|
Adenomatous Polyposis Coli
|
0.080 |
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
|
0.080 |
Biomarker
|
disease |
BEFREE |
Methylation in the promoter region is 62.4% (73/117) for APC and 60.7% (71/117) for MGMT in our CRC patients.
|
19309276 |
2009 |
|
Adenomatous Polyposis Coli
|
0.080 |
PosttranslationalModification
|
disease |
BEFREE |
APC and MGMT promoter methylation data were consistent and reproducible throughout the dilutions and all three replicates in the methylated DNA dilution matrix and between two experiments in clinical samples.
|
19179456 |
2009 |
|
Adenomatous Polyposis Coli
|
0.080 |
Biomarker
|
disease |
BEFREE |
The frequency of hypermethylation was 12.5% (4/32) for MINT1, 40.0% (16/40) for MINT2, 25.0% (10/40) for MINT31, 25.7% (9/35) for p16, 7.7% (3/39) for hMLH1, 26.5% (9/34) for MGMT, and 35.9% (14/39) for APC.
|
17620311 |
2008 |
|
Adenomatous Polyposis Coli
|
0.080 |
GeneticVariation
|
disease |
BEFREE |
There was no relationship of hypermethylation of any gene, including MGMT, with G-to-A or C-to-T transitions in KRAS or P53, although APC hypermethylation was associated with P53 mutation (P < 0.0002).
|
18451217 |
2008 |
|
Adenomatous Polyposis Coli
|
0.080 |
GeneticVariation
|
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
|
0.080 |
AlteredExpression
|
disease |
BEFREE |
Our results show that loss of expression of MGMT occurs more frequently in cancer than in adenoma in both sporadic and FAP patients, and that loss of expression of MGMT is associated with hypermethylation of the promoter area of MGMT gene.
|
12720298 |
2003 |
|
Adenomatous Polyposis Coli
|
0.080 |
GeneticVariation
|
disease |
BEFREE |
Of the primary tumors, 73 of 90 (81%) displayed promoter hypermethylation in at least one of the genes studied: 17% (15 of 90) at p16 (CDKN2A); 16% (14 of 90) at O(6)-methylguanine-DNA-methyltransferase; 8% (7 of 90) at GSTP1; 72% (65 of 90) at APC; and 17% (15 of 90) at DAPK.
|
12684406 |
2003 |
|
Adenomatous Polyposis Coli
|
0.080 |
AlteredExpression
|
disease |
LHGDN |
Our results show that loss of expression of MGMT occurs more frequently in cancer than in adenoma in both sporadic and FAP patients, and that loss of expression of MGMT is associated with hypermethylation of the promoter area of MGMT gene.
|
12720298 |
2003 |