Fig. 5
From: Clonal selection confers distinct evolutionary trajectories in BRAF-driven cancers
BRAF-variant identity and multiplicity regulates tumor responses to targeted therapies. a Cells with higher BRAF variants copies per cell (and higher CCF) were more sensitive to MEK1/2 (AZD6244 or PD318088) or BRAF (PLX-4032) inhibition. AUC, area under the curve. CCF values for individual cells are designated by the heatmap. b NSG mice bearing PDX with the indicated BRAF mutation and copies per cell were treated with dabrafenib (BRAFi) and trametinib (MEKi). Data are expressed as the mean ± s.d. The P-value of the χ2-test between the control and treatment groups was <0.05, <0.001, <0.0001. c Schematic depicting the co-culturing of cells expressing BRAFV600E or BRAFG466V and vector alone. After 48 of Dox-induction, cells were treated with either d dabrafenib (BRAFi) or e trametinib (MEKi). Cellular survival was measured 5 days after drug treatment. Data are expressed as the area under the curve (AUC) and represent the mean ± s.e.m. of at least three independent experiments
