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rdf:type |
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lifeskim:mentions |
umls-concept:C0016053,
umls-concept:C0026882,
umls-concept:C0042285,
umls-concept:C0079784,
umls-concept:C0332324,
umls-concept:C0597357,
umls-concept:C0683598,
umls-concept:C0879468,
umls-concept:C0935989,
umls-concept:C1150625,
umls-concept:C1171350,
umls-concept:C1706382
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pubmed:issue |
1
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pubmed:dateCreated |
2006-1-6
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pubmed:abstractText |
The kinase inhibitor imatinib is used in the treatment of chronic myeloid leukaemia, where it targets the intracellular Bcr-Abl tyrosine kinase, and gastrointestinal stromal tumours, where it targets either the KIT or PDGF tyrosine kinase receptors. Here, we report that imatinib is also an effective inhibitor of the closely related FMS receptor for macrophage colony stimulating factor and that mutation of Asp 802 of FMS to Val confers imatinib resistance. Imatinib readily reverted the transformed phenotype of haemopoietic and fibroblast cell lines that express the oncogene v-fms and also inhibited the growth of the Bacl.2F5 macrophage cell line. The cellular IC50 value of imatinib for FMS was similar to those for Bcr-Abl and KIT. Consequently, imatinib may also prove effective for the treatment of diseases whose progression is dependent upon macrophage-colony stimulating factor, this includes certain aspects of cancer and inflammation.
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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/Antineoplastic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Aspartic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Fusion Proteins, bcr-abl,
http://linkedlifedata.com/resource/pubmed/chemical/Macrophage Colony-Stimulating Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Oncogene Protein v-cbl,
http://linkedlifedata.com/resource/pubmed/chemical/Piperazines,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-crk,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-kit,
http://linkedlifedata.com/resource/pubmed/chemical/Pyrimidines,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Macrophage...,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor Protein-Tyrosine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Valine,
http://linkedlifedata.com/resource/pubmed/chemical/imatinib
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0950-9232
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
5
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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 |
147-51
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:16170366-Animals,
pubmed-meshheading:16170366-Antineoplastic Agents,
pubmed-meshheading:16170366-Aspartic Acid,
pubmed-meshheading:16170366-Disease Progression,
pubmed-meshheading:16170366-Dose-Response Relationship, Drug,
pubmed-meshheading:16170366-Down-Regulation,
pubmed-meshheading:16170366-Drug Resistance, Neoplasm,
pubmed-meshheading:16170366-Fusion Proteins, bcr-abl,
pubmed-meshheading:16170366-Humans,
pubmed-meshheading:16170366-Inflammation,
pubmed-meshheading:16170366-Inhibitory Concentration 50,
pubmed-meshheading:16170366-Macrophage Colony-Stimulating Factor,
pubmed-meshheading:16170366-Mice,
pubmed-meshheading:16170366-Mutation,
pubmed-meshheading:16170366-Neoplasms,
pubmed-meshheading:16170366-Oncogene Protein v-cbl,
pubmed-meshheading:16170366-Phosphorylation,
pubmed-meshheading:16170366-Piperazines,
pubmed-meshheading:16170366-Protein Structure, Tertiary,
pubmed-meshheading:16170366-Proto-Oncogene Proteins c-crk,
pubmed-meshheading:16170366-Proto-Oncogene Proteins c-kit,
pubmed-meshheading:16170366-Pyrimidines,
pubmed-meshheading:16170366-Rats,
pubmed-meshheading:16170366-Receptor, Macrophage Colony-Stimulating Factor,
pubmed-meshheading:16170366-Receptor Protein-Tyrosine Kinases,
pubmed-meshheading:16170366-Signal Transduction,
pubmed-meshheading:16170366-Time Factors,
pubmed-meshheading:16170366-Valine
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pubmed:year |
2006
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pubmed:articleTitle |
FMS receptor for M-CSF (CSF-1) is sensitive to the kinase inhibitor imatinib and mutation of Asp-802 to Val confers resistance.
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pubmed:affiliation |
Institute of Reproductive and Developmental Biology, Imperial College London, Hammersmith Campus, London, UK.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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