Supplementary Figures S1-S15 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer

Supplementary Figure S1. High bTMB is associated with the presence of specific mutations. Supplementary Figure S2. ROC analysis to determine optimal bTMB cutoff. Supplementary Figure S3. High correlation between bTMB determined from WES and a 152- gene targeted sequencing panel. Supplementary Figure S4. Association between high cfDNA yield and shorter PFS. Supplementary Figure S5. High baseline tumor fraction is associated with shorter PFS. Supplementary Figure S6. bTMB scores are not associated with sites of metastatic spread. Supplementary Figure S7. Specific oncogenic signaling pathways are more frequently altered in patients with high bTMB and bCNB scores. Supplementary Figure S8. Genomic landscape of all patients at baseline. Supplementary Figure S9. bTMB and bCNB at baseline vs. progression. Supplementary Figure S10. Correlation between baseline bCNB and bTMB. Supplementary Figure S11. Comparison of ctDNA dynamics as measured by ctDNA fraction and bCNB during treatment and progression. Supplementary Figure S12. Genome-wide plots of copy number changes across treatment time points. Supplementary Figure S13. Copy number changes detected for RB1 and BRCA2 genes across treatment time points. Supplementary Figure S14. Relationship between ctDNA fraction and bTMB and bCNB Supplementary Figure S15. Relationship between tumor fraction and bCNB.