Abstract
The bcr-abl oncogene, present in 95% of patients with chronic myelogenous leukemia (CML), has been implicated as the cause of this disease. A compound, designed to inhibit the Abl protein tyrosine kinase, was evaluated for its effects on cells containing the Bcr-Abl fusion protein. Cellular proliferation and tumor formation by Bcr-Abl-expressing cells were specifically inhibited by this compound. In colony-forming assays of peripheral blood or bone marrow from patients with CML, there was a 92-98% decrease in the number of bcr-abl colonies formed but no inhibition of normal colony formation. This compound may be useful in the treatment of bcr-abl-positive leukemias.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Benzamides
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Blood Cells / drug effects
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Bone Marrow / drug effects
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Dose-Response Relationship, Drug
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Enzyme Inhibitors / pharmacology*
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Evaluation Studies as Topic
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Fusion Proteins, bcr-abl*
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Humans
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Imatinib Mesylate
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Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy*
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Mice
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Piperazines / pharmacology*
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Protein-Tyrosine Kinases / antagonists & inhibitors*
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Proto-Oncogene Proteins c-abl / antagonists & inhibitors*
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Pyrimidines / pharmacology*
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Stem Cells / drug effects
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Tumor Cells, Cultured
Substances
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Benzamides
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Enzyme Inhibitors
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Piperazines
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Pyrimidines
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Imatinib Mesylate
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Protein-Tyrosine Kinases
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Fusion Proteins, bcr-abl
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Proto-Oncogene Proteins c-abl