Fig. 5: The immune landscape of the high-risk and low-risk patients in multiple melanoma cohorts.
From: Synthetic viability induces resistance to immune checkpoint inhibitors in cancer cells

Significant differential of 29 immune signatures scores from He et al. (a) and Bagaev et al. (b) estimated by the ssGSEA method between low-risk and high-risk patients across melanoma cohorts. c The proportions of high immune and low immune infiltration estimated by 29 immune signatures from He et al. in the high-risk and low-risk melanoma patients. The P values were computed by Fisher’s exact test. d Significant differential of correlation coefficients among 29 immune signatures from He et al. between high-risk and low-risk patients in TCGA SKCM dataset. e Significant differential immune signatures score from Thorsson et al. between high-risk and low-risk melanoma patients. Significant differential expression of chemokines (f), MHC (g), co-inhibitors (h), and co-stimulators (i) genes between low-risk and high-risk patients across melanoma cohorts. The P values were calculated from one-sided Wilcoxon rank-sum test with FDR-adjusted. Fold change (FC) values were calculated by ratio of mean gene expression from low-risk and high-risk patients. For P value, * denotes P < 0.05, ** denotes P < 0.01, and *** denotes P < 0.001.