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cells, pubmed, melanoma, cell, figure, scholar, google, jun, resistance, supplementary, braf, cas, state, resistant, expression, upregulation, signaling, cancer, central, persistent, mechanism, alterations, mesenchymal, inhibitor, treatment, table, gene, analysis, vemurafenib, data, nature, parental, line, usa, kinase, genes, inhibition, patients, early, invasive, adaptive, rtkresistance, signature, lines, switch, shortterm, inhibitors, response, phenotype, pkc,

Topics {✒️}

nature portfolio privacy policy global phospho-tyr/thr/ser profiles author information authors neural-crest cell marker open software development mutant b-raf-regulated inhibitor advertising org/rnai/public/resources/protocols rank–rank-hypergeometric overlap method dharmacon/thermo scientific drug-resistant bcr-abl mutants stem cell research melanoma research alliance thermo fisher scientific open-label 0/ reprints growth-factor-driven resistance platelet-derived growth factor oncogenic b-raf kinase ets-1/rhoc signaling regulates transcription factor c-jun caltech-ucla joint center rank–rank hypergeometric overlap rank-rank hypergeometric overlap braf-mutated metastatic melanoma exon-level microarray analysis ras-family member rras2 short-term persisting cell mutant nras-driven resistance oxidant-induced hepatocyte death combine isoform-specific activity systems-wide resistance programs nras-based resistance mechanism cancer research mutant braf melanomas—dependence growth-arrested cell population rtk-resistance mechanism resembles permutation-based kolmogorov–smirnoff raf/mek inhibition independent growth-arrested persistent state mass-spectrometry data set plx4032/4720-induced cell death nature 2002 nature 2010 nature 2012 nature 2014 nature 2011 nature 2000 nature 2013

Questions {❓}

• Melanoma stem cells—are there devils in the detail?

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         datePublished:2016-09-06T00:00:00Z
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      headline:JUN dependency in distinct early and late BRAF inhibition adaptation states of melanoma
      description:A prominent mechanism of acquired resistance to BRAF inhibitors in BRAFV600-mutant melanoma is associated with the upregulation of receptor tyrosine kinases. Evidences suggested that this resistance mechanism is part of a more complex cellular adaptation process. Using an integrative strategy, we found this mechanism to invoke extensive transcriptomic, (phospho-) proteomic and phenotypic alterations that accompany a cellular transition to a de-differentiated, mesenchymal and invasive state. Even short-term BRAF-inhibitor exposure leads to an early adaptive, differentiation state change—characterized by a slow-cycling, persistent state. The early persistent state is distinct from the late proliferative, resistant state. However, both differentiation states share common signaling alterations including JUN upregulation. Motivated by the similarities, we found that co-targeting of BRAF and JUN is synergistic in killing fully resistant cells; and when used up-front, co-targeting substantially impairs the formation of the persistent subpopulation. We confirmed that JUN upregulation is a common response to BRAF inhibitor treatment in clinically treated patient tumors. Our findings demonstrate that events shared between early- and late-adaptation states provide candidate up-front co-treatment targets.
      datePublished:2016-09-06T00:00:00Z
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         Cancer therapeutic resistance
         Melanoma
         Proteomic analysis
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         Stem Cells
         Cell Culture
         Cell Cycle Analysis
         Cell Physiology
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