Fig. 2: NGFRhi melanomas are resistant to multiple therapies.
From: Reversal of pre-existing NGFR-driven tumor and immune therapy resistance
a Colony formation assay on IFNγ treatment on D10 and D10-TR cells. Tumor cells were treated for 7 days with IFNγ (which was refreshed on day 4) and stained with crystal violet. Quantification in b. b Quantification of IFNγ and TNF treatment for 7 days on D10 and D10-TR cells (medium was refreshed on day 4). Error bars represent S.D. of three independent replicates. Statistical analysis by unpaired t-test; *p < 0.05, ***p < 0.001. c Cytotoxicity assay in D10 parental versus TR cells for BRAF + MEKi. Titrations were performed with a 10:1 ratio of BRAFi:MEKi concentration. Error bars represent S.D. of three biological replicates; the experiment was performed in four independent replicates (as quantified in d). d Quantification of three cell lines for BRAF/MEKi sensitivity in parental versus TR lines. BRAF inhibitor dabrafenib was given at 10 nM and MEK inhibitor trametinib at 1 nM. Error bars represent S.D. of four independent replicates. Statistical analysis by Mann–Whitney test; *p < 0.05. e Cell count in parental and TR cells of the D10 cell line, treated continuously with 1000 nM of dabrafenib. Error bars represent S.D. of two independent replicates. Statistical analysis by Mann–Whitney test; *p < 0.05. f Average NGFR expression in PDX samples from melanoma. Error bars represent S.D. Statistical analysis by unpaired t-test. *p < 0.05. g NGFR immunohistochemistry score for patient samples prior to and on BRAF + MEK inhibition, divided in responders (R) and nonresponders (NR). Statistical analysis by Mann–Whitney, **p < 0.01. Source data are provided as a Source Data file.
