Fig. 7
Association of EGFR amplification with TAM subtypes and risk score. a, b The distribution of GISTIC2.0 assigned G-scores for recurrent focal amplifications (red) and deletions (blue) in glioma Cluster 1 (a) and Cluster 2 (b) patients. c Violin plot showing the differential levels of CCL2 mRNA [log2(TPM + 1)] expression between TCGA glioma patients with (n = 103) or without (n = 391) EGFR amplification. d, f Violin plots representing the differential levels of deconvoluted TAM-SPP1 (d) and TAM-CCL3 (f) proportions between TCGA glioma patients with (n = 103) or without (n = 391) EGFR amplification. e, g Violin plots showing the differential signature scores of marker genes for TAM-SPP1 (e) and TAM-CCL3 (g) between TCGA glioma patients with (n = 103) or without (n = 391) EGFR amplification. h Violin plot showing the differential levels of risk score between TCGA glioma patients with (n = 103) or without (n = 391) EGFR amplification. i, k Sankey plots visualizing the relationship between EGFR amplification, IDH mutation, TAM-SPP1 and risk score levels. j Kaplan-Meier curve of overall survival in EGFR amplified patients according to the high and low TAM-SPP1 levels. l Kaplan-Meier curve of overall survival in EGFR non-amplified and IDH mutant patients according to high- and low-risk scores calculated based on the prognostic model. Statistical significance was assessed by unpaired two-tailed Student’s t-test for (c–h) and by two-sided log-rank test for (j, l). *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001