Fig. 6

TSPO overexpression marks oncogenic signaling, extracellular matrix organization and immune system interaction patterns. Heatmap with annotation and unsupervised clustering of differentially expressed genes of 9 TSPO-low vs. 9 TSPO-high GBM cases analyzed with RNA-Seq (TSPO mRNA expression median split) (a). Follow-up analyses in Reactome/ FUMA with the differentially expressed genes predominantly showed three functional clusters among the top 50 overrepresented pathways (Reactome: FDR ≤ 0.25, FUMA: padj ≤ 0.05): ECM organization, immune system interaction, and malignant/oncogenic pathways (b). GSEA using Hallmark gene sets revealed 30 significant gene sets (FDR ≤ 0.05, NES > 2.0) from these three functional clusters (c) and an enrichment of oncogenic signature transcripts in TSPO-high cases (FDR ≤ 0.05, FWR ≤ 0.05) (d). Significances are displayed as follows: p > 0.05 = n.s., p < 0.05 = *, p < 0.01 = **, p < 0.001 = ***. CL: classical, ECM: extracellular matrix, FDR: false discovery rate, FUMA: Functional Mapping and Annotation, FWR: familywise-error rate, GBM: glioblastoma, GSEA: gene set enrichment analysis, IDH: isocitrate dehydrogenase, IDH-wt: IDH-wildtype, MES: mesenchymal, NES: normalized enrichment score, PRO: proneural