Supplementary Tables and Figures. from Cetuximab Resistance in Squamous Carcinomas of the Upper Aerodigestive Tract Is Driven by Receptor Tyrosine Kinase Plasticity: Potential for mAb Mixtures

Abstract

<p>Table S1 contains IC50 values for cetuximab inhibition, EGFR mutation and amplification status of tested cell lines. Figure S1 shows cetuximab binding to surface EGFR on HN5 and cetuximab resistant HN5 cell lines. Figure S2 shows EGFR levels in parental HN5 cells and cetuximab resistant clones. Figure S3 Overexposed image of immunoblot presented in Figure 2B. Figure S4 shows EGFR degradation upon treatment with anti-EGFR 2mixture for 48h. Figure S5 shows LNA-mediated knockdown of EGFR inhibit growth and proliferation of HN5, HN5 CR2, and HN5 CR14. Figure S6 EGFR levels in FaDu versus cetuximab resistant FaDu cell lines. Figure S7 HER3 and IGF1R plasticity as a mechanism of acquired cetuximab resistance in HN5 CR14. Figure S8 Full dose-response curves of cetuximab and EGFR+HER3+IGF1R 5 mixture in a panel of SCCUAT cell lines.</p>