Data that we present throughout this study demonstrates that under nutrient rich conditions (e.g., as cells invade away from pancreatic PanIN or PDAC lesions and move through circulation) TGFβ can cooperate with collagen ECM proteins via ITGA1-dependent mechanisms to establish viable mesenchymal populations that are required for systemic spread and survival of PDAC tumor cells. Here, TGFB1 is linked to neoplasm.