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Helicobacter pylori-Induced Signaling Pathways Contribute to Intestinal Metaplasia and Gastric Carcinogenesis

Helicobacter pylori (H. pylori) induces chronic gastric inflammation, atrophic gastritis, intestinal metaplasia, and cancer. Although the risk of gastric cancer increases exponentially with the extent of atrophic gastritis, the precise mechanisms of gastric carcinogenesis have not been fully elucida...

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Detalles Bibliográficos
Autores principales: Sue, Soichiro, Shibata, Wataru, Maeda, Shin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4441984/
https://www.ncbi.nlm.nih.gov/pubmed/26064948
http://dx.doi.org/10.1155/2015/737621
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author Sue, Soichiro
Shibata, Wataru
Maeda, Shin
author_facet Sue, Soichiro
Shibata, Wataru
Maeda, Shin
author_sort Sue, Soichiro
collection PubMed
description Helicobacter pylori (H. pylori) induces chronic gastric inflammation, atrophic gastritis, intestinal metaplasia, and cancer. Although the risk of gastric cancer increases exponentially with the extent of atrophic gastritis, the precise mechanisms of gastric carcinogenesis have not been fully elucidated. H. pylori induces genetic and epigenetic changes in gastric epithelial cells through activating intracellular signaling pathways in a cagPAI-dependent manner. H. pylori eventually induces gastric cancer with chromosomal instability (CIN) or microsatellite instability (MSI), which are classified as two major subtypes of gastric cancer. Elucidation of the precise mechanisms of gastric carcinogenesis will also be important for cancer therapy.
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spelling pubmed-44419842015-06-10 Helicobacter pylori-Induced Signaling Pathways Contribute to Intestinal Metaplasia and Gastric Carcinogenesis Sue, Soichiro Shibata, Wataru Maeda, Shin Biomed Res Int Review Article Helicobacter pylori (H. pylori) induces chronic gastric inflammation, atrophic gastritis, intestinal metaplasia, and cancer. Although the risk of gastric cancer increases exponentially with the extent of atrophic gastritis, the precise mechanisms of gastric carcinogenesis have not been fully elucidated. H. pylori induces genetic and epigenetic changes in gastric epithelial cells through activating intracellular signaling pathways in a cagPAI-dependent manner. H. pylori eventually induces gastric cancer with chromosomal instability (CIN) or microsatellite instability (MSI), which are classified as two major subtypes of gastric cancer. Elucidation of the precise mechanisms of gastric carcinogenesis will also be important for cancer therapy. Hindawi Publishing Corporation 2015 2015-05-10 /pmc/articles/PMC4441984/ /pubmed/26064948 http://dx.doi.org/10.1155/2015/737621 Text en Copyright © 2015 Soichiro Sue et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Sue, Soichiro
Shibata, Wataru
Maeda, Shin
Helicobacter pylori-Induced Signaling Pathways Contribute to Intestinal Metaplasia and Gastric Carcinogenesis
title Helicobacter pylori-Induced Signaling Pathways Contribute to Intestinal Metaplasia and Gastric Carcinogenesis
title_full Helicobacter pylori-Induced Signaling Pathways Contribute to Intestinal Metaplasia and Gastric Carcinogenesis
title_fullStr Helicobacter pylori-Induced Signaling Pathways Contribute to Intestinal Metaplasia and Gastric Carcinogenesis
title_full_unstemmed Helicobacter pylori-Induced Signaling Pathways Contribute to Intestinal Metaplasia and Gastric Carcinogenesis
title_short Helicobacter pylori-Induced Signaling Pathways Contribute to Intestinal Metaplasia and Gastric Carcinogenesis
title_sort helicobacter pylori-induced signaling pathways contribute to intestinal metaplasia and gastric carcinogenesis
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4441984/
https://www.ncbi.nlm.nih.gov/pubmed/26064948
http://dx.doi.org/10.1155/2015/737621
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