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. Author manuscript; available in PMC: 2019 Jan 1.
Published in final edited form as: Mol Cancer Ther. 2017 Nov 13;17(1):84–95. doi: 10.1158/1535-7163.MCT-17-0705

Figure 2. PLX8394 effectively inhibits ERK1/2 signaling in patient tumors comparable to dabrafenib/trametinib treatment.

Figure 2

A. H&E and IHC analysis of pERK1/2 staining from a representative mutant BRAF patient sample (TJU-MEL-27A) treated with either DMSO, vemurafenib (1 μM), combo (1 μM dabrafenib/16 nM trametinib) or PLX8394 (0.5 μM). B. Quantitation of A across a panel of 6 different mutant BRAF melanoma patient samples. C. Western blot analysis of ERK1/2 signaling and PARP cleavage from a representative patient sample (TJU-MEL-27A). D. Western blot quantitation of the normalized pERK1/2 to ERK2 signal from 5 patient samples. E. RPPA data from mutant BRAF patient samples were analyzed via GSEA. Patient explants treated with vemurafenib (left) and PLX8394 (right), were grouped and compared to DMSO treated samples. Enrichment of the Programmed Cell Death/Apoptosis and Cell Cycle Arrest GO pathways and corresponding changes in RPPA determined protein levels compared to DMSO are shown. Pathway nodes and protein levels for all treatments are on the same scale (bottom left).