Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
|
pubmed:dateCreated |
1992-10-19
|
pubmed:abstractText |
To evaluate the potential role of IGF-I and insulin as growth-promoting factors in malignant lymphocyte development, we examined established T-acute lymphoblastic leukemic (ALL) cell lines with increasing stage of differentiation, HSB2, HUT78, CEM, MOLT3, Jurkat, JM-P, JM-886, and four established preB- and B-ALL cell lines REH, SKW6 CESS, BJAB for production of IGF-I and growth in the presence of antibodies, directed against IGF-I or insulin or their receptors. Basal DNA synthesis of the early differentiated T-cell lines HSB2 and HUT78, as well as the B-cell line REH, could be inhibited in a dose-dependent manner by both monoclonal antibodies against IGF-I (ASC41) and antibodies against the IGF-I receptor (alpha-IR3), suggesting that IGF-I acts as an auto- or paracrine growth factor for these cells via the IGF-I receptor. From these cells HUT78 and REH secreted IGF-I into cell culture medium. DNA synthesis of the further differentiated T-cell lines CEM and MOLT3 was inhibited by alpha-IR3 and antibodies directed against the insulin receptor (RPN.538) and against insulin (RPN.1661). These results suggest that insulin via the IGF-I receptor or insulin receptor can function as an autocrine or paracrine growth factor in these T-ALLs. Proliferation of the most differentiated T-ALL Jurkat and JMP was inhibited only by alpha-IR3 and 2C2, an antibody directed against the IGF-II receptor, suggesting that IGF-I or IGF-II acting via the IGF-I receptor or IGF-II receptor may be involved in proliferation of these cell lines. Inhibition of the DNA synthesis by RPN.538 and RPN.1661 indicate a more important role for insulin in growth of leukemias of the B-ALL cell lines SKW6 and CESS.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/DNA, Neoplasm,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin-Like Growth Factor I,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Somatomedin
|
pubmed:status |
MEDLINE
|
pubmed:month |
Aug
|
pubmed:issn |
0145-2126
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
16
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
807-14
|
pubmed:dateRevised |
2011-11-17
|
pubmed:meshHeading |
pubmed-meshheading:1326686-Antibodies, Monoclonal,
pubmed-meshheading:1326686-Cell Division,
pubmed-meshheading:1326686-DNA, Neoplasm,
pubmed-meshheading:1326686-Humans,
pubmed-meshheading:1326686-Insulin,
pubmed-meshheading:1326686-Insulin-Like Growth Factor I,
pubmed-meshheading:1326686-Precursor Cell Lymphoblastic Leukemia-Lymphoma,
pubmed-meshheading:1326686-Receptor, Insulin,
pubmed-meshheading:1326686-Receptors, Cell Surface,
pubmed-meshheading:1326686-Receptors, Somatomedin,
pubmed-meshheading:1326686-Tumor Cells, Cultured
|
pubmed:year |
1992
|
pubmed:articleTitle |
Influence of antibodies against IGF-I, insulin or their receptors on proliferation of human acute lymphoblastic leukemia cell lines.
|
pubmed:affiliation |
Department of Pediatrics, University of Heidelberg, F.R.G.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|