Abstract
The EGFR pathway has emerged as a key target in non-small-cell lung cancer. EGF receptor (EGFR) inhibition in non-small-cell lung cancer is achieved via small molecular tyrosine kinase inhibitors, such as erlotinib or gefitinib, or monoclonal antibodies such as cetuximab. A growing body of evidence is identifying potential molecular predictors of response and toxicity. This includes tumor-related molecular markers, such as EGFR mutation and copy number, as well as germline markers such as polymorphisms in EGFR or EGFR pathway-related genes. This review focuses on the current state of knowledge of predictors of response and toxicity to EGFR inhibitors in lung cancer.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Antibodies, Monoclonal / adverse effects
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Antibodies, Monoclonal / pharmacology
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Antibodies, Monoclonal / therapeutic use*
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Antineoplastic Agents / adverse effects
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Antineoplastic Agents / pharmacology
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Antineoplastic Agents / therapeutic use*
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Biomarkers, Tumor / analysis
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Biomarkers, Tumor / genetics
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Carcinoma, Non-Small-Cell Lung / drug therapy*
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Carcinoma, Non-Small-Cell Lung / metabolism
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Carcinoma, Non-Small-Cell Lung / pathology
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Clinical Trials as Topic
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Disease-Free Survival
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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 / metabolism
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Lung Neoplasms / pathology
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Polymorphism, Genetic
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Protein-Tyrosine Kinases / antagonists & inhibitors
Substances
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Antibodies, Monoclonal
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Antineoplastic Agents
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Biomarkers, Tumor
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EGFR protein, human
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ErbB Receptors
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Protein-Tyrosine Kinases