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. 2021 Sep 20;24(4):541–553. doi: 10.1093/neuonc/noab212

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© The Author(s) 2021. Published by Oxford University Press on behalf of the Society for Neuro-Oncology.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Fig. 1 — TGF-β signaling is upregulated in GBM compared to IDH-mutant and 1p/19q co-deleted oligodendroglioma. Analysis of TCGA data comparing IDH-wt GBM and IDH-mutant and 1p/19q co-deleted oligodendroglioma. (a) TGFB1 and TGFB2 are upregulated in IDH-wt tumors. (b) GO term analysis reveals pathways related to extracellular matrix. (c) Heatmap of genes related to the top 20 GO terms where either TGFB1 or TGFB2 is present. (d) TGF-β responsive genes identified from the literature. (e) Analysis of drugs related to gene expression signature by connectivity map reveals that TGF-β inhibitors are one of the top candidate drugs that inhibit IDH-wt GBM signature. Abbreviations: GBM, glioblastoma; GO, Gene Ontology; IDH, isocitrate dehydrogenase; TCGA, The Cancer Genome Atlas; TGF-β, transforming growth factor-beta.