Linked Life Data

7509210

Source:http://linkedlifedata.com/resource/pubmed/id/7509210

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1994-3-29
pubmed:abstractText
Custom-made monoclonal anti-idiotype antibodies (anti-Id MoAbs) have been tested as a treatment modality in 34 non-Hodgkin's lymphoma (NHL) patients. Partial or complete tumor remissions have been induced with this treatment in 68% of these patients. One mechanism by which anti-idiotype antibodies may have induced these tumor responses is via a direct antiproliferative effect on the tumor cells, resulting in apoptosis. Primary NHL cells do not proliferate well enough in vitro to test this hypothesis directly. Therefore, we studied the effect of anti-idiotype antibodies on signal transduction through the surface Ig receptor as measured by the induction of cellular protein tyrosine phosphorylation. To assess whether bcl-2 protein could protect lymphoma cells from death induced by anti-Id MoAb, we also measured the level of bcl-2 protein in the same tumor cells. We found a strong correlation between the ability of an anti-Id MoAb to induce an increase in tyrosine phosphorylation in vitro and its ability to induce a tumor regression in the patient. By contrast, the level of bcl-2 expressed by the tumor cells was not correlated with clinical response to anti-Id MoAb treatment.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
83
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
899-906
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Lymphoma regression induced by monoclonal anti-idiotypic antibodies correlates with their ability to induce Ig signal transduction and is not prevented by tumor expression of high levels of bcl-2 protein.
pubmed:affiliation
Department of Medicine, Stanford University Medical Center, CA 94305-5306.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't