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. 2020 May 26;12(6):1364. doi: 10.3390/cancers12061364

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Mechanisms of resistance to mitogen-activated protein kinase (MAPK)-targeted therapies in melanoma. Melanoma cells evade targeted therapies by acquiring additional genetic alterations or through non-genetic mechanisms. LOF: loss of function; MEK: mitogen-activated protein kinase kinase; ERK: extracellular signal-regulated kinase; NF1: neurofibromatosis 1; RTK: receptor tyrosine kinase; MET: hepatocyte growth factor receptor; NGFR: nerve growth factor receptor; PDGFR: platelet derived growth factor receptor; EGFR: epidermal growth factor receptor; IGF1R: insulin-like growth factor 1 receptor; AXL: AXL receptor tyrosine kinase; PTEN: phosphatase and Tensin homolog; PI3K: phosphoinositide 3-kinase; MITF: microphthalmia-associated transcription factor; SOX10: SRY-box transcription Factor 10 (SOX10); YAP1: Yes-associated protein 1; AhR: aryl hydrocarbon receptor.