ArticleCancer science2006
Helicobacter pylori infection stimulates intestinalization of endocrine cells in glandular stomach of Mongolian gerbils.
Article in Cancer science, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Perspectives on gastric cancer: the central role of gastrin in carcinogenesis byFrontiers in oncology · 2026Review
- Diversity in bacterium-host interactions within the species Helicobacter heilmannii sensu stricto.Veterinary research · 2013Article
- Animal models to study the role of long-term hypergastrinemia in gastric carcinogenesis.Journal of biomedicine & biotechnology · 2011Review
- In vitro differentiation of Runx3-/- p53-/- gastric epithelial cells into intestinal type cells.Cancer science · 2008Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intestinal metaplasia has been investigated extensively as a possible premalignant condition for stomach cancer but its pathogenesis is still not fully understood. In the present study, we examined the relationship between endocrine and mucous cell marker expression periodically after Helicobacter pylori infection in the Mongolian gerbil model. The numbers of chromogranin A (CgA)-positive, gastrin-positive and gastric inhibitory polypeptide (GIP)-positive cells in H. pylori-infected groups was increased significantly compared with the non-infected case. However, CgA-positive and gastrin-positive cells then decreased from 50 through 100 experimental weeks after H. pylori infection, whereas GIP-positive cells increased. Coexistence of gastrin-positive and GIP-positive cells was detected in the same gastric and intestinal mixed phenotypic glandular-type glands. In conclusion, the endocrine cell phenotype is in line with that of the mucous counterpart in the glands of H. pylori-infected Mongolian gerbil stomach, supporting the concept that development of intestinal metaplasia is due to the abnormal differentiation of a stem cell.
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