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).
Highlights
Since Trousseau described the correlation between cancer and thrombosis in 1867 [1], there has been no consensus regarding the etiology connecting the two
We have shown that heparanase is able to degrade heparin and low-molecular-weight heparin (LMWH) [3]
We found that a substantial proportion of cancer patients suffering from venous thromboembolism (VTE) and treated with standard LMWH doses had subtherapeutic anti-Xa activity [4]
Summary
Since Trousseau described the correlation between cancer and thrombosis in 1867 [1], there has been no consensus regarding the etiology connecting the two. Poor performance status of patients with cancer has been correlated with a higher risk of thrombosis (Figure 1). This may be due to stasis as well as an indication of the aggressive nature of the malignancy in these patients that results in degradation of their functional capabilities. By the tumor mass, poor performance status, and bed rest following surgical procedures; (2) iatrogenic, iatrogenic, due to treatment with antineoplastic medications; and (3) secretion of heparanase from due to treatment with antineoplastic medications; and (3) secretion of heparanase from malignant malignant tumors that results in degradation of endogenous heparin. We propose stratifying cancer-related hypercoagulability into two main types. We will initially thewill classical mechanism cancer-associated thrombosis tumor-secreted heparanase Degradation of endogenous heparin by tumor-secreted heparanase (type I)
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