Supplementary Tables S1-S11 from Blocking Genomic Instability Prevents Acquired Resistance to MAPK Inhibitor Therapy in Melanoma

Table S1: Clinical characteristics of patients who donated MAPKi-sensitive/-naive and acquired MAPKi-resistant melanoma. Table S2: Genomic alterations, chromothripsis, and ecDNA-/CGR-amplicons detected in MAPKi-sensitive/-naive and acquired MAPKi-resistant melanoma genomes. Table S3: Genes amplified by ecDNAs, CGRs, and linear amplicons along with copy numbers in MAPKi-sensitive/-naïve and acquired MAPKi-resistant melanoma genomes. Table S4: Co-occurrence of resistance-associated genetic alterations (identified in prior studies) with resistance-driver ecDNA and CGR amplicons (identified in the current study). Table S5: Normalized RNA-seq-based transcript expression in MAPKi-sensitive/-naïve and acquired-resistant tumors. Table S6: MAPK-reactivation amplicons in acquired resistance, copy numbers, and amplicon sub-types. Table S7: MAPKi-resistant genes amplified by ecDNAs and CGRs utilized for pathway enrichment analysis. Table S8: Enhancers associated with ecDNAs and CGRs in MAPKi-sensitive/-naive and acquired MAPKi-resistant melanoma genomes. Table S9: Frequencies of enriched SBS signatures reflecting defective DNA repair mechanisms within chromothripsis and non-chromothriptic regions in MAPKi-sensitive (n = 16) and acquired-resistant (n = 31) tumors. Table S10: ecDNAs, CGRs, copy numbers, and associated genes in human melanoma cell lines (M229, M249) on vehicle treatment and early on treatment. Table S11: ecDNAs, CGRs, copy numbers, associated genes in vehicle-treated and early on-treatment PDX tumors.