Linked Life Data

11518409

Source:http://linkedlifedata.com/resource/pubmed/id/11518409

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2001-8-23
pubmed:abstractText
Osteochondromas are chondro-osseous protuberances that occur in metaphyses of long bones. The cartilaginous cap is assumed to be responsible for the growth of the lesions during childhood and adolescence, but mitotic figures are rarely seen in the cap. Therefore, another cell population, probably mesenchymal cells, is responsible for proliferation and growth. Residual mesenchymal cells capable of rapid proliferation are difficult to detect due to lack of specific histologic features. Two specific markers for mesenchymal cells, FGF receptor 3 (FGFR3) and collagen type IIa, have been described. Osteochondroma mesenchymal cells are found in the soft tissues overlying the cartilage cap. The surrounding areas of typical cartilage are negative for both mesenchymal cell associated antigens. The soft tissues overlying the cartilage do not have cartilaginous features. The undifferentiated cells overlying the exostosis yield in culture a rapidly proliferating homogenous population of fibroblast-like cells. Expression at the mRNA level of FGF9, FGFR3, and collagen type IIa is found in these cells, but not in skin fibroblasts from afflicted or healthy individuals. Exogenous administration of TGFbeta1 to cultures of hereditary multiple exostosis eliminates FGF9 expression. These results indicate fibrous regions contain the mesenchymal cells responsible for osteochondroma growth.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0147-7447
pubmed:author
pubmed:issnType
Print
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
783-7
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Role of FGF9 and FGF receptor 3 in osteochondroma formation.
pubmed:affiliation
Department of Clinical Biochemistry, Sackler School of Medicine, Tel-Aviv University, Ramat-Aviv, Israel.
pubmed:publicationType
Journal Article