Deletion of vascular endothelial growth factor in myeloid cells accelerates tumorigenesis

Angoiogenesis and tumorigenesis: mixed messages from VEGF VEGF (vascular endothelial growth factor) is an important angiogenic factor that has been implicated in tumorigenesis. Two papers now show that the function of VEGF is far more complex, as VEFG can negatively regulate angiogenesis and limit tumorigenesis. In one study, Greenberg et al. found that VEGF can inhibit angiogenesis, by impeding the function of the PDGF (platelet-derived growth factor) receptor on pericytes, leading to a loss of pericyte coverage of blood vessels. This involves the formation of heterodimers between the receptors for VEGF and PDGF. In another paper, Stockmann et al. deleted VEGF production in myeloid cells, but not other cell types. Unexpectedly, they found more rapid tumour development in these mice, at the same time as attenuated tumour vascularization and the formation of morphologically and functionally normalized blood vessels. In contrast, tumours lacking VEGF altogether grew more slowly.