Source:http://linkedlifedata.com/resource/pubmed/id/10595736
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
10
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| pubmed:dateCreated |
2000-1-4
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| pubmed:abstractText |
The status of genetic alterations in ulcerative colitis (UC)-associated neoplasia (UCAN) was investigated focusing on microsatellite instability (MSI) which is seen in a certain fraction of colorectal carcinomas, and adenomatous polyposis coli (APC) gene and K-ras gene, in which mutations occur in the early stage of sporadic colorectal tumorigenesis. Thirty-one UCAN from 15 UC patients who had undergone colorectal resection at our institution were investigated. There were 8 lesions of invasive carcinoma, 15 high-grade dysplasia (HGD) and 8 low-grade dysplasia (LGD). DNA was extracted from each neoplastic lesion and corresponding non-neoplastic tissue by a microdissection method. MSI status at 9 microsatellite loci, loss of heterozygosity (LOH) at the APC locus, and K-ras codon 12 point mutation were examined. As for MSI, 4/31 (13%) UCAN (carcinoma: 1/8 (13%), HGD: 2/15 (13%), LGD: 1/8 (13%)) were MSI-high (3 or more unstable loci) and 12/31 (39%) UCAN (carcinoma: 3/8 (38%), HGD: 6/15 (40%), LGD: 3/8 (38%)) were MSI-low (1 or 2 unstable loci). LOH at the APC locus was not found in 9 UCAN from 6 informative (heterozygous) cases. The K-ras mutation rate of UCAN was 3/31 (9.7%) (carcinoma: 2/8 (25%), HGD: 1/15 (7%) and LGD: 0/8). MSI is relatively common in UCAN and is present at the early stage of tumorigenesis of UCAN, while the involvement of genetic alterations of the APC gene and K-ras gene is small. MSI may be one of the mechanisms of the increased neoplastic risk in UC, and UCAN may develop through a different carcinogenic pathway from sporadic carcinomas.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Oct
|
| pubmed:issn |
0910-5050
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
90
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
1081-7
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| pubmed:dateRevised |
2004-11-17
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| pubmed:meshHeading |
pubmed-meshheading:10595736-Adult,
pubmed-meshheading:10595736-Age of Onset,
pubmed-meshheading:10595736-Aged,
pubmed-meshheading:10595736-Colitis, Ulcerative,
pubmed-meshheading:10595736-Colorectal Neoplasms,
pubmed-meshheading:10595736-Female,
pubmed-meshheading:10595736-Genes, APC,
pubmed-meshheading:10595736-Genes, ras,
pubmed-meshheading:10595736-Genetic Markers,
pubmed-meshheading:10595736-Humans,
pubmed-meshheading:10595736-Loss of Heterozygosity,
pubmed-meshheading:10595736-Male,
pubmed-meshheading:10595736-Microsatellite Repeats,
pubmed-meshheading:10595736-Middle Aged,
pubmed-meshheading:10595736-Neoplasm Invasiveness,
pubmed-meshheading:10595736-Neoplasm Staging,
pubmed-meshheading:10595736-Point Mutation,
pubmed-meshheading:10595736-Retrospective Studies
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| pubmed:year |
1999
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| pubmed:articleTitle |
Genetic alterations in ulcerative colitis-associated neoplasia focusing on APC, K-ras gene and microsatellite instability.
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| pubmed:affiliation |
Department of Surgical Oncology, School of Medicine, The University of Tokyo. umetani-1su@h.u-tokyo.ac.jp
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| pubmed:publicationType |
Journal Article
|