Legends to Supplementary Figures from Radiation Resistance in KRAS-Mutated Lung Cancer Is Enabled by Stem-like Properties Mediated by an Osteopontin–EGFR Pathway

Fig. S1. Importance of mutant KRAS status for cellular and clinical radioresistance. Fig. S2. Characterization of the CSC-like features of KRAS mutant NSCLC cells. Fig. S3. Pathway analysis of differentially expressed genes in KRAS mutant vs wild-type NCI-H1703 cells. Fig. S4. Factors influencing the radioresistance of NSCLC cell lines with mutant KRAS. Fig. S5. Role of SPP1/osteopontin expression in KRAS mutant and wild-type NSCLC cell lines and tumors. Fig. S6. Characterization of MLCC alterations in KRAS mutant NSCLC. Fig. S7. BIM regulation and importance of p53/p16 alterations in KRASmut NSCLC.