ArticleWorld journal of gastroenterology2006
Mechanisms inactivating the gene for E-cadherin in sporadic gastric carcinomas.
Article 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 14 papers.
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Who cites it
14 citing papers in PubMed, 50 citations in OpenAlex.
- Article
- Novel Variants and Copy Number Variation in CDH1 Gene in Iranian Patients with Sporadic Diffuse Gastric Cancer.Journal of gastrointestinal cancer · 2019Article
- CDH1 somatic alterations in Mexican patients with diffuse and mixed sporadic gastric cancer.BMC cancer · 2019Article
- Diffuse Gastric Cancer: A Summary of Analogous Contributing Factors for Its Molecular Pathogenicity.International journal of molecular sciences · 2018Review
- Proposed Molecular and miRNA Classification of Gastric Cancer.International journal of molecular sciences · 2018Review
- Molecular classifications of gastric cancers: Novel insights and possible future applications.World journal of gastrointestinal oncology · 2017Review
- Silencing of CtBP1 suppresses the migration in human glioma cells.Journal of molecular histology · 2016Article
- Lauren classification and individualized chemotherapy in gastric cancer.Oncology letters · 2016Article
- Deregulation of ARID1A, CDH1, cMET and PIK3CA and target-related microRNA expression in gastric cancer.Oncotarget · 2015Article
- Clinical management of advanced gastric cancer: the role of new molecular drugs.World journal of gastroenterology · 2014Review
- Molecular targeted therapies in advanced gastric cancer: does tumor histology matter?Therapeutic advances in gastroenterology · 2013Article
- Genomic and epigenetic profiles of gastric cancer: potential diagnostic and therapeutic applications.Surgery today · 2011Review
- Relationship between cell adhesion molecules expression and the biological behavior of gastric carcinoma.World journal of gastroenterology · 2008Article
- Enhancer of zeste homolog 2 downregulates E-cadherin by mediating histone H3 methylation in gastric cancer cells.Cancer science · 2008Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo study the role of CDH1/E-cadherin (E-cad) gene alteration profiles including mutation, loss of heterozygosity (LOH), promoter polymorphism and hypermethylation in mechanisms of CDH1 inactivation in gastric carcinoma (GC).
methodsSpecimens were collected surgically from 70 patients with GC. Allelotyping PCR and detection of LOH, denaturing high pressure liquid chromatography and DNA sequencing, restriction fragment length polymorphism analysis, methylation specific PCR, and immunohistochemical staining were used.
resultsPromoter polymorphism was not a major mechanism of E-cad inactivation. Only one truncating mutation was found in a diffuse type tumor (3%). Both LOH and promoter hypermethylation were major mechanisms of E-cad inactivation, but interestingly, there was a negative association between the fraction of allelic loss (LOH) in tumors and hypermethylation of CDH1. Therefore LOH and hypermethylation were two different tumorigenic pathways involved in GC.
conclusionGiven the findings that somatic mutation was extremely low and the relationship between LOH and hypermethylation was inverse, any two combinations of these three factors cannot fulfill the classical two-hit hypothesis of CDH1 inactivation. Thus, other mechanisms operating at the transcriptional level or at the post-translational level might be required to induce E-cadherin inactivation.
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