ReviewWorld journal of gastroenterology2015
Helicobacter pylori-induced inflammation and epigenetic changes during gastric carcinogenesis.
Review in World journal of gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 2 of them syntheses that pooled it.
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
65 citing papers in PubMed, 2 syntheses or guidelines pooled it, 114 citations in OpenAlex.
- Current research status and hotspots of precancerous lesions of gastric cancer: a bibliometric analysis.Frontiers in oncology · 2025Pooled 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
- Vonoprazan-Based Regimen Is More Useful than PPI-Based One as a First-LineCanadian journal of gastroenterology & hepatology · 2017Trial
- Rethinking Oxidative Stress inLife (Basel, Switzerland) · 2026Review
- 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
- Review
- The quantitative proteomics analysis of multi-stage gastric mucosal lesions associated with Helicobacter pylori infection.PloS one · 2026Article
- Rethinking gastric carcinogenesis: a multiscale ecological model of risk beyondFrontiers in microbiology · 2026Review
- DNA Hypermethylation at the Invasive Front of Oral Squamous Cell Carcinoma Confers Poorly Differentiated Characteristics and Promotes Migration of Cancer Cells.Diagnostics (Basel, Switzerland) · 2025Article
- The Potential Role ofMicroorganisms · 2025Review
- Microbiota-driven epigenetic modifications in gastrointestinal cancer: Implications for pathogenesis and therapeutic strategies.World journal of microbiology & biotechnology · 2025Review
- Update on molecular pathogenesis ofWorld journal of gastrointestinal pathophysiology · 2025Review
- Bridging tissue repair and epithelial carcinogenesis: epigenetic memory and field cancerization.Cell death and differentiation · 2025Review
- Gut microbiome-mediated epigenetic modifications in gastric cancer: a comprehensive multiomics analysis.Frontiers in cellular and infection microbiology · 2025Article
- A Nomogram Combining Platelet to Lymphocyte Ratio (PLR) and Systemic Inflammatory Response Index (SIRI) to Predict Patients withJournal of multidisciplinary healthcare · 2025Article
- Microbiome influence in gastric cancer progression and therapeutic strategies.Frontiers in medicine · 2025Review
- Proteomic Characterization of a Lunasin-Enriched Soybean Extract Potentially Useful in the Treatment ofNutrients · 2024Article
- Mutations in Helicobacter pylori infected patients with chronic gastritis, intestinal type of gastric cancer and familial gastric cancer.Hereditary cancer in clinical practice · 2024Article
- LOX-1 acts as an NNature communications · 2024Article
- IL-17 receptor A functions to help maintain barrier integrity and limit activation of immunopathogenic response toInfection and immunity · 2024Article
5 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
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The sequence of events associated with the development of gastric cancer has been described as "the gastric precancerous cascade". This cascade is a dynamic process that includes lesions, such as atrophic gastritis, intestinal metaplasia and dysplasia. According to this model, Helicobacter pylori (H. pylori) infection targets the normal gastric mucosa causing non-atrophic gastritis, an initiating lesion that can be cured by clearing H. pylori with antibiotics or that may then linger in the case of chronic infection and progress to atrophic gastritis. The presence of virulence factors in the infecting H. pylori drives the carcinogenesis process. Independent epidemiological and animal studies have confirmed the sequential progression of these precancerous lesions. Particularly long-term follow-up studies estimated a risk of 0.1% for atrophic gastritis/intestinal metaplasia and 6% in case of dysplasia for the long-term development of gastric cancer. With this in mind, a better understanding of the genetic and epigenetic changes associated with progression of the cascade is critical in determining the risk of gastric cancer associated with H. pylori infection. In this review, we will summarize some of the most relevant mechanisms and focus predominantly but not exclusively on the discussion of gene promoter methylation and miRNAs in this context.
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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.