Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 18, Issue 10, Pages -Publisher
MDPI
DOI: 10.3390/ijms18102063
Keywords
gastric cancer; intestinal metaplasia; Spasmolytic polypeptide expressing metaplasia (SPEM); Helicobacter pylori; stem cells; lineage tracing
Funding
- KAKENHI [17K15927, 16H06749, 17H05081]
- Project for Cancer Research And Therapeutic Evolution (P-CREATE) from the Japan Agency of Medical Research and Development, AMED
- Mochida Memorial Foundation for Medical and Pharmacological Research
- Takeda Science Foundation
- Mitsubishi Foundation, Natural Sciences
- Advanced Research and Development Programs for Medical Innovation (PRIME)
- Grants-in-Aid for Scientific Research [17K15927, 16H06749] Funding Source: KAKEN
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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.
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