ArticleCancer research2008
Regulation of gastric carcinogenesis by Helicobacter pylori virulence factors.
Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 170 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
170 citing papers in PubMed, 1 synthesis or guideline pooled it, 274 citations in OpenAlex.
- Infiltration to infection: key virulence players of Helicobacter pylori pathogenicity.Infection · 2024Pooled it
- Iron deficiency accelerates Helicobacter pylori-induced carcinogenesis in rodents and humans.The Journal of clinical investigation · 2013Trial
- Review
- Contributions of conserved and species-specific CagX (VirB9) domains to the assembly and function of theInfection and immunity · 2026Article
- Mitochondrial Stress inAntioxidants (Basel, Switzerland) · 2026Review
- Managing dangerous liaisons: lessons fromJournal of bacteriology · 2026Review
- UnravelingVaccines · 2025Review
- Bacteria and Carcinogenesis and the Management of Cancer: A Narrative Review.Pathogens (Basel, Switzerland) · 2025Review
- Helicobacter pylori CagA elevates FTO to induce gastric cancer progression via a "hit-and-run" paradigm.Cancer communications (London, England) · 2025Article
- Hypoxia and Hypoxia-Reoxygenation Potentiate Helicobacter pylori Infection and Gastric Epithelial Cell Proliferation.Cancer medicine · 2025Article
- Article
- Review
- Article
- Remodeling of the gastric environment inmSystems · 2024Article
- Control ofMicrobiology spectrum · 2023Article
- Characterization of TelE, a T7SS LXG Effector Exhibiting a Conserved C-Terminal Glycine Zipper Motif Required for Toxicity.Microbiology spectrum · 2023Article
- Review
- The Hippo signaling pathway in gastric cancer.Acta biochimica et biophysica Sinica · 2023Review
- CDK1 bridges NF-κB and β-catenin signaling in response to H. pylori infection in gastric tumorigenesis.Cell reports · 2023Article
- Clinical Pathogenesis, Molecular Mechanisms of Gastric Cancer Development.Current topics in microbiology and immunology · 2023Article
110 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Helicobacter pylori is the strongest known risk factor for gastric adenocarcinoma, and strains that possess the cag secretion system, which translocates the bacterial effector CagA into host cells, augment cancer risk. H. pylori strains that express the vacuolating cytotoxin or the outer membrane protein OipA are similarly associated with severe pathologic outcomes. We previously reported that an in vivo adapted H. pylori strain, 7.13, induces gastric adenocarcinoma in rodent models of gastritis. In the current study, we used carcinogenic strain 7.13 as a prototype to define the role of virulence constituents in H. pylori-mediated carcinogenesis. Mongolian gerbils were infected with wild-type strain 7.13 or cagA(-), vacA(-), or oipA(-) mutants for 12 to 52 weeks. All infected gerbils developed gastritis; however, inflammation was significantly attenuated in animals infected with the cagA(-) but not the vacA(-) or oipA(-) strains. Gastric dysplasia and cancer developed in >50% of gerbils infected with either the wild-type or vacA(-) strain but in none of the animals infected with the cagA(-) strain. Inactivation of oipA decreased beta-catenin nuclear localization in vitro and reduced the incidence of cancer in gerbils. OipA expression was detected significantly more frequently among H. pylori strains isolated from human subjects with gastric cancer precursor lesions versus persons with gastritis alone. These results indicate that loss of CagA prevents the development of cancer in this model. Inactivation of oipA attenuates beta-catenin nuclear translocation and also decreases the incidence of carcinoma. In addition to defining factors that mediate H. pylori-induced cancer, these results provide insight into mechanisms that may regulate the development of other malignancies arising within the context of inflammatory states.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.