Fig 1: The NGFR High state is associated with resistance to MAPK inhibitors in a subset of melanoma patients Immunohistochemical analysis of vemurafenib-naïve tumors from three melanoma patients stained for NGFR, MITF, and Ki-67 (see Materials and Methods for patient clinical information).Covariate single-cell analysis of Ki-67 versus NGFR measured by immunofluorescence in pre-treatment, on-treatment (with dabrafenib and trametinib combination for 2 weeks), and post-relapse tumor biopsies of a BRAF-mutant melanoma patient (see Materials and Methods for patient clinical information).Cell population histograms representing c-Jun variations measured by immunofluorescence in the same patient-matched biopsies as shown in (B).NGFR gene expression changes in 21 matched pairs of pre-treatment and post-resistance tumor biopsies analyzed by RNA sequencing. MITF changes are shown for tumors with a post-resistance NGFR increase (increase = log2 (fold-change) > 0.5, decrease = log2 (fold-change) < -0.5, no change = |log2 (fold-change)| = 0.5). Gene expression data from patients treated with RAF inhibitor, MEK inhibitor, or their combination were analyzed by combining two published datasets (Sun et al, 2014; Hugo et al, 2015).Ranked GSEA plots of top KEGG pathways significantly correlated with NGFR expression in 18 matched pairs of pre-treatment and post-resistance tumor biopsies (Hugo et al, 2015).