ArticleCancer science2004
Eradication of Helicobacter pylori induces apoptosis and inhibits proliferation of heterotopic proliferative glands in infected Mongolian gerbils.
Article in Cancer science, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Managing dangerous liaisons: lessons fromJournal of bacteriology · 2026Review
- Helicobacter pylori as an oncogenic pathogen, revisited.Expert reviews in molecular medicine · 2017Review
- The Protective Effects of 18β-Glycyrrhetinic Acid on Helicobacter pylori-Infected Gastric Mucosa in Mongolian Gerbils.BioMed research international · 2016Article
- Short-term Intervention to Revert Premalignant Lesions as Strategy to Prevent Gastrointestinal Cancers.Journal of cancer prevention · 2013Review
- Helicobacter pylori infection and gastric carcinogenesis in rodent models.Seminars in immunopathology · 2013Review
- Role of bacteria in oncogenesis.Clinical microbiology reviews · 2010Review
- The detection of Helicobacter pylori cag pathogenicity islands (PAIs) and expression of matrix metalloproteinase-7 (MMP-7) in gastric epithelial dysplasia and intramucosal cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2010Article
- Prevention of Gastric Cancer: When is Treatment of Helicobacter Pylori Warranted?Therapeutic advances in gastroenterology · 2008Article
- Helicobacter pylori eradication prevents progression of gastric cancer in hypergastrinemic INS-GAS mice.Cancer research · 2008Article
- Effect of Helicobacter pylori eradication on gastric carcinogenesis.Laboratory investigation; a journal of technical methods and pathology · 2008Article
- Salt and stress synergize H. pylori-induced gastric lesions, cell proliferation, and p21 expression in Mongolian gerbils.Digestive diseases and sciences · 2007Article
- Effects of eradication of Helicobacter pylori on gastric carcinogenesis in experimental models.Journal of gastroenterology · 2007Review
- Helicobacter pylori infection stimulates intestinalization of endocrine cells in glandular stomach of Mongolian gerbils.Cancer science · 2006Article
- Gastric and intestinal phenotypes and histogenesis of advanced glandular stomach cancers in carcinogen-treated, Helicobacter pylori-infected Mongolian gerbils.Cancer science · 2006Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mongolian gerbils infected with Helicobacter pylori (H. pylori ) develop heterotopic proliferative glands (HPGs) in the glandular stomach submucosa. To investigate the effects of H. pylori eradication on cell turnover in HPGs, three antibiotics, lansoprazole, amoxicillin and clarithromycin, were administered at 50 or 75 weeks after inoculation of H. pylori, and the stomachs were excised for histological examination at 1, 2, 4, 8 or 25 weeks thereafter. The HPGs were classified into gastric type (G-type) and others (GI + I-type), which included both pure intestinal (I-type) and gastric-and-intestinal mixed type (GI-type). Apoptosis and cell proliferation were evaluated by means of TUNEL assay and BrdU labeling, respectively. At 8 weeks post-eradication, apoptotic indices were significantly increased in the eradication group (G-type: 2.5%; GI + I-type: 7.2%) compared to the non-eradication group (G-type: 0.6%; GI + I-type: 2.1%: P < 0.01), while BrdU labeling indices were significantly decreased (G-type: 1.9%; GI + I-type: 6.8% as compared with 4.3% and 13.2%, respectively, P < 0.01 for both). At 25 weeks, the apoptotic indices were similarly higher [G-type: 0.4 (eradication group) vs. 0.2% (non-eradication group); GI + I-type: 5.8 vs. 1.1%, both P < 0.01], and the BrdU labeling indices (G-type: 0.8 vs. 2.2%, P < 0.01; GI + I-type: 5.1 vs. 11%, P < 0.05) continued to be lower in HPGs. Furthermore, there were highly significant reductions in the areas of HPGs at 8 and 25 weeks post-eradication. These findings demonstrated that eradication results in apoptosis and reduction of proliferation of HPGs in H. pylori-infected gerbils, these lesions thus being apparently reversible through regulation of cell kinetics.
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