ReviewWorld journal of gastroenterology2006
Helicobacter pylori eradication to prevent gastric cancer: underlying molecular and cellular mechanisms.
Review in World journal of gastroenterology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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
17 citing papers in PubMed, 33 citations in OpenAlex.
- Genetic association ofEcancermedicalscience · 2026Article
- Early detection of gastric cancer after Helicobacter pylori eradication due to endoscopic surveillance.Helicobacter · 2018Article
- Association between TNF-α rs1799964 and RAF1 rs1051208 MicroRNA binding site SNP and gastric cancer susceptibility in an Iranian population.Gastroenterology and hepatology from bed to bench · 2017Article
- Hematologic manifestations of Helicobacter pylori infection.World journal of gastroenterology · 2014Review
- Endoscopic surveillance strategy after endoscopic resection for early gastric cancer.World journal of gastrointestinal pathophysiology · 2014Review
- VEZT, a novel putative tumor suppressor, suppresses the growth and tumorigenicity of gastric cancer.PloS one · 2013Article
- Immunoexpression of cyclooxygenase-2 in primary gastric carcinomas and lymph node metastases.World journal of gastroenterology · 2012Article
- DNA repair enzyme polymorphisms and oxidative stress in a Turkish population with gastric carcinoma.Molecular biology reports · 2011Article
- Combined effect of miR-146a rs2910164 G/C polymorphism and Toll-like receptor 4 +3725 G/C polymorphism on the risk of severe gastric atrophy in Japanese.Digestive diseases and sciences · 2011Article
- New insights into the inactivation of gastric tumor suppressor RUNX3: the role of H. pylori infection.Journal of cellular biochemistry · 2011Review
- No associations of Toll-like receptor 2 (TLR2) -196 to -174del polymorphism with the risk of Helicobacter pylori seropositivity, gastric atrophy, and gastric cancer in Japanese.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2010Article
- Genetic predisposition to Helicobacter pylori-induced gastric precancerous conditions.World journal of gastrointestinal oncology · 2010Article
- Short-term celecoxib intervention is a safe and effective chemopreventive for gastric carcinogenesis based on a Mongolian gerbil model.World journal of gastroenterology · 2009Article
- Epigenetics: connecting environment and genotype to phenotype and disease.Journal of dental research · 2009Review
- Significant association of RUNX3 T/A polymorphism at intron 3 (rs760805) with the risk of gastric atrophy in Helicobacter pylori seropositive Japanese.Journal of gastroenterology · 2009Article
- NAT2 polymorphism in Omani gastric cancer patients-risk predisposition and clinicopathological associations.World journal of gastroenterology · 2007Article
- Leukotriene BOncoimmunologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Numerous cellular and molecular events have been described in development of gastric cancer. In this article, we overviewed roles of Helicobacter pylori (H pylori) infection on some of the important events in gastric carcinogenesis and discussed whether these cellular and molecular events are reversible after cure of the infection. There are several bacterial components affecting gastric epithelial kinetics and promotion of gastric carcinogenesis. The bacterium also increases risks of genetic instability and mutations due to NO and other reactive oxygen species. Epigenetic silencing of tumor suppressor genes such as RUNX3 may alter the frequency of phenotype change of gastric glands to those with intestinal metaplasia. Host factors such as increased expression of growth factors, cytokines and COX-2 have been also reported in non-cancerous tissue in H pylori-positive subjects. It is noteworthy that most of the above phenomena are reversed after the cure of the infection. However, some of them including overexpression of COX-2 continue to exist and may increase risks for carcinogenesis in metaplastic or dysplastic mucosa even after successful H pylori eradication. Thus, H pylori eradication may not completely abolish the risk for gastric carcinogenesis. Efficiency of the cure of the infection in suppressing gastric cancer depends on the timing and the target population, and warrant further investigation.
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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.