Abstract
Targeted therapies aimed at inhibiting oncogenic tyrosine kinases are becoming commonplace in the treatment of cancer. The EML4-ALK fusion gene was first identified as a potentially targetable oncogenic driver in non-small cell lung cancer in 2007. A small molecule ALK inhibitor, crizotinib, may now be on the verge of approval by the US Food and Drug Administration for the treatment of ALK-rearranged lung cancer. Here we review the discovery of EML4-ALK, the development of clinical diagnostics for ALK rearrangements, the clinical epidemiology of lung cancers driven by EML4-ALK, and ongoing ALK inhibitor-based clinical trials.
MeSH terms
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Carcinoma, Non-Small-Cell Lung* / diagnosis
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Carcinoma, Non-Small-Cell Lung* / epidemiology
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Carcinoma, Non-Small-Cell Lung* / genetics
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Carcinoma, Non-Small-Cell Lung* / metabolism
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Carcinoma, Non-Small-Cell Lung* / therapy
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Crizotinib
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Genetic Therapy
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Humans
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Lung Neoplasms* / diagnosis
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Lung Neoplasms* / epidemiology
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Lung Neoplasms* / genetics
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Lung Neoplasms* / metabolism
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Lung Neoplasms* / therapy
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Oncogene Proteins, Fusion / genetics*
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Oncogene Proteins, Fusion / metabolism
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Pyrazoles / therapeutic use
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Pyridines / therapeutic use
Substances
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EML4-ALK fusion protein, human
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Oncogene Proteins, Fusion
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Pyrazoles
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Pyridines
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Crizotinib