The Combination of Vemurafenib and Procaspase-3 Activation Is Synergistic in Mutant BRAF Melanomas

The development of vemurafenib resistance limits the long-term efficacy of this drug for treatment of metastatic melanomas with the (V600E)BRAF mutation. Inhibition of downstream MAPK signaling with vemurafenib induces apoptotic cell death mediated by caspase-3, suggesting that addition of a procasp...

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Veröffentlicht in:	Molecular cancer therapeutics 2016-08, Vol.15 (8), p.1859-1869
Hauptverfasser:	Peh, Jessie, Fan, Timothy M, Wycislo, Kathryn L, Roth, Howard S, Hergenrother, Paul J
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Antineoplastic Agents - pharmacology Apoptosis - drug effects Apoptosis - genetics Caspase 3 - metabolism Cell Line, Tumor Cell Proliferation - drug effects Disease Models, Animal Drug Resistance, Neoplasm Drug Synergism Humans Hydrazones - pharmacology Indoles - pharmacology Melanoma - drug therapy Melanoma - genetics Melanoma - metabolism Melanoma - pathology Mice Mutation Phosphorylation Piperazines - pharmacology Proto-Oncogene Proteins B-raf - genetics Sulfonamides - pharmacology Tumor Burden - drug effects Xenograft Model Antitumor Assays
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