Abstract
Slow-cycling BRAF melanoma cells are notoriously resistant to standard chemotherapy or targeted therapy but the underlying mechanism remains elusive. Now a new study unlocks this mystery and offers novel insights into developing more effective therapeutic interventions.
MeSH terms
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Antineoplastic Agents / therapeutic use
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Drug Resistance, Neoplasm*
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ErbB Receptors / antagonists & inhibitors
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ErbB Receptors / genetics
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ErbB Receptors / metabolism
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Humans
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Indoles / therapeutic use
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Melanoma / drug therapy
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Melanoma / metabolism*
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Melanoma / pathology
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Microphthalmia-Associated Transcription Factor / metabolism
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Mutation
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Phenotype
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Protein Kinase Inhibitors / therapeutic use
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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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Proto-Oncogene Proteins B-raf / metabolism
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RNA Interference
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RNA, Small Interfering / metabolism
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SOXE Transcription Factors / metabolism*
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Sulfonamides / therapeutic use
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Vemurafenib
Substances
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Antineoplastic Agents
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Indoles
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Microphthalmia-Associated Transcription Factor
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Protein Kinase Inhibitors
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RNA, Small Interfering
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SOX10 protein, human
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SOXE Transcription Factors
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Sulfonamides
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Vemurafenib
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EGFR protein, human
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ErbB Receptors
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BRAF protein, human
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Proto-Oncogene Proteins B-raf