Abstract
Although the majority of patients with EGFR-mutant lung cancer respond well to EGF receptor (EGFR) tyrosine kinase inhibitors (TKI), all patients eventually develop resistance. The mechanism of acquired resistance is still unknown for a considerable subset of cases. This study reveals the NF1 tumor suppressor gene as a new mediator of resistance to EGFR TKIs and provides a mechanistic rationale for developing combination therapies.
©2014 AACR.
MeSH terms
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Antineoplastic Agents / pharmacology
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Antineoplastic Agents / therapeutic use*
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Drug Resistance, Neoplasm*
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ErbB Receptors / antagonists & inhibitors
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ErbB Receptors / genetics
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Humans
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Lung Neoplasms / drug therapy*
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Lung Neoplasms / genetics
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Mutation
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Neurofibromin 1 / genetics*
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Protein Kinase Inhibitors / pharmacology
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Protein Kinase Inhibitors / therapeutic use*
Substances
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Antineoplastic Agents
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Neurofibromin 1
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Protein Kinase Inhibitors
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ErbB Receptors