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Semin Thromb Hemost
DOI: 10.1055/a-2799-0557
Review Article

Extracellular Vesicles Drive Coagulopathy Across Hematologic Cancers

Authors

  • Charlotte Gran 

    1   Department of Molecular Medicine and Surgery, Coagulation Research, Karolinska Institutet, Stockholm, Sweden
    2   Clinical Chemistry, Medical Diagnostics, Karolinska University Hospital, Stockholm, Sweden

  • Sanna Norén

    3   Department of Medicine Huddinge, Gastroenterology and Rheumatology Unit, Karolinska Institute, Stockholm, Sweden
    4   Department of Hepatology, Karolinska University Hospital, Stockholm, Sweden

  • Jovan P. Antovic

    1   Department of Molecular Medicine and Surgery, Coagulation Research, Karolinska Institutet, Stockholm, Sweden
    2   Clinical Chemistry, Medical Diagnostics, Karolinska University Hospital, Stockholm, Sweden

Funding Information This work was supported by the Swedish Cancer Society (Grant Number 22 2109Fk).
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Abstract

Coagulopathies are common in hematological malignancies and can cause life-threatening bleeding or thrombosis. Extracellular vesicles (EVs), including exosomes, microvesicles, and apoptotic bodies, carry cargo that reflects their cellular origin. They frequently express tissue factor (TF) and expose phosphatidylserine (PS), which initiate and amplify coagulation and can also transport fibrinolytic mediators that modulate plasmin generation. Procoagulant EVs are commonly assessed using TF- and PS-dependent functional assays, global hemostasis tests such as overall hemostatic potential, and flow cytometric phenotyping. Clinical and experimental data show elevated EV numbers and activity at diagnosis in several hematological malignancies. In acute leukemias, EV-associated procoagulant activity often declines with treatment yet may remain above control levels, consistent with residual risk. In plasma cell disorders and myeloproliferative neoplasms, platelet-derived and TF/PS-positive EVs are frequently increased and have been linked to enhanced thrombin generation. EVs appear to play key roles across leukemias, multiple myeloma, lymphoid, and myeloproliferative neoplasms. However, considerable methodological heterogeneity, including differences in preanalytical handling, EV isolation, characterization, and activity measurement, limits comparability and clinical translation. Disease-specific mechanistic studies are needed to clarify how EVs modulate hemostasis in different hematologic malignancies. In parallel, standardized protocols and adequately powered clinical studies are required to validate EVs as biomarkers.

Keywords

cancer and thrombosis/hemostasis - hypercoagulability - thrombosis - mechanistic - laboratory diagnostics - extracellular vesicle


Publication History

Received: 06 October 2025

Accepted: 27 January 2026

Accepted Manuscript online:
12 February 2026

Article published online:
24 February 2026

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