Abstract
We present the case of a patient with rapidly accelerated fibrosarcoma gene F (BRAF) mutated adenocarcinoma of the lung, responding to BRAF inhibitor dabrafenib after progressing on vemurafenib followed by docetaxel. The present case illustrates the potential benefit of successful rechallenge with a BRAF inhibitor, a well known phenomenon observed in other oncogenic driven molecular subtypes of non-small cell lung cancer (NSCLC) such as epidermal growth factor receptor mutation. Rechallenge with a BRAF inhibitor in BRAF mutated NSCLC should be considered, particularly in the absence of alternative therpateutic options.
Keywords:
Adenocarcinoma; BRAF mutation; Lung; NSCLC; Rechallenge; Resistance.
Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.
MeSH terms
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Adenocarcinoma / diagnosis
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Adenocarcinoma / drug therapy*
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Adenocarcinoma / genetics*
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Antineoplastic Agents / therapeutic use
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Carcinoma, Bronchogenic / diagnosis
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Carcinoma, Bronchogenic / drug therapy*
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Carcinoma, Bronchogenic / genetics*
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DNA Mutational Analysis
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Disease Progression
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Drug Resistance, Neoplasm
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Humans
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Imidazoles / therapeutic use*
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Indoles / therapeutic use
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Lung Neoplasms / diagnosis
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Lung Neoplasms / drug therapy*
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Lung Neoplasms / genetics*
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Male
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Middle Aged
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Mutation*
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Neoplasm Staging
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Oximes / therapeutic use*
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Positron-Emission Tomography
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Proto-Oncogene Proteins B-raf / antagonists & inhibitors
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Proto-Oncogene Proteins B-raf / genetics*
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Retreatment
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Sulfonamides / therapeutic use
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Tomography, X-Ray Computed
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Treatment Outcome
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Vemurafenib
Substances
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Antineoplastic Agents
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Imidazoles
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Indoles
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Oximes
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Sulfonamides
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Vemurafenib
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Proto-Oncogene Proteins B-raf
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dabrafenib