Antiangiogenic cancer therapy targets the formation of new blood vessels used to support tumor growth. Although many of these agents are currently being tested in clinical trials, no reliable way to monitor the effects of many, if not most, of these therapeutic agents on the inhibition of the complicated process of angiogenesis exists. Dr. Robert S. Kerbel from Women's College Health Sciences Centre in Toronto and colleagues, including Dr. Francesco Bertolini of the European Institute of Oncology in Milan and Dr. Robert D'Amato of Harvard University, examined whether circulating levels of a class of specific blood cells that contribute to the formation of tumor vessels provide any useful information about the effectiveness of angiogenesis inhibitors.
The researchers found that levels of circulating endothelial cells (CECs) and circulating endothelial progenitor cells (CEPs) are quite varied depending on the genetic background of an animal. However, within a particular strain of mice, levels of these cells are influenced by known regulators of blood vessel formation and correlate remarkably with the ability to induce tumor blood vessel growth and the response to antiangiogenic therapy. Importantly, treatment with a drug that interfered with the major signaling receptor for vascular endothelial growth factor (VEGF), a key regulator of blood vessel development, caused a dose-dependent reduction in CEPs. The reduction in CEPs closely reflected the previously established antitumor activity of this VEGF inhibitor, and the optimal decline in CECs and CEPs was reached
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