ABSTRACT
The last 20 years have yielded signifi cant advances in our understanding of the relationship between cancer biology, cancer-associated hemostatic activation, and the subsequent development of venous thromboembolism (VTE). Hemostatic activation can occur in patients with a variety of tumor types but may not translate into the development of clinically evident thrombosis due to the presence or absence of additional risk factors (1,2). Although arterial events can also occur in patients with malignancy, VTE is more frequently observed (1-3). Patients with cancer have at least a sevenfold increased risk of VTE compared to patients without cancer and the risk may be up to 20-fold in patients with metastatic disease (4). Various studies report the incidence of clinically signifi cant VTE as 1% to 43% among cancer patients, depending on the type
and stage of tumor, modality of cancer treatment, contributing risk factors, and comorbidities (5,6).
