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Int. J. Mol. Sci. 2017, 18(10), 2063; doi:10.3390/ijms18102063

Metaplasia in the Stomach—Precursor of Gastric Cancer?

Graduate School of Medicine, Department of Gastroenterology, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
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Received: 1 September 2017 / Revised: 23 September 2017 / Accepted: 25 September 2017 / Published: 27 September 2017
(This article belongs to the Special Issue Cancer Stem Cells)
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Abstract

Despite a significant decrease in the incidence of gastric cancer in Western countries over the past century, gastric cancer is still one of the leading causes of cancer-related deaths worldwide. Most human gastric cancers develop after long-term Helicobacter pylori infection via the Correa pathway: the progression is from gastritis, atrophy, intestinal metaplasia, dysplasia, to cancer. However, it remains unclear whether metaplasia is a direct precursor of gastric cancer or merely a marker of high cancer risk. Here, we review human studies on the relationship between metaplasia and cancer in the stomach, data from mouse models of metaplasia regarding the mechanism of metaplasia development, and the cellular responses induced by H. pylori infection. View Full-Text
Keywords: gastric cancer; intestinal metaplasia; Spasmolytic polypeptide expressing metaplasia (SPEM); Helicobacter pylori; stem cells; lineage tracing gastric cancer; intestinal metaplasia; Spasmolytic polypeptide expressing metaplasia (SPEM); Helicobacter pylori; stem cells; lineage tracing
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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. (CC BY 4.0).

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Kinoshita, H.; Hayakawa, Y.; Koike, K. Metaplasia in the Stomach—Precursor of Gastric Cancer? Int. J. Mol. Sci. 2017, 18, 2063.

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