Abstract
Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) deliver high response rates with relatively modest toxicity in patients with advanced EGFR-mutated non-small cell lung cancer. Despite this, nearly all tumors eventually develop resistance to first-line therapy. At present, the only standard treatment option for patients with acquired resistance is cytotoxic chemotherapy. In this article, we review the latest research into methods of targeting acquired resistance to EGFR TKI therapy, including third-generation EGFR TKIs that target the T790M resistance mutation and other novel agents in development.
MeSH terms
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Afatinib
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Antineoplastic Agents / pharmacology
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Antineoplastic Agents / therapeutic use*
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Carcinoma, Non-Small-Cell Lung / drug therapy*
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Carcinoma, Non-Small-Cell Lung / genetics
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Carcinoma, Non-Small-Cell Lung / pathology
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Cetuximab / pharmacology
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Cetuximab / 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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Erlotinib Hydrochloride / pharmacology
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Erlotinib Hydrochloride / therapeutic use
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Gefitinib
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Humans
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Lung / drug effects*
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Lung / metabolism
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Lung / pathology
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Lung Neoplasms / drug therapy*
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Lung Neoplasms / genetics
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Lung Neoplasms / pathology
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Point Mutation*
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Protein Kinase Inhibitors / pharmacology
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Protein Kinase Inhibitors / therapeutic use*
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Quinazolines / pharmacology
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Quinazolines / therapeutic use
Substances
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Antineoplastic Agents
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Protein Kinase Inhibitors
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Quinazolines
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Afatinib
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Erlotinib Hydrochloride
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EGFR protein, human
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ErbB Receptors
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Cetuximab
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Gefitinib