The results suggest that APC hypermethylation is an age-specific marker of gastric carcinogenesis, and the concordance of this event with CDH1 hypermethylation suggests that the Wnt pathway has an important role in gastric carcinogenesis.
It is well known that germ line mutations in the cis-element of tumor suppressor genes such as mismatch repair (MMR) genes, the adenomatous polyposis coli (APC) gene and the E-cadherin (CDH1) gene are involved in Lynch syndrome, familial adenomatous polyposis and hereditary diffuse gastric cancer, respectively.
Sixty cases (49 well-differentiated and 11 poorly differentiated) were investigated for methylation of adenomatous polyposis coli (APC) and E-cadherin promoters, the loss of heterozygosity (LOH) at APC locus and beta-catenin and E-cadherin expression by immunohistochemistry.
The concordance between CDH1 and APC methylation in IDCs and paired circulating DNA underscores the utility of serum DNA as a non-invasive tool for methylation analysis in IDC patients.
This paper focuses on changes in E-cadherin (CDH1), adenomatous polyposis coli (APC), and beta-catenin (CTNNB1) in 50 tumors of the central nervous system.
Twenty-two laryngeal squamous cell carcinomas were analyzed in our study regarding genetic changes of two tumor suppressor genes: Adenomatous polyposis coli (APC) and E-cadherin (CDH1).
Mutation analysis of the mutation cluster region of the APC gene, determination of gene promoter methylation status of the APC-1A and E-cadherin genes, and immunohistochemical analysis of APC, E-cadherin, and beta-catenin were performed using paraffin-embedded tumor tissue.
The methylation frequencies of the genes tested in NSCLC specimens were 52% for E-cadherin (CDH1), 41% for RAS association domain family protein (RASSF1A), 38% for fragile histidine triad (FHIT) and adenomatous polyposis coli (APC), 27% for retinoic acid receptor beta (RARbeta) and H-cadherin (CDH13), 20% for p16INK4A, 0.8% for O6-methylguanine-DNA-methyltransferase (MGMT), and 0% for glutathione S-transferase P1 (GSTP1).
Our results suggest that alterations, both in APC and E-cadherin genes, are involved in the evolution and progression of clear cell renal cell carcinoma.
This suggests that the normal APC and E-cadherin protein expressions in benign epithelium are progressively and independently lost in the sporadic colorectal cancers.
This suggests that the normal APC and E-cadherin protein expressions in benign epithelium are progressively and independently lost in the sporadic colorectal cancers.
Moreover, to assess whether mutations of genes interacting with APC can substitute or act in association with APC alterations, we sequenced both CTNNB1 (beta-catenin) and CDH1 (E-cadherin) genes.No CTNNB1 or CDH1 mutations were found.