Abstract
Background: Progression from intestinal metaplasia to neoplasia has not been demonstrated experimentally. The hypothesis that gastric adenocarcinoma arises from intestinal metaplasia was tested in a Mongolian gerbil model of Helicobacter pylori (H. pylori) infection. Methods: One hundred and fourteen specific pathogen-free gerbils were divided in five groups, A and D: infected with H. pylori and administered the carcinogen N-methyl-N-nitrosourea (MNU); C and E: received MNU; B: H. pylori, but no MNU. Animals were killed at 41 weeks, stomachs were mapped, and the relationship between metaplasia and cancer was assessed. Results: Intestinal metaplasia occurred more frequently in the H. pylori-infected, MNU-treated gerbils than in those receiving H. pylori inoculation only (P < 0.01). Carcinomas arose only in H. pylori-infected animals receiving MNU (8 well differentiated, 2 poorly differentiated, and 10 signet ring). Intestinal metaplasia occurred more frequently in association with intestinal-type carcinoma. Conclusions: Intestinal metaplasia and adenocarcinoma arise in stomachs subjected to the same injuries (in this study, H. pylori and MNU). Only two intestinal-type carcinomas were contiguous to intestinal metaplasia; all other tumors developed most commonly at non-metaplastic sites. This suggests that in this animal model H. pylori and MNU induce several phenotypes of gastric cancer, but intestinal metaplasia may be a direct precursor only in a subset of the intestinal-type tumors.
Original language | English (US) |
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Pages (from-to) | 283-290 |
Number of pages | 8 |
Journal | Scandinavian Journal of Gastroenterology |
Volume | 36 |
Issue number | 3 |
DOIs | |
State | Published - Jan 1 2001 |
Keywords
- Animal
- Carcinogenesis
- Gastric cancer
- Helicobacter pylori
- Intestinal metaplasia
- Mongolian gerbil
- N-methyl-N-nitrosourea
- Stomach
ASJC Scopus subject areas
- Gastroenterology