Supplementary Data from A Transcriptionally Definable Subgroup of Triple-Negative Breast and Ovarian Cancer Samples Shows Sensitivity to HSP90 Inhibition

Abstract

<p>Suppl Data and Methods Fig. S1. Flowchart of experimental approach. Fig. S2. Unsupervised hierarchical clustering of breast or ovarian cancer cell lines confirms known subtypes. Fig. S3. Validation of BR/OV-1 and -2 clusters of BRCA and OVCA cell lines. Fig. S4. BR/OV-1 and -2 subgroups of cell lines exhibit differential Hsp90i sensitivity in GDSC database v7. Fig. S5. Support vector machine (SVM) classifier validates robustness of BR/OV-1/2 gene expression classifier to predict BR/OV-1/2 status in an independent dataset. Fig. S6. Validation of BR/OV-1 and -2 subgroups at the (phospho)protein level. Fig. S7. BR/OV-1 and -2 subgroups are distinguishable by proteomics. Fig. S8. Individual dose-response curves for BR/OV-1 and -2 TNBC and OVCA cell lines treated with CCT018159. Fig. S9. Differential sensitivity of BR/OV-1 vs. -2 cell lines to Hsp90 inhibition is lineage-independent. Fig. S10. Individual dose-response curves for TNBC and OVCA cell lines subtyped as BR/OV-1 or -2. Fig. S11. Effects of Hsp90 inhibition on (phospho)protein expression in BR/OV-1 TNBC and OVCA cells. Fig. S12. Effects of Hsp90 inhibition on (phospho)protein expression in BR/OV-2 TNBC and OVCA cells. Fig. S13. Hsp90 inhibition induces apoptosis in BR/OV-2 but not BR/OV-1 TNBC and OVCA cells. Fig. S14. Individual growth curves of OVCA xenografts. Fig. S15. Representative Ki67 IHC and TUNEL images of OVCA xenografts. Fig. S16. Individual growth curves of breast cancer PDX tumors. Fig. S17. Body weight monitoring of mice bearing breast cancer PDX tumors. Fig. S18. Representative Ki67 IHC and TUNEL images of breast cancer PDX tumors. Fig. S19. Assessing homologous recombination deficiency (HRD)-related genetic alterations in tumor models.</p>