Supplementary Figures 1 through 9 from Chemoresistance in Pancreatic Cancer Is Driven by Stroma-Derived Insulin-Like Growth Factors

Fig. S1. Primary M2-like macrophages express IGF-1 and IGF-2. Fig. S2. In the absence of chemotherapy, addition of MCM, IGF blockade or recombinant IGF does not affect proliferation or survival of pancreatic cancer cells. Fig.S3. MCM enhances resistance of pancreatic cancer cells to gemcitabine, 5-FU and paclitaxel in an IGF-dependent manner. Fig. S4. Biopsies from pancreatic cancer patients express activated Insulin and IGF1 receptors and are infiltrated by macrophages. Fig. S5. Mouse orthotopic pancreatic tumors are rich in macrophages and myofibroblasts. Fig. S6. Tumors from KPC mouse model express activated Insulin/IGF1 receptors. Fig. S7. Gating strategy used to FACS-sort tumor cells, immune cells and stromal cells. Fig. S8. Primary pancreatic myofibroblasts secrete IGF-1 and IGF-2. Fig. S9. IGF-1 and IGF-2 are expressed in the tumor microenvironment of PDA patients. Fig. S10. Gating strategies used to analyse tumor infiltrated immune cell populations. Fig. S11. IGF blockade decreases activation of Insulin and IGF1 receptors in pancreatic tumors. Fig. S12. Combination of 5-FU and paclitaxel with BI 836845 in a syngeneic orthotopic pancreatic cancer model.