


From the * James P. Wilmot Cancer Center and the Department of Medicine, University of Rochester, Rochester, NY;
University of Southern California-Keck School of Medicine and the Kenneth J. Norris Jr. Comprehensive Cancer Center, Los Angeles, CA;
Department of Internal Medicine, University of California-Davis, Sacramento, CA; University of California, Davis, Sacramento, CA;
Department of Medicine, Duke University School of Medicine, and the Duke Comprehensive Cancer Center, Durham, NC
Authors disclosures of potential conflicts of interest are found at the end of this article.
Address reprint requests to Gary H. Lyman, MD, MPH, Department of Medicine, Duke University School of Medicine and the Duke Comprehensive Cancer Center, 2424 Erwin Road, Box 602, Durham, NC 27705, e-mail: Gary.Lyman{at}duke.edu
Overview: Cancer-associated thrombosis is a frequent complication of cancer and cancer treatment, with a clear increase in incidence reported in recent studies. Epidemiologic studies have demonstrated that patients with cancer who develop venous thromboembolism (VTE) have reduced survival. VTE has multiple clinical consequences in patients with cancer, including the need for long-term anticoagulation, a risk of bleeding complications, and a continuing risk of recurrent VTE. Thrombosis also has been shown to be the second leading cause of death in patients with cancer and is associated with decreased short-term as well as long-term survival. VTE has been associated with a number of specific risk factors, including the type and stage of cancer, surgery and other cancer treatments, and certain patient comorbidities, as well as recently identified biomarkers. A risk model recently has been developed to aid in the identification of patients with cancer at highest risk for VTE. Population-based studies as well as prospective clinical trials in patients with cancer have shown that many chemotherapeutic drugs alone or in combination can significantly increase the risk of VTE. Newer targeted therapeutic agents and antiangiogenic drugs, although often demonstrating a low thrombotic risk when administered alone, are associated with a greatly increased risk when combined with conventional chemotherapeutic agents.