Supplementary Materials

The PDF file includes:

  • Materials and Methods
  • Fig. S1. Identification of differential enhancer activation between GSCs and DGCs.
  • Fig. S2. DHODH promotes GSC growth.
  • Fig. S3. CADS1859 and CADT456 are important for GSC proliferation.
  • Fig. S4. Validation of knockdown efficacy of shRNAs directed against CAD.
  • Fig. S5. CAD regulates primary GSC growth and self-renewal.
  • Fig. S6. DHODH regulates primary GSC growth and self-renewal.
  • Fig. S7. CAD and DHODH are essential for primary GSC maintenance.
  • Fig. S8. Expression of pyrimidine synthesis genes remains unchanged across glioblastoma specimens harboring different driver mutations.
  • Fig. S9. EGFR regulates CADT456 phosphorylation through the MAPK-ERK pathway.
  • Fig. S10. PTEN deletion promotes CADS1859 phosphorylation through the PI3K-AKT pathway.
  • Fig. S11. PTEN deletion promotes CADS1859 phosphorylation through the PI3K-AKT-TORC1 but not the TORC2 pathway.
  • Fig. S12. Combinatorial blockade of de novo pyrimidine synthesis in GSCs by the DHODH inhibitor teriflunomide and EGFR or PI3K inhibition.
  • Fig. S13. Sensitivity of GSCs to inhibitor treatments.
  • Fig. S14. Impact of targeted therapies on signal transduction pathways in vivo.
  • Fig. S15. Combined targeting of pyrimidine synthesis inhibits GSC tumorigenesis in vivo.
  • Fig. S16. Pairwise correlation analysis of pyrimidine pathway genes and gene enrichment analysis.
  • Fig. S17. Proposed model of combined targeting of pyrimidine synthesis in GSCs.
  • Legend for data file S1
  • References (6172)

[Download PDF]

Other Supplementary Material for this manuscript includes the following: