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Cancer-associated thrombosis.

Jeffrey I Zwicker1, Barbara C Furie, Bruce Furie

  • 1Center for Hemostasis and Thrombosis Research, Beth Israel Deaconess Medical Center and the Department of Medicine, Harvard Medical School, Boston, MA 02115, United States. jzwicker@bidmc.harvard.edu

Critical Reviews in Oncology/Hematology
|February 13, 2007
PubMed
Summary

Malignancy is linked to a hypercoagulable state, with elevated coagulation markers and inflammatory cytokines observed in cancer patients. The exact molecular mechanisms driving cancer-associated thrombosis are still under investigation.

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Area of Science:

  • Oncology
  • Hematology
  • Molecular Biology

Background:

  • Strong evidence links malignancy with venous thromboembolic events.
  • Cancer is recognized as a hypercoagulable state, supported by laboratory markers of coagulation activation.
  • Elevated levels of inflammatory cytokines, coagulation proteins, and procoagulant microparticles are observed in cancer patients.

Purpose of the Study:

  • To investigate the molecular basis of cancer-associated thrombosis.
  • To determine the contribution of various factors to thrombus formation in malignancy.

Main Methods:

  • Analysis of laboratory markers of coagulation activation (e.g., thrombin-antithrombin complex, prothrombin fragments 1+2).
  • Measurement of inflammatory cytokines (e.g., tumor necrosis factor, interferon-gamma).

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  • Assessment of coagulation proteins (e.g., tissue factor, factor VIII) and procoagulant microparticles.

    • Main Results:

    • Laboratory markers confirm malignancy as a hypercoagulable state.
    • Elevated levels of specific inflammatory cytokines, coagulation proteins, and microparticles are noted in patients with malignancy.
    • The precise molecular underpinnings of cancer-associated thrombosis remain to be fully elucidated.

    Conclusions:

    • Malignancy significantly increases the risk of venous thromboembolic events.
    • While several factors contribute to a hypercoagulable state in cancer, the molecular basis for thrombosis is complex and requires further research.
    • The roles of chemotherapeutics, tumor cells, endothelium, and circulating procoagulants in thrombus formation are active areas of investigation.