: December 31, 2015
Revised: January 19, 2016
Accepted: January 30, 2016
Article in press: January 30, 2016
Published online: May 14, 2016
Processing time: 154 Days and 5.3 Hours
Core Tip
Core tip: Columnar metaplasia of the esophagus, whether specialized or not, is a hallmark of gastroesophageal reflux disease. Current information suggests that intestinal metaplasia in the esophagus arises from gastric-type metaplasia. In this study, we have demonstrated that Helicobacter pylori (H. pylori) cagA+ can colonize esophageal gastric-type metaplastic mucosa, and that DNA methylation of tumor suppressor genes could be related to H. pylori cagA+ infection, which in turn, may predispose to precancerous lesions, including intestinal metaplasia.