Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1985-1-24
pubmed:abstractText
The humoral hypercalcemia of malignancy (HHM) is a syndrome caused by tumor cells releasing unknown circulating factors which stimulate osteoclastic bone resorption. In the D6 variant of the rat Leydig cell tumor model of HHM, we found that tumor extracts and tumor cell conditioned medium contained a macromolecular bone resorbing factor which coeluted on column chromatography with transforming growth factor activity (TGF). This observation led to the hypothesis that the tumor-derived bone resorbing factor was a TGF which interacts with the epidermal growth factor (EGF) receptor. To test this hypothesis, we examined the effects of two classes of antisera to the EGF receptor on bone resorption stimulated by conditioned medium from Leydig D6 tumor cells using organ cultures of fetal rat long bones. The antiserum which blocks the binding of EGF to its receptor inhibited bone resorption stimulated by tumor conditioned medium and by EGF. The second antiserum to the EGF receptor which does not block EGF binding or biological activity had no effect on bone resorption stimulated by either tumor conditioned medium or EGF. Neither antiserum had any effect on bone resorption stimulated by parathyroid hormone (PTH). These results indicate that the tumor-derived bone resorbing factor is dependent upon the availability of EGF receptors for its activity and are consistent with it being a TGF.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
116
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
469-71
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1985
pubmed:articleTitle
EGF receptor antiserum inhibits bone resorbing activity produced by a rat Leydig cell tumor associated with the humoral hypercalcemia of malignancy.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't