Abstract
Imatinib mesylate has been reported to produce positive results in atypical chronic myeloproliferative disorders (CMD) with chromosomal translocations that disrupt the platelet-derived growth factor receptor beta gene (PDGFRB). We used imatinib to treat a 49-year old man with atypical CMD in accelerated phase and the H4 (D10S170)-PDGFRB fusion gene. After 3 months of treatment, we observed grade 4 hematologic toxicity and a lack of response.
MeSH terms
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Benzamides
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Biomarkers
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Chromosomes, Human, Pair 10 / genetics
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Chromosomes, Human, Pair 10 / ultrastructure
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Chromosomes, Human, Pair 5 / genetics
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Chromosomes, Human, Pair 5 / ultrastructure
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Disease Progression
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Drug Resistance
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Enzyme Inhibitors / adverse effects
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Enzyme Inhibitors / pharmacology
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Enzyme Inhibitors / therapeutic use*
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Gene Rearrangement
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Humans
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Hydroxyurea / therapeutic use
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Imatinib Mesylate
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Leukocytosis / drug therapy
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Leukocytosis / etiology
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Male
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Middle Aged
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Mutant Proteins / genetics*
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Oncogene Proteins, Fusion
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Piperazines / adverse effects
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Piperazines / pharmacology
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Piperazines / therapeutic use*
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Primary Myelofibrosis / complications
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Primary Myelofibrosis / drug therapy*
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Primary Myelofibrosis / genetics
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Pyrimidines / adverse effects
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Pyrimidines / pharmacology
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Pyrimidines / therapeutic use*
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Splenectomy
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Splenomegaly / etiology
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Splenomegaly / surgery
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Thrombocytopenia / chemically induced
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Thrombocytopenia / etiology
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Translocation, Genetic
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Treatment Failure
Substances
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Benzamides
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Biomarkers
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Enzyme Inhibitors
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H4-PDGFRB fusion protein, human
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Mutant Proteins
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Oncogene Proteins, Fusion
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Piperazines
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Pyrimidines
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Imatinib Mesylate
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Hydroxyurea