Abstract
In this issue of Blood, Zimmerman and colleagues demonstrate that the tyrosine kinase inhibitor (TKI) crenolanib effectively suppresses growth of leukemic cells harboring both FLT3-ITD and FLT3-TKD mutations, the latter of which are increasingly seen to emerge as resistant mutations after FMS-like tyrosine kinase 3 (FLT3) inhibitor therapy.
MeSH terms
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Animals
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Antineoplastic Agents / therapeutic use*
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Benzimidazoles / therapeutic use*
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Female
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Humans
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Leukemia, Myeloid, Acute / drug therapy*
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Leukemia, Myeloid, Acute / enzymology*
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Male
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Piperidines / therapeutic use*
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Protein Kinase Inhibitors / therapeutic use*
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fms-Like Tyrosine Kinase 3 / antagonists & inhibitors*
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fms-Like Tyrosine Kinase 3 / genetics*
Substances
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Antineoplastic Agents
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Benzimidazoles
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Piperidines
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Protein Kinase Inhibitors
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FLT3 protein, human
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fms-Like Tyrosine Kinase 3
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crenolanib