ReviewCurrent opinion in infectious diseases2016
Molecular mechanisms of gastric cancer initiation and progression by Helicobacter pylori.
Review in Current opinion in infectious diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 29 citations in OpenAlex.
- Helicobacter pylori infection activates the HIF-1α/ALS2/Rab5 signaling axis in gastric cells.Cell communication and signaling : CCS · 2026Article
- A vicious cycle inducer in gastric pathogenesis: implication of Helicobacter pylori.Archives of microbiology · 2026Review
- The Double-Edged Sword of Genomic DNA Methylation: Orchestrating Gastric Carcinogenesis and Shaping Precision Oncology.Oncology research · 2026Review
- Article
- Clinical and Endoscopic-Histological Features of Multifocal and Corpus-Restricted Atrophic Gastritis Patients With Non-Cardia Gastric Cancer or Dysplasia: A Multicenter, Cross-Sectional Study.Clinical and translational gastroenterology · 2025Article
- Review
- Gastric microbiota: an emerging player in gastric cancer.Frontiers in microbiology · 2023Review
- circXRCC5 foster gastric cancer growth and metastasis by the HNRNPC/circXRCC5/miR-655-3p/RREB1/UBA2 positive feedback loop.Cancer gene therapy · 2022Article
- Kinases and therapeutics in pathogen mediated gastric cancer.Molecular biology reports · 2022Review
- Microbiota and cancer: current understanding and mechanistic implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- Article
- Role of Bacteria in the Incidence of Common GIT Cancers: The Dialectical Role of Integrated Bacterial DNA in Human Carcinogenesis.Infection and drug resistance · 2021Review
- Could Periodontal Disease through PeriopathogenJournal of clinical medicine · 2020Review
- Review
- Article
- The dual role of alpha7 nicotinic acetylcholine receptor in inflammation-associated gastrointestinal cancers.Heliyon · 2020Review
- The role of non-American journal of cancer research · 2020Review
- Osteopontin b and c Splice isoforms in Leukemias and Solid Tumors: Angiogenesis Alongside ChemoresistanceAsian Pacific journal of cancer prevention : APJCP · 2018Review
- Increased Abundance of Clostridium and Fusobacterium in Gastric Microbiota of Patients with Gastric Cancer in Taiwan.Scientific reports · 2018Article
- Amino-Terminal Processing ofFrontiers in microbiology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
purpose of reviewInfection with the Gram-negative, microaerophilic pathogen Helicobacter pylori results in gastric cancer in a subset of infected individuals. As such, H. pylori is the only WHO classified bacterial class I carcinogen. Numerous studies have identified mechanisms by which H. pylori alters host cell signaling pathways to cause disease. The purpose of this review is to highlight recent studies that explore mechanisms associated with induction of gastric cancer. RECENT
findingsOver the last year and a half, new mechanisms contributing to the etiology of H. pylori-associated gastric cancer development have been discovered. In addition to utilizing the oncogenic CagA toxin to alter host cell signaling pathways, H. pylori also induces host DNA damage and alters DNA methylation to perturb downstream signaling. Furthermore, H. pylori activates numerous host cell pathways and proteins that result in epithelial-to-mesenchymal transition and induction of cell survival and proliferation. SUMMARY: Mounting evidence suggests that H. pylori promotes gastric carcinogenesis using a multifactorial approach. Intriguingly, many of the targeted pathways and mechanisms show commonality with diverse forms of cancer.
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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.