Unlocking Phenotypic Plasticity has been recently recognized as a Halmark of cancer. Metastatic dissemination in pancreatic ductal adenocarcinoma (PDAC) has been attributed to epithelial-mesenchymal transition (EMT). EMT has been associated with cell migration, proliferation and resistance to therapy. Importantly, it has been suggested that reversing the EMT to a mesenchymal-epithelial transition (MET) can improve PDAC treatment. This project intends to identify new molecular targets against metastatic drug-resistant pancreatic cancer cells, taking advantage of proteomic and ultrastructure cellular analysis, and of an in vivo study using resistant cells xenografted in mice.