Potential mechanisms of cancer-related hypercoagulability

Nicola J. Nasser, Jana Fox, Abed Agbarya

Research output: Contribution to journalReview article

5 Scopus citations

Abstract

The association between cancer and thrombosis has been known for over a century and a half. However, the mechanisms that underlie this correlation are not fully characterized. Hypercoagulability in cancer patients can be classified into two main categories: Type I and Type II. Type I occurs when the balance of endogenous heparin production and degradation is disturbed, with increased degradation of endogenous heparin by tumor-secreted heparanase. Type II hypercoagulability includes all the other etiologies, with factors related to the patient, the tumor, and/or the treatment. Patients with poor performance status are at higher risk of venous thromboembolism (VTE). Tumors can result in VTE through direct pressure on blood vessels, resulting in stasis. Several medications for cancer are correlated with a high risk of thrombosis. These include hormonal therapy (e.g., tamoxifen), chemotherapy (e.g., cisplatin, thalidomide and asparaginase), molecular targeted therapy (e.g., lenvatinib, osimertinib), and anti-angiogenesis monoclonal antibodies (e.g., bevacizumab and ramucirumab).

Original languageEnglish (US)
Article number566
JournalCancers
Volume12
Issue number3
DOIs
StatePublished - Mar 2020

Keywords

  • Cancer
  • Endogenous heparin
  • Heparan sulfate
  • Heparanase
  • Thrombosis

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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