ArticleJournal of gastroenterology2014
Enhanced expression of activation-induced cytidine deaminase in human gastric mucosa infected by Helicobacter pylori and its decrease following eradication.
Article in Journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 29 citations in OpenAlex.
- Therapy with omeprazole modulates regulatory T cell/T helper 17 immune response in children with duodenal ulcers.Inflammopharmacology · 2018Trial
- Rethinking gastric carcinogenesis: a multiscale ecological model of risk beyondFrontiers in microbiology · 2026Review
- Article
- Identification and Verification of Potential Biomarkers in Gastric Cancer By Integrated Bioinformatic Analysis.Frontiers in genetics · 2022Article
- Genetic Pathogenesis of Inflammation-Associated Cancers in Digestive Organs.Pathogens (Basel, Switzerland) · 2021Review
- Comparison of the Clinicopathological Characteristics and Genetic Alterations Between Patients with Gastric Cancer with or WithoutThe oncologist · 2019Article
- Helicobacter pylori as an oncogenic pathogen, revisited.Expert reviews in molecular medicine · 2017Review
- Modulation of p53 during bacterial infections.Nature reviews. Microbiology · 2015Review
- AID, p53 and MLH1 expression in early gastric neoplasms and the correlation with the background mucosa.Oncology letters · 2015Article
- Helicobacter pylori virulence factor CagA promotes tumorigenesis of gastric cancer via multiple signaling pathways.Cell communication and signaling : CCS · 2015Review
- Gastric Carcinogenesis and Underlying Molecular Mechanisms: Helicobacter pylori and Novel Targeted Therapy.BioMed research international · 2015Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRecent studies have shown important roles for activation-induced cytidine deaminase (AID), an intrinsic genome mutator, in H. pylori-associated gastric cancer development. Here, we evaluated the relationship between H. pylori-induced gastritis and AID expression from human biopsy specimens.
methodsIn 109 patients with dyspeptic symptoms who had undergone endoscopy and received biopsy of the antrum, angulus, and corpus, H. pylori infection was diagnosed by serologic test, (13)C urea breath test, and histological examination. Histological scores of H. pylori, neutrophils, mononuclear cells, atrophy, and intestinal metaplasia (IM) were assessed using the updated Sydney system (USS). Immunohistochemical AID expression of the biopsy specimens was scored.
resultsSixty of 109 (55.0 %) patients were positive for H. pylori and eradication was successful in 48 patients. AID expression in H. pylori-infected mucosa was significantly higher (p < 0.01) than in non-infected mucosa. AID expression was highest in the antrum and was significantly (p < 0.01) reduced toward the proximal portion of the stomach. For USS, multivariate analysis using linear regression revealed that mononuclear cell infiltration (p < 0.01) and IM (p < 0.05) correlated independently with AID expression. After eradication of H. pylori, AID expression was significantly decreased (p < 0.01), but was still higher than that in H. pylori-negative patients in all sites of the stomach.
conclusionsAID expression is elevated in H. pylori-positive patients and is reduced following H. pylori eradication. Moreover, AID expression is highest in the antrum and correlated with severity of chronic inflammation and IM, suggesting an important role for AID in gastric cancer development through gastritis.
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