Adenoma
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The loss of expression of both MLH1 and PMS2 proteins was present in 6.3% of adenomas, 9.1% of adenomas with high-grade dysplasia and 9.4% of colon adenocarcinomas.
|
29976631 |
2018 |
Adenoma
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Patients with an MMR-deficient tumor or adenoma without MLH1 promoter hypermethylation were referred for genetic analysis.
|
30063919 |
2018 |
Adenoma
|
0.100 |
PosttranslationalModification
|
group |
BEFREE |
MLH1 promoter methylation exhibited a poor sensitivity value (< 0.5) in patients with GC compared with adjacent tissues, gastric adenomas, chronic gastritis, normal gastric mucosa, and normal healthy blood samples.
|
29334683 |
2018 |
Adenoma
|
0.100 |
PosttranslationalModification
|
group |
BEFREE |
MLH1-93 G/a polymorphism is associated with MLH1 promoter methylation and protein loss in dysplastic sessile serrated adenomas with BRAF<sup>V600E</sup> mutation.
|
29304767 |
2018 |
Adenoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
More polyps (mostly adenomas) were detected in MLH1 carriers.
|
29025352 |
2018 |
Adenoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Serrated polyps (hyperplastic polyps, sessile or traditional serrated adenomas), which can arise in a sporadic or polyposis setting, predispose to colorectal cancer (CRC), especially those with microsatellite instability (MSI) due to MLH1 promoter methylation (MLH1<sup>me+</sup>).
|
27329244 |
2017 |
Adenoma
|
0.100 |
Biomarker
|
group |
BEFREE |
When a precursor polyp was identified, MLH1-hypermethylated BRAF wild-type colorectal carcinomas arose from precursor polyps resembling conventional tubular/tubulovillous adenomas in contrast to MLH1-deficient BRAF-mutated colorectal carcinomas, which arose from precursor sessile serrated adenomas (P<0.001).
|
27438990 |
2016 |
Adenoma
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Advanced traditional serrated adenomas retained MLH1 expression in 97%, showed strong p53 staining in 55%, and nuclear β-catenin staining in 40%.
|
25216220 |
2015 |
Adenoma
|
0.100 |
Biomarker
|
group |
BEFREE |
To clarify differences in WNT signaling activation in association with MLH1 methylation or BRAF/KRAS mutations between serrated and conventional routes, we performed β-catenin immunostaining, methylation-specific PCR for MLH1 and WNT signaling associated genes such as AXIN2, APC, and MCC and secreted frizzled-related proteins (SFRPs), and direct sequencing of BRAF/KRAS in 27 SSA/Ps, 14 SSA/Ps with high-grade dysplasia and 9 SSA/Ps with submucosal carcinoma, as well as 19 conventional adenomas, 26 adenomas with high-grade dysplasia and 25 adenomas with submucosal carcinoma.
|
24925057 |
2015 |
Adenoma
|
0.100 |
PosttranslationalModification
|
group |
BEFREE |
We conclude that hypermethylation of MLH1, when occurs in an adenoma cell with BRAF oncogenic mutational activation, drives the pathway for MSI cancer by providing the cells with a mutator phenotype.
|
24964857 |
2014 |
Adenoma
|
0.100 |
Biomarker
|
group |
BEFREE |
The APC/β-catenin pathway was not altered, while MLH1 immunostaining was negative in RCTs and positive in adenomas and normal mucosa.
|
23425390 |
2013 |
Adenoma
|
0.100 |
PosttranslationalModification
|
group |
BEFREE |
Short-term folate supplementation in physiological doses has no effect on ESR1 and MLH1 methylation in colonic mucosa of individuals with adenoma.
|
23328702 |
2012 |
Adenoma
|
0.100 |
Biomarker
|
group |
BEFREE |
Of these patients, the MSI test and MLH1 immunohistochemistry were performed in the available tissue samples from patients with advanced adenomas.
|
22361441 |
2012 |
Adenoma
|
0.100 |
Biomarker
|
group |
BEFREE |
These data suggest that CpG island methylation in hMSH2 and MGMT, but not hMLH1, is closely related to carcinogenesis in colorectal carcinomas presenting with a conventional adenoma-carcinoma sequence.
|
21706233 |
2011 |
Adenoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
KRAS codon 12/13 and 59/61 and BRAF V600E mutations, MSI, and MGMT and hMLH1 methylation and expression in 42 serrated adenocarcinomas and 17 serrated adenomas were compared with those in 59 non-serrated colorectal carcinomas (CRCs) and nine adenomas.
|
21457162 |
2011 |
Adenoma
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Six (33%) of 18 EPCs showed loss of Mlh1 expression, but rarely in adenomas and CIAs (p=0.008).
|
18097574 |
2008 |
Adenoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Polyps coded as hyperplastic polyps (HP) from subjects with Lynch syndrome and FCF enrolled in the HNPCC-register at the Hvidovre University Hospital as well as adenomas from this population were retrieved and reviewed for features of SSP.
|
17929199 |
2008 |
Adenoma
|
0.100 |
PosttranslationalModification
|
group |
BEFREE |
There was no significant difference in methylation of HIC1, MINT1, MINT31, and p16. hMLH1 methylation was absent in all tubulovillous/villous adenomas and seen in only 2 (7%) tubular adenomas.
|
17950780 |
2008 |
Adenoma
|
0.100 |
PosttranslationalModification
|
group |
BEFREE |
Methylation of ASC/TMS1 was more common in right-sided tumors (p = 0.02), concordant with hMLH1 methylation (p = 0.03) and is a late stage event, occurring in 0 of 18 tubular adenomas, 0 of 12 villous adenomas, 2 of 44 (5%) Stage 1 cancers, 8 of 31 (26%) Stage 2 cancers, 8 of 21 (38%) Stage 3 cancers and 2 of 19 (11%) Stage 4 cancers.
|
17986858 |
2007 |
Adenoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
To cast light on the contribution of methylation to genesis of ulcerative colitis (UC)-associated tumors, promoter methylation and expression of O6-methylguanine DNA methyltransferase (MGMT), hMLH1, p16INK4, and E-cadherin were examined in 14 low-grade dysplasias (LGDs), 15 high-grade dysplasias (HGDs), and 14 adenocarcinomas associated with UC and, for comparison, in 30 sporadic adenomas with LGD, 30 adenomas with HGD, and 60 adenocarcinomas, using methylation-specific polymerase chain reaction and immunohistochemical analysis.
|
17276933 |
2007 |
Adenoma
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Methylations of MGMT, CDKN2A (p16) and MLH1 were detected in 28, 33 and 9% of the 101 flat-type adenomas, respectively.
|
17143260 |
2007 |
Adenoma
|
0.100 |
PosttranslationalModification
|
group |
BEFREE |
MLH1 methylation in the Lynch syndrome adenomas suggests gene methylation might have a role in the initiation of these neoplasms.
|
17278092 |
2007 |
Adenoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
However, risk associated with the hMLH1-93A variant differed by smoking: smoking-associated risks were stronger among those with variant -93AA or -93AG genotypes, showing a twofold greater risk of adenoma with >25 pack-years of smoking compared with nonsmokers, and a corresponding eightfold greater risk of hyperplastic polyps (genotype smoking: p-interaction=0.02 for hyperplastic polyps and p-interaction=0.08 for adenomas).
|
16771955 |
2006 |
Adenoma
|
0.100 |
PosttranslationalModification
|
group |
BEFREE |
An hMLH1 methylation defect was seen in only one adenoma (1.3%), from a patient who had a synchronous cancer showing the same defect.
|
16902913 |
2006 |
Adenoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Utilizing real-time PCR (MethyLight), we quantified DNA methylation in five CIMP-specific gene promoters [CACNA1G (calcium channel, voltage-dependent, T type alpha-1G subunit), CDKN2A (p16/INK4A), CRABP1 (cellular retinoic acid binding protein-1), MLH1 and NEUROG1 (neurogenin 1)] and MGMT in six synchronous carcinoma pairs (12 carcinomas) and eight synchronous carcinoma and adenoma pairs (16 tumors).
|
16699497 |
2006 |