Supplementary Figures 1-14; Supplementary Tables 1-3 from A Monoclonal Antibody to ADAM17 Inhibits Tumor Growth by Inhibiting EGFR and Non–EGFR-Mediated Pathways

Le résumé fourni par la source

Supplementary Figures 1-14; Supplementary Tables 1-3. Supplementary Figure 1. Lead antibody 80PH3 is a potent inhibitor of recombinant ADAM17 Supplementary Figure 2. 80PH3 is not a potent inhibitor of cellular ADAM17 Supplementary Figure 3. MEDI3622 is highly selective for ADAM17 and does not inhibit ADAM10 or MMP12 Supplementary Figure 4. MEDI3622 does not compete for binding to cellular ADAM17 with the ADAM17 monoclonal antibody 9301 Supplementary Figure 5. MEDI3622 inhibits cellular mouse ADAM17 Supplementary Figure 6. Cell surface levels of HER pathway proteins in OE21 esophageal cancer cells Supplementary Figure 7. The half-life of MEDI3622 in rats is approximately 8 days Supplementary Figure 8. Several phosphorylation sites in EGFR are inhibited by MEDI3622 Supplementary Figure 9. Exposure to MEDI3622 reduces levels of phospho-SRC and phospho-YES Supplementary Figure 10. Percent activated EGFR predicts cetuximab sensitivity in a series of Head and Neck PDX models Supplementary Figure 11. Proliferation of COLO205 colon cancer cells is independent of the HER pathways Supplementary Figure 12. MEDI3622 does not inhibit HER pathways in Colo205 tumors Supplementary Figure 13. Predictive value of ADAM17, EGFR, HER2, and HER3 mRNA levels for sensitivity of cell lines to MEDI3622 Supplementary Figure 14. Sensitivity to MEDI3622 is not predicted my mRNA levels of ADAM1, HER2 OR HER3 in head and neck PDX models Supplementary Table 1. Correlation of MEDI3622 and cetuximab anti-proliferative activity Supplementary Table 2. Identification of ADAM17 substrates in COLO205 cells by SILAC proteomics Supplementary Table 3. Identification of ADAM17 substrates in H358 lung cancer cells by SILAC proteomics

Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.