ArticleProceedings of the National Academy of Sciences of the United States of America2005
Activation of beta-catenin by carcinogenic Helicobacter pylori.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 290 papers.
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
290 citing papers in PubMed, 470 citations in OpenAlex.
- Host andGut microbes · 2026Article
- Review
- Multiple TonB-dependent transport systems inInfection and immunity · 2026Article
- The dual role of gastric microbiota dysbiosis in gastric cancer progression and therapy.International journal of clinical oncology · 2026Review
- The "Hit-and-Run" legacy: epigenetic locking and the survival switch in H. pylori-associated gastric cancer.Cell death discovery · 2026Review
- Rethinking Oxidative Stress inLife (Basel, Switzerland) · 2026Review
- Spatial transcriptomics defines IM-crypt as a premalignant niche with bidirectional divergence in early gastric carcinogenesis.Communications biology · 2026Article
- Tumor-resident bacteria in gastrointestinal cancers: from regulatory mechanisms to clinical implications.Cancer biology & medicine · 2026Review
- Managing dangerous liaisons: lessons fromJournal of bacteriology · 2026Review
- Microbiome modulation of tumorigenesis and immune responses.Journal of biomedical science · 2026Review
- Advancements in understanding tumor-resident bacteria and their application in cancer therapy.Military Medical Research · 2025Review
- Gut microbiota in cancer initiation, development and therapy.Science China. Life sciences · 2025Review
- Article
- Microbiota and gastric cancer: from molecular mechanisms to therapeutic strategies.Frontiers in cellular and infection microbiology · 2025Review
- Microbial oncogenesis within the gastric niche: how the gastric microbiota influencesFrontiers in microbiology · 2025Review
- A landscape review with novel criteria to evaluate microbial drivers for cancer: priorities for innovative research targeting excessive cancer mortality in sub-Saharan Africa.Frontiers in cellular and infection microbiology · 2025Review
- The intersection ofFrontiers in cellular and infection microbiology · 2025Review
- Cultivation and molecular characterization of viable Helicobacter pylori from the root canal of 170 deciduous teeth of children.Cell communication and signaling : CCS · 2024Article
- Prognostic impact and reasons for variability by tumor location in gastric cancer.World journal of gastroenterology · 2024Article
- Staphylococcus aureus lipid factors modulate melanoma cell clustering and invasion.Disease models & mechanisms · 2024Article
230 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
15 authors at 1 institution in 1 country.
Funding
Abstract
Persistent gastritis induced by Helicobacter pylori is the strongest known risk factor for adenocarcinoma of the distal stomach, yet only a fraction of colonized persons ever develop gastric cancer. The H. pylori cytotoxin-associated gene (cag) pathogenicity island encodes a type IV secretion system that delivers the bacterial effector CagA into host cells after bacterial attachment, and cag+ strains augment gastric cancer risk. A host effector that is aberrantly activated in gastric cancer precursor lesions is beta-catenin, and activation of beta-catenin leads to targeted transcriptional up-regulation of genes implicated in carcinogenesis. We report that in vivo adaptation endowed an H. pylori strain with the ability to rapidly and reproducibly induce gastric dysplasia and adenocarcinoma in a rodent model of gastritis. Compared with its parental noncarcinogenic isolate, the oncogenic H. pylori strain selectively activates beta-catenin in model gastric epithelia, which is dependent on translocation of CagA into host epithelial cells. Beta-catenin nuclear accumulation is increased in gastric epithelium harvested from gerbils infected with the H. pylori carcinogenic strain as well as from persons carrying cag+ vs. cag- strains or uninfected persons. These results indicate that H. pylori-induced dysregulation of beta-catenin-dependent pathways may explain in part the augmentation in the risk of gastric cancer conferred by this pathogen.
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.