Abstract
Third-generation mutant-specific EGFR tyrosine kinase inhibitors are showing robust clinical activity, particularly in lung cancers harboring the EGFR(T790M) mutation, yet acquired resistance to these agents emerges. Additional mutations in EGFR can confer resistance that, depending on their genomic context, could determine new drug sensitivities of the cancer cells.
©2015 American Association for Cancer Research.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Comment
MeSH terms
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Acrylamides / pharmacology*
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Alleles*
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Animals
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Antineoplastic Agents / pharmacology*
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Drug Resistance, Neoplasm / genetics*
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ErbB Receptors / antagonists & inhibitors*
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ErbB Receptors / genetics*
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Humans
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Mutation*
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Protein Kinase Inhibitors / pharmacology*
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Pyrimidines / pharmacology*
Substances
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Acrylamides
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Antineoplastic Agents
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Protein Kinase Inhibitors
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Pyrimidines
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ErbB Receptors