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Potential Mechanisms of Cancer-Related Hypercoagulability

Department of Radiation Oncology, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, New York, NY 10467, USA
Institute of Oncology, Bnai Zion Medical Center, Haifa 31048, Israel
Author to whom correspondence should be addressed.
Cancers 2020, 12(3), 566;
Received: 3 February 2020 / Revised: 25 February 2020 / Accepted: 26 February 2020 / Published: 29 February 2020
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). View Full-Text
Keywords: cancer; thrombosis; endogenous heparin; heparanase; heparan sulfate cancer; thrombosis; endogenous heparin; heparanase; heparan sulfate
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MDPI and ACS Style

Nasser, N.J.; Fox, J.; Agbarya, A. Potential Mechanisms of Cancer-Related Hypercoagulability. Cancers 2020, 12, 566.

AMA Style

Nasser NJ, Fox J, Agbarya A. Potential Mechanisms of Cancer-Related Hypercoagulability. Cancers. 2020; 12(3):566.

Chicago/Turabian Style

Nasser, Nicola J.; Fox, Jana; Agbarya, Abed. 2020. "Potential Mechanisms of Cancer-Related Hypercoagulability" Cancers 12, no. 3: 566.

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