ArticleCurrent topics in microbiology and immunology2023
Impact of the Helicobacter pylori Oncoprotein CagA in Gastric Carcinogenesis.
Article in Current topics in microbiology and immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 13 citations in OpenAlex.
- Host andGut microbes · 2026Article
- Review
- Berberine and Berberine-Derived Compounds as Promising Weapons AgainstPharmaceuticals (Basel, Switzerland) · 2026Review
- CagA promotes gastric cancer stemness and metastasis via DNMT1-mediated epigenetic silencing of BEX1.Cancer gene therapy · 2026Article
- Contributions of conserved and species-specific CagX (VirB9) domains to the assembly and function of theInfection and immunity · 2026Article
- Cryptic redundancy between PAR1b and PAR1a, two members of the PAR1 kinase family, in the survival of PAR1b-knockout mice.Scientific reports · 2026Article
- Mechanisms, functions and therapeutic targeting of protein tyrosine phosphatases.Nature reviews. Molecular cell biology · 2026Review
- Update on the pathogenesis and clinical management ofWorld journal of gastrointestinal pathophysiology · 2025Review
- Extracts from Plectranthus asirensis and Premna resinosa inhibit Helicobacter pylori-induced epithelial cell damage, DNA double-strand breaks and inflammation.Gut pathogens · 2025Article
- Molecular characterization of fourGut microbes · 2025Article
- Helicobacter pylori, microbiota and gastric cancer - principles of microorganism-driven carcinogenesis.Nature reviews. Gastroenterology & hepatology · 2025Review
- Fusobacterium nucleatum confirmed in gastric biopsies of patients without Helicobacter pylori.BMC research notes · 2025Article
- The Influence of Gastric Microbiota and Probiotics inBiomedicines · 2024Review
- Cultivation and molecular characterization of viable Helicobacter pylori from the root canal of 170 deciduous teeth of children.Cell communication and signaling : CCS · 2024Article
- Efficacy and Tolerability of Olaparib Plus Paclitaxel in Patients with Gastric Cancer Associated with Hereditary Breast and Ovarian Cancer.Current oncology (Toronto, Ont.) · 2024Article
- Two remarkable serine/leucine polymorphisms in Helicobacter pylori: functional importance for serine protease HtrA and adhesin BabA.Cell communication and signaling : CCS · 2024Review
- GRB7-mediated enhancement of cell malignant characteristics induced byFrontiers in microbiology · 2024Article
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1 author at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori CagA is the first and only bacterial oncoprotein etiologically associated with human cancer. Upon delivery into gastric epithelial cells via bacterial type IV secretion, CagA acts as a pathogenic/pro-oncogenic scaffold that interacts with and functionally perturbs multiple host proteins such as pro-oncogenic SHP2 phosphatase and polarity-regulating kinase PAR1b/MARK2. Although H. pylori infection is established during early childhood, gastric cancer generally develops in elderly individuals, indicating that oncogenic CagA activity is effectively counteracted at a younger age. Moreover, the eradication of cagA-positive H. pylori cannot cure established gastric cancer, indicating that H. pylori CagA-triggered gastric carcinogenesis proceeds via a hit-and-run mechanism. In addition to its direct oncogenic action, CagA induces BRCAness, a cellular status characterized by replication fork destabilization and loss of error-free homologous recombination-mediated DNA double-strand breaks (DSBs) by inhibiting cytoplasmic-to-nuclear localization of the BRCA1 tumor suppressor. This causes genomic instability that leads to the accumulation of excess mutations in the host cell genome, which may underlie hit-and-run gastric carcinogenesis. The close connection between CagA and BRCAness was corroborated by a recent large-scale case-control study that revealed that the risk of gastric cancer in individuals carrying pathogenic variants of genes that induce BRCAness (such as BRCA1 and BRCA2) dramatically increases upon infection with cagA-positive H. pylori. Accordingly, CagA-mediated BRCAness plays a crucial role in the development of gastric cancer in conjunction with the direct oncogenic action of CagA.
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