Karl H. Plate

TL;DR: It is shown that expression of an endothelial cell-specific mitogen, vascular endothelial growth factor (VEGF), is induced in astrocytoma cells but is dramatically upregulated in two apparently different subsets of glioblastoma cells, which strongly support the concept that tumour angiogenesis is regulated by paracrine mechanisms and identify VEGF as a potential tumourAngiogenesis factor in vivo.

TL;DR: It is reported that embryonic angiogenesis in mice was not affected by deficiency of PlGF, andTransplantation of wild-type bone marrow rescued the impairedAngiogenesis and collateral growth in Pgf−/− mice, indicating that PlGF might have contributed to vessel growth in the adult by mobilizing bone-marrow–derived cells.

TL;DR: The biological relevance of the VEGF/Flk-1 receptor/ligand system for angiogenesis is investigated using a retrovirus encoding a dominant-negative mutant of the Flk- 1/VEGF receptor to infect endothelial target cells in vivo, and tumour growth is prevented in nude mice.

TL;DR: The results indicate that chronic vascular insufficiency and, possibly, insufficient Vegf-dependent neuroprotection lead to the select degeneration of motor neurons.

TL;DR: In situ hybridization showed that VEGF is expressed in vivo in rat glioma cells which reside along necrotic areas and therefore closely mimicks the expression pattern of V EGF observed in human glioblastoma, consistent with a role for VEGf in tumor- and hypoxia-induced angiogenesis.