ReviewPhysiological reviews2010
Role of innate immunity in Helicobacter pylori-induced gastric malignancy.
Review in Physiological reviews, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 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
124 citing papers in PubMed, 2 syntheses or guidelines pooled it, 229 citations in OpenAlex.
- Toll-Like Receptor 1 Locus Re-examined in a Genome-Wide Association Study Update on Anti-Helicobacter pylori IgG Titers.Gastroenterology · 2022Pooled it
- Association between tumor necrosis factor β 252 A/G polymorphism and risk of gastric cancer: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013Pooled it
- Bacterial contributions to cancer development: mechanisms, dysbiosis, and cross-cancer associations.Infectious agents and cancer · 2026Review
- Protumorigenic Responses of CEACAM6 in Helicobacter pylori-Infected Gastric Cancer Cells.Journal of cellular and molecular medicine · 2026Article
- Review
- SMTdb: A Comprehensive Spatial Meta-Transcriptome Resource in Cancer.Molecular biology and evolution · 2025Article
- Research progress on monocyte/macrophage in the development of gastric cancer.Future oncology (London, England) · 2025Review
- Phytochemical Analysis, Computational Study, and in vitro Assay ofJournal of experimental pharmacology · 2025Article
- Toll-like Receptor 4 Signaling Mediates Gastritis and Gastric Cancer.Current molecular medicine · 2025Review
- Unravelling the role of intratumoral bacteria in digestive system cancers: current insights and future perspectives.Journal of translational medicine · 2024Review
- Current research on the interaction between Helicobacter pylori and macrophages.Molecular biology reports · 2024Review
- The Most Recent Insights into the Roots of Gastric Cancer.Life (Basel, Switzerland) · 2024Review
- BRD4 Empowers Macrophages to Fight Helicobacter pylori.Cellular and molecular gastroenterology and hepatology · 2024Article
- The immunopathogenesis ofFrontiers in microbiology · 2024Review
- Cross-talk betweenFrontiers in cellular and infection microbiology · 2024Article
- BRD4 Regulates Glycolysis-Dependent Nos2 Expression in Macrophages Upon H pylori Infection.Cellular and molecular gastroenterology and hepatology · 2024Article
- Investigating the Molecular Mechanisms Underlying Early Response to Inflammation andInternational journal of molecular sciences · 2023Article
- Reactive Oxygen Species andAntioxidants (Basel, Switzerland) · 2023Review
- Immune response modulation in inflammatory bowel diseases byWorld journal of gastroenterology · 2023Review
- Identification of PTPN20 as an innate immunity-related gene in gastric cancer with Helicobacter pylori infection.Frontiers in immunology · 2023Article
64 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
3 authors at 2 institutions in 1 country.
Funding
Abstract
Helicobacter pylori colonizes the majority of persons worldwide, and the ensuing gastric inflammatory response is the strongest singular risk factor for peptic ulceration and gastric cancer. However, only a fraction of colonized individuals ever develop clinically significant outcomes. Disease risk is combinatorial and can be modified by bacterial factors, host responses, and/or specific interactions between host and microbe. Several H. pylori constituents that are required for colonization or virulence have been identified, and their ability to manipulate the host innate immune response will be the focus of this review. Identification of bacterial and host mediators that augment disease risk has profound ramifications for both biomedical researchers and clinicians as such findings will not only provide mechanistic insights into inflammatory carcinogenesis but may also serve to identify high-risk populations of H. pylori-infected individuals who can then be targeted for therapeutic intervention.
Indexed as
Identifiers
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.