Abstract
Paradoxical activation of the mitogen-activated protein kinase pathway can cause secondary malignancies in patients treated with inhibitors of BRAF(V600) proteins. Characterization of a patient with concurrent BRAF-mutant melanoma and NRAS-mutant leukemia treated intermittently with combined BRAF and MEK inhibition provides new insights into the potential clinical and molecular effects of this therapeutic strategy.
©2014 AACR.
MeSH terms
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Antineoplastic Agents / therapeutic use*
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Antineoplastic Combined Chemotherapy Protocols
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Clinical Trials as Topic
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Enzyme Inhibitors / therapeutic use
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GTP Phosphohydrolases / antagonists & inhibitors*
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Humans
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Leukemia / drug therapy*
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Leukemia / genetics
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Leukemia / pathology
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Melanoma / drug therapy*
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Melanoma / genetics
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Melanoma / pathology
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Melanoma / secondary
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Membrane Proteins / antagonists & inhibitors*
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Mutation
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Proto-Oncogene Proteins B-raf / genetics*
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Proto-Oncogene Proteins B-raf / metabolism
Substances
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Antineoplastic Agents
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Enzyme Inhibitors
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Membrane Proteins
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Proto-Oncogene Proteins B-raf
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GTP Phosphohydrolases
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NRAS protein, human