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AXL is not necessary for maintenance of intrinsic resistance.
AXL is not necessary for maintenance of intrinsic resistance. A, effects of AXL overexpression on survival of drug-sensitive BRAFV600-mutant melanoma cell lines following 4-day treatment with PLX4720 (RAFi, 2 μmol/L), AZD6244 (MEKi, 200 nmol/L), PLX AZD6244, or VTX11E (ERKi, 2 μmol/L). MEK1 is a negative control; RAF1 is a positive control for RAFi resistance. Data are mean ± standard deviation. Asterisks beneath graph indicate P < 0.01 (two-tailed t test) relative to the same cell line, expressing MEK1, and treated with the same drug. B, effects of AXL overexpression on phosphorylation of AKT and maintenance of ERK phosphorylation following overnight treatment with MAPK pathway inhibitors. D, DMSO; P, 2 μmol/L PLX4720; A, 200 nmol/L AZD6244; PA, PLX AZD6244; and E, VTX11E, 2 μmol/L. MEK1 is a negative control; RAF1 is a positive control for pERK reactivation following RAFi treatment. C, effects of AXL inhibitors on induction of pAKT and rescue of pERK following AXL overexpression. R428, 500 nmol/L; XL184, 3 μmol/L; XL880, 100 nmol/L; in the presence or absence of 2 μmol/L PLX4720. shAXL is a positive control. D, effects of AXL inhibitors on pAKT and pERK levels in intrinsically resistant cell lines in the presence or absence of PLX4720. E, effects of AXL inhibitors on intrinsic resistance to PLX4720. David J. Konieczkowski et al. Cancer Discovery 2014;4: ©2014 by American Association for Cancer Research
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