ReviewRedox report : communications in free radical research2011
Redox biology and gastric carcinogenesis: the role of Helicobacter pylori.
Review in Redox report : communications in free radical research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 63 papers, 4 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
63 citing papers in PubMed, 4 syntheses or guidelines pooled it, 122 citations in OpenAlex.
- Infiltration to infection: key virulence players of Helicobacter pylori pathogenicity.Infection · 2024Pooled it
- Can a diet rich in Brassicaceae help controlFrontiers in medicine · 2024Pooled it
- A meta-analysis of the association between the presence of Helicobacter pylori and periodontal diseases.Medicine · 2019Pooled it
- Helicobacter pylori infection and esophageal cancer risk: an updated meta-analysis.World journal of gastroenterology · 2013Pooled it
- Advances in dermatology using DNA aptamer "Aptamin C" innovation: Oxidative stress prevention and effect maximization of vitamin C through antioxidation.Journal of cosmetic dermatology · 2020Trial
- Increased protein carbonylation and decreased antioxidant status in anemic H. pylori infected patients: effect of treatment.Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology AssociationTrial
- Article
- Redox-regulated cell death in gastric cancer: Molecular insights and therapeutic opportunities.Journal of physiology and biochemistry · 2026Review
- Antioxidant and Cytoprotective Effects of Chilean Macroalgae Against Oxidative Stress-Induced Damage in Gastric Epithelial Cells.Nutrients · 2026Article
- Rethinking Oxidative Stress inLife (Basel, Switzerland) · 2026Review
- Impact of oxidative and antioxidative potential on cancer risk: the Japan Public Health Center-based Prospective Study.British journal of cancer · 2026Article
- From gut to mouth: salivary signatures of carcinogenic microbiota.Frontiers in cellular and infection microbiology · 2026Review
- Helicobacter pylori and gastric cancer: mechanisms and new perspectives.Journal of hematology & oncology · 2025Review
- Alginate Oligosaccharides Protect Gastric Epithelial Cells against Oxidative Stress Damage through Induction of the Nrf2 Pathway.Antioxidants (Basel, Switzerland) · 2024Article
- mRNA Expression and Methylation of theBiomarker insights · 2024Article
- Pivotal role ofFrontiers in medicine · 2024Review
- 300-fold higher neuro- and immunotoxicity from low-redox transformation of carbamazepine.Toxicology reports · 2023Article
- Association between the presence and genotype ofExperimental and therapeutic medicine · 2023Article
- Reactive Oxygen Species andAntioxidants (Basel, Switzerland) · 2023Review
- Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Almost half the world's population is infected by Helicobacter pylori (H. pylori). This bacterium increases the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in human stomach, and this has been reported to impact upon gastric inflammation and carcinogenesis. However, the precise mechanism by which H. pylori induces gastric carcinogenesis is presently unclear. Although the main source of ROS/RNS production is possibly the host neutrophil, H. pylori itself produces O₂•⁻. Furthermore, its cytotoxin induces ROS production by gastric epithelial cells, which might affect intracellular signal transduction, resulting in gastric carcinogenesis. Excessive ROS production in gastric epithelial cells can cause DNA damage and thus might be involved in gastric carcinogenesis. Understanding the molecular mechanism of H. pylori-induced carcinogenesis is important for developing new strategies against gastric cancer.
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.