Abstract
CDK4 is preclinically validated as a therapeutic target in PAX3-FOXO1 fusion gene-positive rhabdomyosarcomas. Pharmacologic targeting showed sensitivity but, contrary to expectation, CDK4 genomic amplification and overexpression associated with 25% of cases that exhibited the lowest sensitivities. This emphasizes the importance of tumor-specific preclinical studies to define and understand drug sensitivity.
©2015 American Association for Cancer Research.
Publication types
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Research Support, Non-U.S. Gov't
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Comment
MeSH terms
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Animals
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Cyclin-Dependent Kinase 4 / antagonists & inhibitors*
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Cyclin-Dependent Kinase 4 / genetics*
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Cyclin-Dependent Kinase 6 / antagonists & inhibitors*
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Drug Resistance, Neoplasm / genetics*
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Female
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Gene Amplification*
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Humans
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Oncogene Proteins, Fusion / genetics*
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Protein Kinase Inhibitors / pharmacology*
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Rhabdomyosarcoma / genetics*
Substances
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Oncogene Proteins, Fusion
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Protein Kinase Inhibitors
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Cyclin-Dependent Kinase 4
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Cyclin-Dependent Kinase 6