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rdf:type |
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lifeskim:mentions |
umls-concept:C0007634,
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0023418,
umls-concept:C0044602,
umls-concept:C0085862,
umls-concept:C0086418,
umls-concept:C0162638,
umls-concept:C1150587,
umls-concept:C1299583,
umls-concept:C1367731,
umls-concept:C1512310,
umls-concept:C1549571,
umls-concept:C1608386,
umls-concept:C1704259,
umls-concept:C1705632,
umls-concept:C1705987
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pubmed:issue |
9
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pubmed:dateCreated |
2001-8-7
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pubmed:abstractText |
Increasing resistance to chemotherapeutic regimes remains a serious problem in the treatment of acute myeloid leukaemia. We have shown that phosphatidylinositol (PI) 3-kinase inhibition significantly sensitises the AML derived cell line, HL60 to chemotherapeutic drug- and Fas-induced apoptosis. PI3-kinase inhibition significantly potentiates cytotoxic drug-induced c-jun N-terminal kinase (JNK) activation, reported to be a requirement for apoptosis. However, JNK inhibition does not enhance cell viability following treatment with drug and inhibitor. Furthermore, PI3-kinase inhibition significantly increases sensitivity to apoptosis mediated by an exogenous receptor agonist, again by a JNK independent mechanism. These results suggest that PI3-kinase inhibitors could be of significant therapeutic importance, lowering the threshold for apoptosis induced by both chemotherapy and cell-mediated immune response.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD95,
http://linkedlifedata.com/resource/pubmed/chemical/Antineoplastic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/FASLG protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Fas Ligand Protein,
http://linkedlifedata.com/resource/pubmed/chemical/JNK Mitogen-Activated Protein...,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphatidylinositol 3-Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-akt,
http://linkedlifedata.com/resource/pubmed/chemical/Tretinoin,
http://linkedlifedata.com/resource/pubmed/chemical/anti-Fas monoclonal antibody
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0145-2126
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
25
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
801-11
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:11489474-Antibodies, Monoclonal,
pubmed-meshheading:11489474-Antigens, CD95,
pubmed-meshheading:11489474-Antineoplastic Agents,
pubmed-meshheading:11489474-Apoptosis,
pubmed-meshheading:11489474-Enzyme Activation,
pubmed-meshheading:11489474-Fas Ligand Protein,
pubmed-meshheading:11489474-HL-60 Cells,
pubmed-meshheading:11489474-Humans,
pubmed-meshheading:11489474-JNK Mitogen-Activated Protein Kinases,
pubmed-meshheading:11489474-Leukemia,
pubmed-meshheading:11489474-Membrane Glycoproteins,
pubmed-meshheading:11489474-Mitogen-Activated Protein Kinases,
pubmed-meshheading:11489474-Phosphatidylinositol 3-Kinases,
pubmed-meshheading:11489474-Phosphorylation,
pubmed-meshheading:11489474-Protein-Serine-Threonine Kinases,
pubmed-meshheading:11489474-Proto-Oncogene Proteins,
pubmed-meshheading:11489474-Proto-Oncogene Proteins c-akt,
pubmed-meshheading:11489474-Transcription, Genetic,
pubmed-meshheading:11489474-Tretinoin
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pubmed:year |
2001
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pubmed:articleTitle |
Inhibition of PI3-kinase sensitises HL60 human leukaemia cells to both chemotherapeutic drug- and Fas-induced apoptosis by a JNK independent pathway.
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pubmed:affiliation |
Tumour Biology Laboratory, Department of Biochemistry, University College Cork, Prospect Row, Cork, Ireland.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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