0000000000460625
AUTHOR
Nicla Borrelli
Additional file 7 of A receptor-antibody hybrid hampering MET-driven metastatic spread
Additional file 7: Supplementary Fig. 7. Serum concentration of AbDec-L1 after single i.v. administration to Sprague Dawley rats at different time points.
Additional file 3 of A receptor-antibody hybrid hampering MET-driven metastatic spread
Additional file 3: Supplementary Fig. 3. IVIS images of lungs excised from hHGF-ki mice that received intra-pancreatic injection of HPAF-II cells.
Additional file 6 of A receptor-antibody hybrid hampering MET-driven metastatic spread
Additional file 6: Supplementary Fig. 6. Analysis of CL-901 primary tumors treated with AbDec-L1.
Additional file 2 of A receptor-antibody hybrid hampering MET-driven metastatic spread
Additional file 2: Supplementary Fig. 2. IVIS images of livers excised from hHGF-ki mice that received intra-pancreatic injection of Capan-1 cells.
Additional file 5 of A receptor-antibody hybrid hampering MET-driven metastatic spread
Additional file 5: Supplementary Fig. 5. IVIS images of organs excised from hHGF-ki mice that received sub-cuteaneous injection of CL-901 cells.
Additional file 4 of A receptor-antibody hybrid hampering MET-driven metastatic spread
Additional file 4: Supplementary Fig. 4. Immunohistochemical analysis of MET phosphorylation in pancreatic primary tumors treated with AbDec-L1.
Additional file 1 of A receptor-antibody hybrid hampering MET-driven metastatic spread
Additional file 1: Supplementary Fig. 1. IVIS analysis of primary tumors excised from mice that received intra-pancreatic injections of Capan-1 or HPAF-II pancreatic cancer cells.
A receptor-antibody hybrid hampering MET-driven metastatic spread
AbstractBackgroundThe receptor encoded by the MET oncogene and its ligand Hepatocyte Growth Factor (HGF) are at the core of the invasive-metastatic behavior. In a number of instances genetic alterations result in ligand-independent onset of malignancy (METaddiction). More frequently, ligand stimulation of wild-type MET contributes to progression toward metastasis (METexpedience). Thus, while MET inhibitors alone are effective in the first case, combination therapy with ligand inhibitors is required in the second condition.MethodsIn this paper, we generated hybrid molecules gathering HGF and MET inhibitory properties. This has been achieved by ‘head-to-tail’ or ‘tail-to-head’ fusion of a sin…