Supplementary Figures and Tables from Resistance to RET-Inhibition in RET-Rearranged NSCLC Is Mediated By Reactivation of RAS/MAPK Signaling

Supplementary Figures 1-8 Fig. S1: Cell viability of LC-2/ad, PR1, and PR2 cells treated with alectinib or cabozantinib. Fig. S2: RET break-apart FISH analysis of LC-2/ad, PR1, PR2, and H2228. Fig. S3: Phosphatase inhibitor treatment of PR1 and PR2 restores phospho-RET. Fig S4: NRAS Q61K increases NRAS GTP loading and induces RET inhibitor resistance in TPC1 cells. Fig S5: PR1 cells remain resistant to ponatinib after withdrawal from chronic ponatinib treatment. Fig S6: PR2 cells have lost RET signaling dependence. Fig S7: AXL signaling contributes to EGFR-mediated resistance to ROS1 inhibitors in HCC78-TAER cells. Fig S8: PR2 cells demonstrate plasticity when withdrawn from chronic ponatinib and display dual dependence on RET and EGFR. Supplementary Tables 1-3 Table S1: Normalized gene expression of RTKs in LC-2/ad, PR1 and PR2 cells. Table S2: Normalized gene expression of RTK ligands in LC-2/ad, PR1 and PR2 cells. Table S3: Normalized gene expression of protein tyrosine phosphatases in LC-2/ad, PR1, and PR2 cell lines.