Abstract
The fusion gene EML4-ALK (echinoderm microtubule-associated protein-like 4 gene and the anaplastic lymphoma kinase gene) was recently identified as a novel genetic alteration in non-small cell lung cancer (NSCLC). EML4-ALK translocations correlate with specific clinical and pathological features, in particular lack of EGFR and K-ras mutations, and may be associated with resistance to EGFR tyrosine-kinase inhibitors (TKIs). Here, we report a case of a patient with a concomitant EGFR mutation and ALK translocation resistant to erlotinib. Considering this report, ALK status should be investigated in unexplained cases of EGFR-TKI-resistance of EGFR mutated NSCLCs.
Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.
MeSH terms
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Anaplastic Lymphoma Kinase
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Antineoplastic Agents / therapeutic use
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Carcinoma, Non-Small-Cell Lung / genetics*
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Carcinoma, Non-Small-Cell Lung / pathology
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Cell Cycle Proteins / genetics*
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Drug Resistance, Neoplasm / genetics
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ErbB Receptors / genetics*
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Erlotinib Hydrochloride
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Genes, ras / genetics
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Humans
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In Situ Hybridization, Fluorescence
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Lung Neoplasms / genetics*
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Lung Neoplasms / pathology
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Male
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Microtubule-Associated Proteins / genetics*
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Middle Aged
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Mutation / genetics*
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Oncogene Proteins, Fusion / genetics
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Quinazolines / antagonists & inhibitors
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Quinazolines / therapeutic use
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Receptor Protein-Tyrosine Kinases / genetics*
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Serine Endopeptidases / genetics*
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Translocation, Genetic
Substances
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Antineoplastic Agents
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Cell Cycle Proteins
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Microtubule-Associated Proteins
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Oncogene Proteins, Fusion
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Quinazolines
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Erlotinib Hydrochloride
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ALK protein, human
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Anaplastic Lymphoma Kinase
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ErbB Receptors
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Receptor Protein-Tyrosine Kinases
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EML4 protein, human
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Serine Endopeptidases