Triggering Tumor Immunity through Angiogenesis Targeting Available to Purchase

Whereas nascent tumors fulfill their metabolic requirements for oxygen and nutrients through diffusion from the existing vasculature, advanced lesions engender the formation of new blood vessels to support progressive tumor growth and to effectuate tissue invasion and metastasis (1). Angiogenesis reflects the complex interplay of multiple cell types, whose functions are orchestrated by an array of growth factors, adhesion molecules, and extracellular matrix components. Among the many signals contributing to tumor blood vessel development, the major vascular endothelial growth factor isoform vascular endothelial growth factor (VEGF)-A subserves a crucial role (2). VEGF-A induces endothelial cell proliferation and vascular permeability through the receptor tyrosine kinase VEGF receptor 2 (VEGF-R2; KDR, Flk-1), while stimulating the recruitment and activation of hematopoietic precursors and mature myeloid cells through VEGF-R1 (Flt-1; ref. 3). This elicited cross-talk of vascular elements and immune cells recapitulates physiologic mechanisms critical to wound healing, although...