Next Article in Journal
A Preclinical Embryonic Zebrafish Xenograft Model to Investigate CAR T Cells in Vivo
Next Article in Special Issue
Thromboprophylaxis in the End-of-Life Cancer Care: The Update
Previous Article in Journal
Systematic Review of Patient-Reported Outcomes following Surgical Treatment of Lymphedema
Previous Article in Special Issue
Primary Thromboprophylaxis in Ambulatory Cancer Patients: Where Do We Stand?
Open AccessReview

Potential Mechanisms of Cancer-Related Hypercoagulability

1
Department of Radiation Oncology, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, New York, NY 10467, USA
2
Institute of Oncology, Bnai Zion Medical Center, Haifa 31048, Israel
*
Author to whom correspondence should be addressed.
Cancers 2020, 12(3), 566; https://doi.org/10.3390/cancers12030566
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
Show Figures

Graphical abstract

MDPI and ACS Style

Nasser, N.J.; Fox, J.; Agbarya, A. Potential Mechanisms of Cancer-Related Hypercoagulability. Cancers 2020, 12, 566. https://doi.org/10.3390/cancers12030566

AMA Style

Nasser NJ, Fox J, Agbarya A. Potential Mechanisms of Cancer-Related Hypercoagulability. Cancers. 2020; 12(3):566. https://doi.org/10.3390/cancers12030566

Chicago/Turabian Style

Nasser, Nicola J.; Fox, Jana; Agbarya, Abed. 2020. "Potential Mechanisms of Cancer-Related Hypercoagulability" Cancers 12, no. 3: 566. https://doi.org/10.3390/cancers12030566

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Search more from Scilit
 
Search
Back to TopTop