Abstract
Research over the last decade has determined that the gene rearrangement involving the anaplastic lymphoma kinase (ALK) gene is an oncogenic driver in approximately 5% of patients with non-small cell lung carcinoma (NSCLC). This review describes the discovery of the ALK translocation, development of ALK directed therapy, and acquired resistance to ALK directed therapy with a focus on the clinical data and efficacy of the most recently approved ALK inhibitor, ceritinib.
Keywords:
ALK translocation; NSCLC; ceritinib.
© The Author(s), 2015.
MeSH terms
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Anaplastic Lymphoma Kinase
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Animals
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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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Drug Resistance, Neoplasm
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Gene Rearrangement
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Humans
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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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Protein Kinase Inhibitors / pharmacology
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Protein Kinase Inhibitors / therapeutic use
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Pyrimidines / pharmacology
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Pyrimidines / therapeutic use*
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Receptor Protein-Tyrosine Kinases / antagonists & inhibitors
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Receptor Protein-Tyrosine Kinases / genetics
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Sulfones / pharmacology
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Sulfones / therapeutic use*
Substances
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Antineoplastic Agents
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Protein Kinase Inhibitors
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Pyrimidines
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Sulfones
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ALK protein, human
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Anaplastic Lymphoma Kinase
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Receptor Protein-Tyrosine Kinases
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ceritinib