ArticleWorld journal of gastroenterology2005
Helicobacter pylori infection in relation to E-cadherin gene promoter polymorphism and hypermethylation in sporadic gastric carcinomas.
Article in World journal of gastroenterology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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.
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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.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- The clinicopathological significance of CDH1 in gastric cancer: a meta-analysis and systematic review.Drug design, development and therapy · 2015Pooled it
- Role of E-cadherin in epithelial barrier dysfunction: implications for bacterial infection, inflammation, and disease pathogenesis.Frontiers in cellular and infection microbiology · 2025Review
- Association of CDH1 -160 C → A and -347 G→ GA polymorphisms and expression of E-cadherin and gastric cancer: A case-control study.Turkish journal of surgery · 2021Article
- Inhibition of DNA Methylation at theACS omega · 2016Article
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- Epithelial-mesenchymal transition mediated tumourigenesis in the gastrointestinal tract.World journal of gastroenterology · 2008Review
- Promoter hypermethylation of CDH1, FHIT, MTAP and PLAGL1 in gastric adenocarcinoma in individuals from Northern Brazil.World journal of gastroenterology · 2007Article
- Association of e-cadherin gene CDH1 polymorphism -160 C/A with susceptibility to develop vitiligo.Anais brasileiros de dermatologiaArticle
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo study Helicobacter pylori (H. pylori) infection in relation to E-cadherin (E-cad) promoter polymorphism and hypermethylation in GCs.
methodsSpecimens were taken from representative cancerous lesions and adjacent non-cancerous epithelia of 67 resected GCs. H. pylori was detected by real-time PCR of the cagA gene from non-neoplastic epithelium. E-cad promoter polymorphism and hypermethylation were determined by restriction fragment length polymorphism analysis and methylation-specific PCR, respectively. Expression of E-cad protein was determined by immunohistochemistry.
resultsH. pylori was found in 57% of patients with GC. H. pylori infection was more frequently found in tumors with the -160C/C genotype than those with the -160C/A and -160A/A genotypes (74% vs 47%, P = 0.02). H. pylori infection was associated with E-cad methylation in non-neoplastic epithelium; however, no significant difference in H. pylori was observed between methylated and unmethylated cancerous lesions.
conclusionPatients with the -160C/C genotype might require H. pylori infection to promote the inactivation of CDH1, suggesting that H. pylori infection might affect GC in an initial stage because polymorphism is germ line. Mechanism of hypermethylation of CDH1 promoter in GC is complex, and H. pylori infection might affect it in an initial stage.
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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.