|
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 |
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 |
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 |
AlteredExpression
|
group |
BEFREE |
We therefore investigated hMLH1 hypermethylation, hMLH1 expression and MSI in a group of early gastric cancers and gastric adenomas.
|
11313962 |
2001 |
|
Adenoma
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Loss of hMLH-1 expression was seen in 1/10 (10%) hyperplasias, 3/12 (25.0%) adenomas, and 1/7 (14.3%) carcinomas.
|
12641777 |
2003 |
|
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 |
AlteredExpression
|
group |
BEFREE |
Thirty percent of IPMC tumors and 25% of IPMA tumors showed MSI-L. All IPMCs and IPMAs showed normal expression of both hMLH1 and hMSH2.
|
12448010 |
2002 |
|
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 |
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 |
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 |
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 |
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 |
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 |
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 |
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 |
PosttranslationalModification
|
group |
BEFREE |
These findings indicate that the inactivation of hMLH1 gene expression by promoter methylation is an early event and might be the origin of MSI-positive gastric adenomas.
|
11710827 |
2001 |
|
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 |
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 |
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 |
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 |
Biomarker
|
group |
BEFREE |
We have found that methylated MGMT, CDKN2A, and MLH1 occur in 49%, 34%, and 7% of adenomas and in 5%, 10%, and 7% of hyperplastic polyps, respectively, and that they are more common in histologically advanced adenomas.
|
15709190 |
2005 |
|
Adenoma
|
0.100 |
Biomarker
|
group |
BEFREE |
Mixed polyps, particularly those with carcinoma, showed loss of hMLH1 (33%), MGMT (37%), and even hMSH2 (11%) with significantly higher frequency compared to hyperplastic polyps, conventional adenomas, and serrated adenomas.
|
15712188 |
2005 |
|
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 |
Biomarker
|
group |
BEFREE |
The effect of the HNPCC gene is to accelerate the progression of adenoma to carcinoma, but not to initiate adenoma development.
|
7523876 |
1994 |