Abstract
Anaplastic lymphoma kinase (ALK) gene rearrangements are found in approximately 5% of non-small cell lung carcinoma patients and confer sensitivity to ALK inhibitors such as crizotinib. The particular ALK fusion expressed may have an impact on protein stability and sensitivity to crizotinib, and this may underlie the heterogeneity in responses observed in the clinic.
©2012 AACR.
MeSH terms
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Anaplastic Lymphoma Kinase
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Biomarkers, Pharmacological / metabolism
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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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Cell Proliferation
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Crizotinib
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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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Oncogene Proteins, Fusion* / genetics
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Oncogene Proteins, Fusion* / isolation & purification
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Oncogene Proteins, Fusion* / metabolism
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Protein Kinase Inhibitors / administration & dosage
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Protein Stability
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Pyrazoles / administration & dosage
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Pyridines / administration & dosage
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Receptor Protein-Tyrosine Kinases* / genetics
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Receptor Protein-Tyrosine Kinases* / metabolism
Substances
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Biomarkers, Pharmacological
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EML4-ALK fusion protein, human
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Oncogene Proteins, Fusion
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Protein Kinase Inhibitors
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Pyrazoles
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Pyridines
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Crizotinib
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ALK protein, human
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Anaplastic Lymphoma Kinase
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Receptor Protein-Tyrosine Kinases