Fig. 1: Overview of the proteogenomic landscape of gliomas.
A Summary of significantly mutated genes from 187 exomes. The right panel: percentage of samples affected. The left panel: the comparison of mutational frequencies of driver mutations across different brain locations. The top panel: the count of mutations per sample. The middle panel: the clinical characteristics of each sample. The central heat map: distribution of significant mutations across the sequenced samples, color-coded by mutation type; and bottom panel: the distribution of SCNAs across the sequenced samples. frequent focal somatic copy-number alterations including gains (pink), amplification (red), loss (pale blue) or deletion (dark blue). B The heatmap indicated the mutational status of the two exclusively mutated genes: EGFR and IDH1 (two-sided fisher exact test, p = 0.0014). The heatmap indicated the distribution of significant mutations across the sequenced samples, mutated samples were color-coded in black; The histological grade of each sample were depicted on the top. C, D The bar plot described the pathways enriched by the proteins upregulated in mutant samples (red), by proteins upregulated in WT samples (blue) (IDH1-mutant: C EGFR-mutant: D) (p value was evaluated by hypergeometric test and adjusted by BH correction). E, F The protein–protein interaction networks constructed by the proteins altered significantly in the mutant samples. Proteins were color-coded based on the fold changes between the mutant and wild-type samples, displayed in log10 scale. (IDH1-mutant: E, EGFR-mutant: F). G The heatmap presented the biological downstream pathways associated with EGFR and IDH1 mutations. Each column represented a patient sample and rows from top to the bottom indicated EGFR and IDH1 mutational status, pathways’ GSVA scores, the expression of pathway related proteins. For protein expression: color of each cell showed z scored FOT of proteins across the proteomic subgroups. Source data are provided as Source Data files.
