Supplementary Figures 1 through 17 and Supplementary Tables 1 and 2 from Activating Mutations in <i>PIK3CB</i> Confer Resistance to PI3K Inhibition and Define a Novel Oncogenic Role for p110β

Abstract

<p>Supplementary Figure S1. Inhibition of AKT and S6 phosphorylation. Supplementary Figure S2. Cell growth inhibition by a panel of compounds. Supplementary Figure S3. Effect of GDC-0980 on AKT and S6 phosphorylation. Supplementary Figure S4. Cell growth inhibition by a panel of compounds. Supplementary Figure S5. Inhibition of AKT phosphorylation. Supplementary Figure S6. Cell growth inhibition by a panel of anti-cancer agents. Supplementary Figure S7. The alignment of C-terminus of Human p110 family. Supplementary Figure S8. Droplet digital PCR (ddPCR) detection of PIK3CB D1067Y mutation. Supplementary Figure S9. Detection of copy number variation. Supplementary Figure S10. A. Cell growth inhibition by GDC-0941. B. Droplet digital PCR (ddPCR) analysis of PTEN-null GDC-0941 resistant cell lines. Supplementary Figure S11. Droplet digital PCR detection of PIK3CB D1067V mutation. Supplementary Figure S12. PIK3CB mutant expressing EVSA-T cells are less sensitive to PI3K inhibitors. Supplementary Figure S13. Inhibition of AKT and S6 phosphorylation. Supplementary Figure S14. p110β dependency of A498. Supplementary Figure S15. ATP competition assay. Supplementary Figure S16. Relative quantification of baseline AKT phosphorylation levels in EVSA-T parental cells and resistant clones. Supplementary Figure S17. Signal profile in Rat-2 stable cell lines. Supplementary Table S1 Compound list. Supplementary Table S2 Whole exome sequencing list of genes mutated in EVSA-T GDC-0941 resistant cells.</p>