Abstract
Clinical tools to accurately describe, evaluate, and predict an individual's response to cancer therapy are a field-wide priority; in many advanced cancers, only 10-20% of individuals will have a clinical benefit from therapy, yet we treat the entire population. Furthermore, many therapies are initially effective, but lose effectiveness over time. Here we describe methods to derive in vitro models of resistance to EGFR tyrosine kinase inhibitors. We additionally describe approaches to characterize possible mechanisms of resistance by genomic and transcriptomic approaches.
MeSH terms
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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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Cell Line, Tumor
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Drug Resistance, Neoplasm / drug effects
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Drug Resistance, Neoplasm / genetics
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Epithelial-Mesenchymal Transition / genetics
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ErbB Receptors / antagonists & inhibitors
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ErbB Receptors / genetics*
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Gefitinib
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Gene Expression Profiling
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Genetic Markers / 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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Oligonucleotide Array Sequence Analysis*
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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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Sequence Analysis, DNA
Substances
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Antineoplastic Agents
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Genetic Markers
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Protein Kinase Inhibitors
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Quinazolines
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ErbB Receptors
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Gefitinib