ReviewGastrointestinal tumors2014
An Update on Helicobacter pylori as the Cause of Gastric Cancer.
Review in Gastrointestinal tumors, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis 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
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Efficacy and Safety of Polaprezinc-Based Therapy versus the Standard Triple Therapy forNutrients · 2022Pooled it
- Article
- Rhein Exhibits Anti-Inflammatory Effects in Chronic Atrophic Gastritis via Nrf2 and MAPK Signaling.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2023Article
- The Anti-Helicobacter pylori effects of Limosilactobacillus reuteri strain 2892 isolated from Camel milk in C57BL/6 mice.World journal of microbiology & biotechnology · 2023Article
- Increased Risk to Develop Hypertension and Carotid Plaques in Patients with Long-LastingJournal of clinical medicine · 2022Article
- Cancer Incidence Characteristic Evolution Based on the National Cancer Registry in Taiwan.Journal of oncology · 2020Article
- CagA orchestrates eEF1A1 and PKCδ to induce interleukin-6 expression inGut pathogens · 2020Article
- Article
- Suicide journey of H. pylori through gastric carcinogenesis: the role of non-H. pylori microbiome and potential consequences for clinical practice.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2019Review
- The power of small changes: Comprehensive analyses of microbial dysbiosis in breast cancer.Biochimica et biophysica acta. Reviews on cancer · 2019Review
- Observational
- Article
- Serum Antibodies against Helicobacter pylori Neutrophil Activating Protein in Carriers of IL-4 C-590T Genetic Polymorphism Amplify the Risk of Gastritis and Gastric Cancer.Iranian biomedical journal · 2017Article
- Glutathione peroxidase 7 suppresses cancer cell growth and is hypermethylated in gastric cancer.Oncotarget · 2017Article
- Helicobacter pylori as an oncogenic pathogen, revisited.Expert reviews in molecular medicine · 2017Review
- Suppressed Helicobacter pylori-associated gastric tumorigenesis in Fat-1 transgenic mice producing endogenous ω-3 polyunsaturated fatty acids.Oncotarget · 2016Article
- Influences of diet and the gut microbiome on epigenetic modulation in cancer and other diseases.Clinical epigenetics · 2015Review
- Clinicopathological Features and Treatment Outcome of Patients with Gastric Cancer in Lagos: Is the Outlook Getting Better?Journal of the West African College of SurgeonsArticle
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 2 countries.
Funding
Abstract
backgroundGastric cancer is the second most common cause of cancer deaths worldwide. The vast majority of gastric cancers are inflammation-related cancers caused by infection with Helicobacter pylori. H. pylori-induced oxidative stress damages DNA, resulting in genetic instability. In addition, H. pylori itself can cause DNA damage and epigenetic changes that trigger genetic instability and neoplastic transformation. SUMMARY: H. pylori strain-specific components act in combination with host factors and environmental and dietary factors to greatly enhance the inflammatory response and thus the cancer risk. Variations in several key factors, such as the cag pathogenicity island and the VacA protein, can trigger a greater inflammatory response in host cells. Genetic polymorphisms in the host such as in the IL-1β gene, and chromosomes 9p21.3 and 10q23 also play a contributing role. Finally, diet is a major external factor that modulates the risk of gastric cancer. KEY MESSAGE: The majority of gastric cancers are inflammation-related cancers caused by infection with H. pylori. Eradication of H. pylori is important for the prevention and treatment of gastric cancer. PRACTICAL IMPLICATIONS: H. pylori eradication results in healing of gastritis and prevention of further H. pylori-induced genetic damage. Eradication of H. pylori prior to development of atrophic gastritis can prevent the development of gastric cancer. Japan has undertaken a nationwide program to identify and eliminate H. pylori, along with surveillance for those who underwent H. pylori eradication too late to eliminate cancer risk. Population-wide eradication of H. pylori will result in gastric cancer becoming a vanishingly rare disease.
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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.