ReviewCell communication and signaling : CCS2015
Helicobacter pylori virulence factor CagA promotes tumorigenesis of gastric cancer via multiple signaling pathways.
Review in Cell communication and signaling : CCS, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers, 4 of them syntheses that pooled it.
What it found
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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
126 citing papers in PubMed, 4 syntheses or guidelines pooled it, 217 citations in OpenAlex.
- Gastric cancer burden and regional disparities among Helicobacter pylori-positive patients in the Americas: a systematic review and meta-analysis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Pooled it
- Gut microbiota and gastrointestinal tumors: insights from a bibliometric analysis.Frontiers in microbiology · 2025Pooled it
- CagA toxin and risk of Helicobacter pylori-infected gastric phenotype: A meta-analysis of observational studies.PloS one · 2024Pooled it
- Helicobacter pylori cagA status and gastric mucosa-associated lymphoid tissue lymphoma: a systematic review and meta-analysis.Journal of health, population, and nutrition · 2022Pooled it
- Health education based on precede-proceed model in eradication evaluation of Helicobacter pylori infection: a retrospective cohort study.BMC gastroenterology · 2025Trial
- Helicobacter pylori triggers gastric mucosal remodeling toward a fetal-like transcriptional program via stromal IL-1β signaling.Nature communications · 2026Article
- Alkaloids Mediate Multi-Level Modulation of Gastric Carcinogenesis: From Antibacterial and Anti-Inflammatory Actions to Antitumor Effects.International journal of molecular sciences · 2026Review
- Beyond Infection: Mitochondrial Reprogramming and Immunometabolic Adaptation inDiseases (Basel, Switzerland) · 2026Article
- Association of IL-10 promoter and IL-12 gene polymorphisms with the risk of symptomatic Helicobacter pylori infection.BMC gastroenterology · 2026Article
- What Does Bacteria Have to Do with Cancer? The Influence of the Body's Microbiota on Cancer in Cats and Dogs.International journal of molecular sciences · 2026Review
- Computational design of a multi-epitope vaccine against Helicobacter pylori targeting CagA, FliD, urease, and OipA with cholera toxin B subunit (CTB) adjuvant.BMC microbiology · 2026Article
- Bacterial Infections Role in Gynecological Cancers Development: Narrative Review.Cancer reports (Hoboken, N.J.) · 2026Review
- Hydrogen Sulfide InhibitsCells · 2026Article
- A vicious cycle inducer in gastric pathogenesis: implication of Helicobacter pylori.Archives of microbiology · 2026Review
- CagA-dependent expression of anti-inflammatory cytokine IL-13 and TNFRSF member Fn14 inFrontiers in microbiology · 2026Article
- Targeting BRD4 in gastric cancer: promoting apoptosis and suppressing tumor progression.Frontiers in pharmacology · 2026Article
- Metabolic reprogramming as a key regulator in Helicobacter pylori-infected gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2026Review
- Molecular mechanisms of bacteria-mediated cancer immunotherapy: from intratumoral microbiota to engineered therapeutics.Frontiers in immunology · 2026Review
- Patchouli alcohol suppressesFrontiers in pharmacology · 2026Article
- Update on the pathogenesis and clinical management ofWorld journal of gastrointestinal pathophysiology · 2025Review
66 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
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori (H. pylori) infection is strongly associated with the development of gastric diseases but also with several extragastric diseases. The clinical outcomes caused by H. pylori infection are considered to be associated with a complex combination of host susceptibility, environmental factors and bacterial isolates. Infections involving H. pylori strains that possess the virulence factor CagA have a worse clinical outcome than those involving CagA-negative strains. It is remarkable that CagA-positive H. pylori increase the risk for gastric cancer over the risk associated with H. pylori infection alone. CagA behaves as a bacterial oncoprotein playing a key role in H. pylori-induced gastric cancer. Activation of oncogenic signaling pathways and inactivation of tumor suppressor pathways are two crucial events in the development of gastric cancer. CagA shows the ability to affect the expression or function of vital protein in oncogenic or tumor suppressor signaling pathways via several molecular mechanisms, such as direct binding or interaction, phosphorylation of vital signaling proteins and methylation of tumor suppressor genes. As a result, CagA continuously dysregulates of these signaling pathways and promotes tumorigenesis. Recent research has enriched our understanding of how CagA effects on these signaling pathways. This review summarizes the results of the most relevant studies, discusses the complex molecular mechanism involved and attempts to delineate the entire signaling pathway.
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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.