ReviewCurrent microbiology2022
Helicobacter Pylori and Gastric Cancer Progression.
Review in Current microbiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 28 citations in OpenAlex.
- Advances inOncology letters · 2026Review
- Feco-prevalence and risk factors of Helicobacter pylori infection among adults with dyspepsia in Mogadishu, Somalia: a cross-sectional study.Gut pathogens · 2026Article
- New advances of nanozymes for the diagnosis and treatment of digestive system diseases (Review).International journal of molecular medicine · 2025Review
- The role of TLRs (microbe recognition receptor) in gastric cancer: An update.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Article
- Interaction Between Hypoxia-Inducible Factor 1-alpha Gene Polymorphism and Helicobacter pylori Infection on Gastric Cancer in a Chinese Tibetan Population.Biochemical genetics · 2025Article
- Comprehensive multiomics analysis of the signatures of gastric mucosal bacteria and plasma metabolites across different stomach microhabitats in the development of gastric cancer.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- Organosulfur Compounds in Garlic for Gastric Cancer Treatment: Anticancer Effects, Overcoming Drug Resistance, and Mechanisms.Recent patents on anti-cancer drug discovery · 2025Review
- MOMASTAntioxidants (Basel, Switzerland) · 2024Article
- Prognostic Value and Therapeutic Significance of CCL Chemokines in Gastric Cancer.Current medicinal chemistry · 2024Article
- Ubiquitin-specific Protease 35 Promotes Gastric Cancer Metastasis by Increasing the Stability of Snail1.International journal of biological sciences · 2024Article
- Review
- The role of microbiota in esophageal squamous cell carcinoma: A review of the literature.Thoracic cancer · 2023Review
- Association of PTGER4 and PRKAA1 genetic polymorphisms with gastric cancer.BMC medical genomics · 2023Article
- Short-chain fatty acids in cancer pathogenesis.Cancer metastasis reviews · 2023Review
- High-Salt Diet ExacerbatesJournal of personalized medicine · 2023Review
- Innate Immune Program in Formation of Tumor-Initiating Cells from Cells-of-Origin of Breast, Prostate, and Ovarian Cancers.Cancers · 2023Review
- An oxidative stress biomarkers predict prognosis in gastric cancer patients receiving immune checkpoint inhibitor.Frontiers in oncology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastric cancer (GC) remains the fifth most common malignant tumor and the third leading cause of cancer death, despite the decline in incidence and mortality worldwide over the past five decades. Currently, the roles of Helicobacter pylori (H. pylori) in the development of GC have been established. The effects of H. pylori are mediated through interactions of H. pylori pathogen-associated molecular patterns (PAMPs) with pattern-recognition receptors (PRRs) located on immune and epithelial cells. It is known that this interaction leads to the generation of reactive oxygen species (ROS), activation of the mechanisms of angiogenesis, epithelial-mesenchymal transformation (EMT), and immunological tolerance. Not all this excludes the possibility that H. pylori may have an effect not only on the induction, but also on the mechanisms of GC progression. In this review, we will consider the main structural elements of the innate immune system and the mechanisms of their interaction with H. pylori; the possible role of H. pylori in GC progression; relationship of H. pylori with clinical and pathological characteristics and prognosis of GC, as well as data on the effect of eradication therapy on long-term results of GC patient treatment.
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.