ReviewArchives of microbiology2026
A vicious cycle inducer in gastric pathogenesis: implication of Helicobacter pylori.
Review in Archives of microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Simultaneous point-of-care detection and virulence typing of Helicobacter pylori using multiplex recombinase polymerase amplification combined with lateral flow strip.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori is a major human pathogen responsible for chronic gastritis, peptic ulcers, and gastric cancer. Its persistence is facilitated by a complex arsenal of virulence factors, including the CagA oncoprotein, the VacA toxin, adhesins, and the ability to form biofilms. While the roles of individual factors are well-studied, the integrated mechanisms by which they collectively drive carcinogenesis remain a critical knowledge gap. This review integrates evidence showing that CagA delivery and type IV secretion-dependent signals create a transient, infection-driven BRCAness (BRCA1/2 pathway deficiency) state, which is a homologous recombination DNA repair deficiency, promoting error-prone repair and genomic instability. Concurrently, CagA-independent pathways, such as T4SS-mediated ADP-heptose delivery and reactive oxygen species generation, contribute to DNA double-strand breaks. The infection further impairs host defenses by disrupting tumor suppressor pathways such as p53, dysregulating immune signaling of NF-κB and JAK/STAT, which results in immune evasion through arginine depletion and impaired antigen presentation. By elucidating the coordinated interplay among virulence factors, DNA damage response impairment, and immune modulation, this review highlights potential intervention nodes that may help disrupt persistent infection and ultimately reduce the risk of H. pylori-associated gastric cancer.
Indexed as
Identifiers
41524903What Socratic 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 Socratic graph.