Linked Life Data

9811473

Source:http://linkedlifedata.com/resource/pubmed/id/9811473

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
18
pubmed:dateCreated
1998-11-16
pubmed:abstractText
Microsatellite instability (MSI) has been detected in endometrial carcinomas occurring in women affected by hereditary nonpolyposis colorectal carcinoma (HNPCC) as well as in 20% of presumably sporadic endometrial tumors. While the MSI+ phenotype observed in endometrial tumors from HNPCC patients is attributed to germ line mutations in mismatch repair (MMR) genes, somatic mutations of known MMR genes are infrequent in MSI+ sporadic endometrial carcinomas. Recently, cytosine methylation of the MLH1 promoter region has been identified in a subset of MSI+ colon primary carcinomas and cell lines. We studied the MLH1 and MSH2 promoter methylation status in 29 presumably sporadic uterine endometrioid carcinomas (UECs), which had previously been characterized for the MSI phenotype and a subset for DNA MMR gene mutational status. We found that 13 (45%) of 29 cases of EC were hypermethylated in the 5' CpG island of MLH1. Hypermethylation of MSH2 was not observed. MLH1 was hypermethylated in 12 (92%) of 13 MSI+ tumors, while only 1 (6%) of 16 MSI- tumors (Fischer's exact test P<O.0001). Other tumor types we tested did not demonstrate MLH1 promoter hypermethylation. Our data suggest that hypermethylation of MLH1, but not of MSH2, is associated with the MSI phenotype in sporadic endometrial carcinomas.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:day
5
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2413-7
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
MLH1 promoter hypermethylation is associated with the microsatellite instability phenotype in sporadic endometrial carcinomas.
pubmed:affiliation
Tumor Biology, The Johns Hopkins Oncology Center, Baltimore, Maryland 21231, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't