Supplementary Text, Figure Legends, Figures S1-S12 from Biomarker Accessible and Chemically Addressable Mechanistic Subtypes of BRAF Melanoma
Supplemental Figure S1. Integrative Analysis of Functional Genomics and Copy Number Variation in Melanoma Cells and Tissues, Supplemental Figure S2. Elastic Net Derived Biomarker Results for Melanoma Survival Genes and Detection of These Biomarkers in TCGA SKCM, Supplemental Figure S3. The SOX10 Regulatory Network Supporting Cell Autonomous Melanoma Cell Growth and Survival, Supplemental Figure S4. SOX10 Addiction Specifies Sensitivity of BRAF Mutant Melanomas to BRAF and MEK Inhibitors In Vitro, Related to Figure 1, Supplemental Figure S5. SOX10 Addiction Specifies Sensitivity of BRAF Mutant Melanomas to BRAF and MEK Inhibitors In Patients, Related to Figure 2, Supplemental Figure S6. Bicluster of melanoma cell lines and chemical compounds in McDermott/Benes GDSC dataset, Related to Figure 3, Supplemental Figure S7. Nomination of TBK1 as a Therapeutic Target for Drug-Resistant Melanoma, Related to Figure 3, Supplemental Figure S8. TBK1/IKKε-Addiction is Conserved In Vivo, Related to Figure 4, Supplemental Figure S9. TBK1/IKKε-Addiction Corresponds to a Cell Autonomous Innate Immune Melanoma Subtype, Related to Figure 5, Supplemental Figure S10. TBK1/IKKε Activate AKT and YAP to Support Survival of the Cell-autonomous Immune Melanoma Subtype, Related to Figure 6, Supplemental Figure S11. 13C glucose and 13C glutamine metabolism at 30m and 2h, Related to Figure 7 and Supplemental Fig. S7, Supplemental Figure S12. Distinct Epigenetic Cell Fate Programs Specify TBK1/IKKε Addiction, Related to Figure 7.