Adenomatous Polyposis Coli
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
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.
|
23504555 |
2013 |
Adenomatous Polyposis Coli
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
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.
|
21134075 |
2011 |
Adenomatous Polyposis Coli
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
DNA was extracted, modified with sodium bisulfite, and subjected to real-time quantitative, methylation-specific polymerase chain reaction analysis for the following genes: adenomatous polyposis coli (APC); cadherin 1, type 1, E-cadherin (epithelial) (CDH1); estrogen receptor 1 (ESR1); cytokine high in normal 1 (HIN1); hyperplastic polyposis protein 1 (HPP1); O-6 methylguanine-DNA methyltransferase (MGMT); neural epidermal growth factor-like 1 (NELL1); splicing factor 3B, 14-kDa subunit (p14); cyclin-dependent kinase (CDK) inhibitor 2B (inhibits CDK4) (p15); retinoic acid receptor beta (RARβ); somatostatin (SST); tachykinin, precursor 1 (TAC1); and tissue inhibitor of metalloproteinase (TIMP) metallopeptidase inhibitor 3 (TIMP3).
|
20572039 |
2010 |
Adenomatous Polyposis Coli
|
0.100 |
Biomarker
|
disease |
BEFREE |
There was no correlation between APC and E-cadherin methylation patterns and the other clinicopathologic features, nor with patient outcome.
|
19900189 |
2010 |
Adenomatous Polyposis Coli
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
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.
|
18632876 |
2008 |
Adenomatous Polyposis Coli
|
0.100 |
Biomarker
|
disease |
BEFREE |
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.
|
18662704 |
2008 |
Adenomatous Polyposis Coli
|
0.100 |
GeneticVariation
|
disease |
LHGDN |
Genetic changes of CDH1, APC, and CTNNB1 found in human brain tumors.
|
17905526 |
2007 |
Adenomatous Polyposis Coli
|
0.100 |
Biomarker
|
disease |
BEFREE |
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.
|
17905526 |
2007 |
Adenomatous Polyposis Coli
|
0.100 |
Biomarker
|
disease |
LHGDN |
Loss of extracellular E-cadherin in the normal mucosa of duodenum and colon of patients with familial adenomatous polyposis.
|
16949915 |
2006 |
Adenomatous Polyposis Coli
|
0.100 |
Biomarker
|
disease |
BEFREE |
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).
|
16259108 |
2005 |
Adenomatous Polyposis Coli
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
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.
|
15361208 |
2004 |
Adenomatous Polyposis Coli
|
0.100 |
Biomarker
|
disease |
BEFREE |
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).
|
15042681 |
2004 |
Adenomatous Polyposis Coli
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
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.
|
15203750 |
2004 |
Adenomatous Polyposis Coli
|
0.100 |
Biomarker
|
disease |
BEFREE |
This suggests that the normal APC and E-cadherin protein expressions in benign epithelium are progressively and independently lost in the sporadic colorectal cancers.
|
12647217 |
2003 |
Adenomatous Polyposis Coli
|
0.100 |
AlteredExpression
|
disease |
LHGDN |
This suggests that the normal APC and E-cadherin protein expressions in benign epithelium are progressively and independently lost in the sporadic colorectal cancers.
|
12647217 |
2003 |
Adenomatous Polyposis Coli
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
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.
|
14691304 |
2003 |