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UNC Blood Research Center

Pancreatic cancer-associated venous thrombosis

Cancer patients have a 4- to 9-fold increased risk of venous thrombosmbolism (VTE) compared with the general population. We are particularly interested in the mechanisms underlying pancreatic cancer-associated thrombosis (CAT), as pancreatic cancer has one of the highest incidences of VTE. Using mouse models of pancreatic CAT, we have identified three key pathways to venous thrombosis: (1) tissue factor-positive extracellular vesicles (TF+EVs), (2) neutrophils and neutrophil extracellular traps (NETs) and (3) plasminogen activator inhibitor-1 (PAI-1).

Pathways of cancer-associated thrombosis. Pathway 1: tumors release TF-positive extracellular vesicles that activate the coagulation cascade and platelets and increase the risk of VTE. Pathway 2: tumors release granulocyte-colony stimulating factor (G-CSF) that increases the number of neutrophils in the circulation and enhances NET formation and the risk of VTE. Pathway 3: tumors release PAI-1 that increases the risk of VTE by inhibiting plasmin generation and fibrinolysis. NET, neutrophil extracellular trap; PAI-1, plasminogen activator inhibitor-1; TF, tissue factor