Source:http://linkedlifedata.com/resource/pubmed/id/11807990
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
|
pubmed:dateCreated |
2002-1-24
|
pubmed:abstractText |
High-frequency microsatellite instability (MSI-H) due to defective DNA mismatch repair occurs in the majority of hereditary nonpolyposis colorectal cancers (HNPCCs) and in a subset of sporadic malignant tumors. Clinicopathologic and genotypic features of MSI-H colorectal tumors in HNPCC patients and those in sporadic cases are very similar but not identical. Correlation between the MSI phenotype and aberrant DNA methylation has been highlighted recently. A strong association between MSI and CpG island methylation has been well characterized in sporadic colorectal cancers with MSI-H but not in those of hereditary origin. To address the issue, we analyzed hereditary and sporadic colorectal cancers for aberrant DNA methylation of target genes using methylation-specific polymerase chain reaction. DNA methylation of the MLH1, CDKN2A, MGMT, THBS1, RARB, APC, and p14ARF genes was found in 0%, 23%, 10%, 3%, 73%, 53%, and 33% of 30 MSI-H cancers in HNPCC patients and in 80%, 55%, 23%, 23%, 58%, 35%, and 50% of 40 sporadic colorectal cancers with MSI-H, respectively. Cases showing methylation at three or more loci of six genes other than MLH1 were defined as CpG island methylator phenotype-positive (CIMP +), and 23% of HNPCC tumors and 53% of sporadic cancers with MSI-H were CIMP+ (P = 0.018). Differences in the extent of CpG island methylation, coupled with the differential involvement of several genes by methylation, in HNPCC tumors and sporadic MSI-H colorectal cancers may be associated with diverging developmental pathways in hereditary and sporadic cancers despite similar MSI-H phenotypes.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:status |
MEDLINE
|
pubmed:month |
Mar
|
pubmed:issn |
1045-2257
|
pubmed:author | |
pubmed:copyrightInfo |
Copyright 2002 Wiley-Liss, Inc.
|
pubmed:issnType |
Print
|
pubmed:volume |
33
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
322-5
|
pubmed:dateRevised |
2006-11-15
|
pubmed:meshHeading |
pubmed-meshheading:11807990-Adenocarcinoma,
pubmed-meshheading:11807990-Colorectal Neoplasms,
pubmed-meshheading:11807990-Colorectal Neoplasms, Hereditary Nonpolyposis,
pubmed-meshheading:11807990-CpG Islands,
pubmed-meshheading:11807990-DNA Methylation,
pubmed-meshheading:11807990-Female,
pubmed-meshheading:11807990-Humans,
pubmed-meshheading:11807990-Microsatellite Repeats,
pubmed-meshheading:11807990-Phenotype
|
pubmed:year |
2002
|
pubmed:articleTitle |
Differential involvement of the hypermethylator phenotype in hereditary and sporadic colorectal cancers with high-frequency microsatellite instability.
|
pubmed:affiliation |
First Department of Internal Medicine, Sapporo Medical University, Sapporo, Japan. h-yama@sapmed.ac.jp
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|