EGFR and pancreatic ductal adenocarcinoma: The resistance mechanism to cetuximab (ctx) in pancreatic ductal adenocarcinoma (PDAC) cells involves the overexpression of active integrin β1, leading to Src-AKT activation and resulting in EGFR ligand-independent proliferation signaling that circumvents the effects of EGFR blockade., a dual-targeting antibody, Ctx-TPP11, by genetically fusing the NRP1-targeting peptide TPP11 to the C terminus of the cetuximab heavy chain was developed that inhibits integrin β1 signaling.