Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1992-7-31
pubmed:abstractText
In tumor cells expressing platelet-derived growth factor (PDGF) ligand(s) and receptor(s), immunoblot analysis established tyrosine phosphorylation of PDGF receptors (PDGFRs) in the absence of any exogenous ligand, implying chronic receptor activation. Exposure to suramin resulted in diminished receptor autophosphorylation and/or up-regulation of receptor protein. In a subset of such tumor lines, there was a marked reduction in DNA synthesis in response to suramin or PDGF-neutralizing antiserum. These findings demonstrate that autocrine PDGF stimulation contributes to proliferation of some human tumors and that agents which interfere with ligand-receptor interactions at the cell surface can significantly interfere in this process.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:volume
7
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1355-9
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Demonstration of an activated platelet-derived growth factor autocrine pathway and its role in human tumor cell proliferation in vitro.
pubmed:affiliation
Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892.
pubmed:publicationType
Journal Article