ABSTRACT

One of the fundamental phenomena to observe in assessing tumor growth and treatment response is vascularity. In order to grow beyond approximately 1-2 mm3, a tumor must recruit and form new vasculature, as it can no longer rely on the passive di›usion of nutrients [1]. During the process known as angiogenesis, several growth factors such as platelet-derived growth factor (PGF), œbroblast growth factor (FGF), and vascular endothelial growth factor (VEGF) are secreted to promote the migration of endothelial cells to the site. However, the vessels produced from tumor-associated angiogenesis di›er from those of normal vasculature. Normal vasculature is arranged as a progression from large arteries feeding into smaller arteries/arterioles which terminate at the capillary bed. From the capillary bed, venules carry the deoxygenated blood to small veins, which empty into larger primary veins. During tumor angiogenesis, the imbalance to antiangiogenic and angiogenic factors can lead to abnormal vasculature formation. Tumor vasculature has been reported to be leaky and poorly constructed, with tortuous topology containing incomplete vessels [1-3].