Ahuva Itin

TL;DR: It is shown that vascular endothelial growth factor (VEGF) probably functions as a hypoxia-inducible angiogenic factor and is specifically induced in a subset of glioblastoma cells distinguished by their immediate proximity to necrotic foci and the clustering of capillaries alongside VEGF-producing cells.

TL;DR: It is shown that regression of retinal capillaries in neonatal rats exposed to high oxygen, is preceded by a shut–off of vascular endothelial growth factor (VEGF) production by nearby neuroglial cells.

TL;DR: It is shown that blood vessels in both a xenografted tumor and primary human tumors contain a sizable fraction of immature blood vessels that have not yet recruited periendothelial cells, suggesting that the unique dependence on VEGF of blood vessels lacking periENDothelial Cells can be exploited to reduce an existing tumor vasculature.

TL;DR: The data suggest a model for VEGF-programmed adult neovascularization highlighting the essential paracrine role of recruited myeloid cells and a role for SDF1 in their perivascular retention.

TL;DR: It is shown that expression of vascular endothelial growth factor (VEGF) is upregulated in chronically hypoxic niches (inner layers) of the spheroid and that expression is reversed when hypoxia is relieved by hyperoxygenation and that stress-induced VEGF activity is taken into account in any attempt to target tumor angiogenesis.