Source:http://linkedlifedata.com/resource/pubmed/id/17160433
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
|
pubmed:dateCreated |
2007-7-6
|
pubmed:abstractText |
Aggressive fibromatosis is a mesenchymal neoplasm associated with mutations resulting in beta-catenin mediated transcriptional activation. Plasminogen activator inhibitor-1 (PAI-1) is expressed at a high level in aggressive fibromatosis, and using transgenic mice, we found that PAI-1 plays an important role in aggressive fibromatosis tumor formation. Familial adenomatous polyposis is associated with Adenomatous Polyposis Coli gene mutations resulting in beta-catenin mediated transcriptional activation, yet only some patients develop aggressive fibromatosis. Since PAI-1 expression is influenced by a promoter 4G/5G polymorphism, we investigated the incidence of this polymorphism in familial adenomatous polyposis patients who did and who did not develop aggressive fibromatosis, as well as sporadic aggressive fibromatosis patients. There was a trend towards association of the 4G allele (associated with high PAI-1 expression) with the development of aggressive fibromatosis in familial adenomatous polyposis patients (50% vs. 19%, P = 0.1). In familial adenomatous polyposis patients who did not develop aggressive fibromatosis, there was a significantly lower proportion of patients with a 4G allele compared to the healthy control (19% vs. 51%, P = 0.0286). The lower incidence of 4G polymorphism in the PAI-1 promoter may be preventive against the development of aggressive fibromatosis. This data provides additional evidence supporting an important role for PAI-1 in the pathogenesis of aggressive fibromatosis.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:issn |
1389-9600
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
6
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
89-95
|
pubmed:dateRevised |
2008-11-21
|
pubmed:meshHeading |
pubmed-meshheading:17160433-Adenomatous Polyposis Coli,
pubmed-meshheading:17160433-Adult,
pubmed-meshheading:17160433-Causality,
pubmed-meshheading:17160433-Comorbidity,
pubmed-meshheading:17160433-Fibromatosis, Aggressive,
pubmed-meshheading:17160433-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:17160433-Genetic Predisposition to Disease,
pubmed-meshheading:17160433-Humans,
pubmed-meshheading:17160433-Incidence,
pubmed-meshheading:17160433-Plasminogen Activator Inhibitor 1,
pubmed-meshheading:17160433-Polymorphism, Genetic,
pubmed-meshheading:17160433-Promoter Regions, Genetic,
pubmed-meshheading:17160433-Severity of Illness Index,
pubmed-meshheading:17160433-Transcriptional Activation
|
pubmed:year |
2007
|
pubmed:articleTitle |
An association between the 4G polymorphism in the PAI-1 promoter and the development of aggressive fibromatosis (desmoid tumor) in familial adenomatous polyposis patients.
|
pubmed:affiliation |
Program in Developmental Biology, The Hospital for Sick Children, University of Toronto, Ontario, Canada.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|