Potential Mechanisms of Cancer-Related Hypercoagulability

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).

microRNAs and Markers of Neutrophil Activation as Predictors of Early Incidental Post-Surgical Pulmonary Embolism in Patients with Intracranial Tumors

“…However, it is different in malignant brain tumors such as glioma than in benign tumors such as meningioma, where operated patients have a risk of VTE up to 26% [4] and 30% [5,6], respectively. The underlying mechanisms responsible for the increased VTE risk seem to be heterogeneous, including factors related to the tumor itself, to the patient, to other physiopathological mechanisms (e.g., inflammation) as well as iatrogenic factors [7,8]. Tumor cells seem to induce hypercoagulability through multiple mechanisms, such as the production of procoagulant and proaggregating molecules (e.g., tissue factor), and the release of pro-inflammatory cytokines that activate endothelial cells, platelets and leukocytes.…”

Prominent Hypercoagulability Associated With Inflammatory State Among Cancer Patients With SARS-CoV-2 Infection

“…Increased procoagulants such as tissue factor, elevated platelet activity, damaged endothelium and blood flow abnormalities may all contribute to hypercoagulability in cancer patients ( 20 ). Cancer patients with poor performance status or receiving several medications such as hormonal therapy or chemotherapy also contributed to risk of hypercoagulability ( 21 ). These aspects of cancer-related hypercoagulability have been known for a long time.…”

Cancer-Associated Thrombosis: Risk Factors, Molecular Mechanisms, Future Management

“…Examples of these medications are hormonal therapy such as tamoxifen, chemotherapy (e.g., paclitaxel, doxorubicin, thalidomide), molecular targeted therapy such as osimertinib, anti-angiogenesis therapy (e.g., bevacizumab, ramucirumab), immunotherapies and radiation therapies. 15 Chemotherapy. Using combination therapy of chemotherapeutic drugs increases the risk of arterial thrombosis occurrence in patients with breast cancer, but the mechanism is not clear.…”

“…Examples of these medications are hormonal therapy such as tamoxifen, chemotherapy (e.g., paclitaxel, doxorubicin, thalidomide), molecular targeted therapy such as osimertinib, anti-angiogenesis therapy (e.g., bevacizumab, ramucirumab), immunotherapies and radiation therapies. 15 …”