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Introduction Venous thromboembolism is one of the most frequent complications in cancer patients and significantly contributes to morbidity and mortality.1 Even without clinical manifestations, cancer patients commonly have hemostatic abnormalities, which worsen as the cancer progresses.2 In acute leukemia, the systemic activation of blood coagulation results in life-threatening consumption coagulopathy and a thrombo-hemorrhagic syndrome.3 The acquisition of a prothrombotic phenotype by tumor cells is an oncogenic-driven event, and is one of the main mechanisms responsible for blood clotting activation in cancer.46 The expression of procoagulant proteins, including tissue factor (TF) and cancer procoagulant, as well as the exposure of anionic phospholipids, contribute to different extents to the prothrombotic phenotype of tumor cells.7,8 Activation of blood coagulation leads to the generation of thrombin, the final effector enzyme of blood coagulation, and to fibrin formation

Conflict of interest Warren Ladiges is a member of the Editorial Board of Aging Pathobiology and Therapeutics

Tebar et al., 1999

doi: 10.1038/s41392-025-02455-w