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The pathogenesis of cancer-associated thrombosis

  • Progress in Hematology
  • Cancer associated thrombosis and bleeding
  • Published:
International Journal of Hematology Aims and scope Submit manuscript

Abstract

Patients with cancer have a higher risk of venous thromboembolism (VTE), including deep vein thrombosis (DVT) and pulmonary embolism (PE), compared to the general population. Cancer-associated thrombosis (CAT) is a thrombotic event that occurs as a complication of cancer or cancer therapy. Major factors determining VTE risk in cancer patients include not only treatment history and patient characteristics, but also cancer type and site. Cancer types can be broadly divided into three groups based on VTE risk: high risk (pancreatic, ovarian, brain, stomach, gynecologic, and hematologic), intermediate risk (colon and lung), and low risk (breast and prostate). This implies that the mechanism of VTE differs between cancer types and that specific VTE pathways may exist for different cancer types. This review summarizes the specific pathways that contribute to VTE in cancer patients, with a particular focus on leukocytosis, neutrophil extracellular traps (NETs), tissue factor (TF), thrombocytosis, podoplanin (PDPN), plasminogen activator inhibitor-1 (PAI-1), the intrinsic coagulation pathway, and von Willebrand factor (VWF).

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Data availability

The datasets generated in the current study are available from the corresponding author on reasonable request.

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The authors would like to thank Editage (www.editage.jp) for English language editing.

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Correspondence to Kohei Tatsumi.

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KT is a member of Medicinal Biology of Thrombosis and Hemostasis established by Nara Medical University and Chugai Pharmaceutical Co., Ltd.

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Tatsumi, K. The pathogenesis of cancer-associated thrombosis. Int J Hematol (2024). https://doi.org/10.1007/s12185-024-03735-x

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