Linked Life Data

10500801

Source:http://linkedlifedata.com/resource/pubmed/id/10500801

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1999-11-4
pubmed:abstractText
It has been suggested that one means by which chemotherapeutic agents exert their effect on leukaemic cells, is via autocrine induction of fas-ligand which then binds to fas (CD95), activates the caspase pathway and results ultimately in apoptotic death. In order to test this hypothesis, we have treated leukaemic cell lines with various chemotherapeutic agents (idarubicin, etoposide, fludarabine and 2-CdA) with and without pre-treatment with fas (ZB4) and fas-ligand (NOK-1) blocking monoclonal antibodies. Cell cycle analysis and quantitation of apoptosis were performed by flow cytometry following propidium iodide staining. HL-60 cells were found to be sensitive to the induction of apoptosis with all drugs tested but were highly resistant to treatment with a fas-ligating antibody (CH11). Apoptosis was neither inhibited in parental CEM cells nor their mdr-expressing drug resistant counterpart, CEM/VLB100 by pre-treatment with either ZB4 or NOK1. In addition, CEM/VLB100 were slightly more sensitive to treatment with CH11 (100 ng/ml) than parental CEM cells (% age apoptosis = 30.35 and 23.675, p = 0.024) and at least as sensitive to recombinant fas-ligand (50 ng/ml) (% age apoptosis = 26.6 and 20.2, p = NS). We conclude that it is unlikely that fas/fas-ligand interactions play a significant role in the induction of apoptosis by these chemotherapeutic agents in the leukaemic cell lines tested.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0065-2598
pubmed:author
pubmed:issnType
Print
pubmed:volume
457
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
259-66
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Inhibition of FAS/FAS-ligand does not block chemotherapy-induced apoptosis in drug sensitive and resistant cells.
pubmed:affiliation
Department of Haematology, St. Bartholomew's and Royal London School of Medicine, United Kingdom. d.s.richardson@mds.qmw.ac.uk
pubmed:publicationType
Journal Article