Werner Risau

TL;DR: Understanding of the molecular basis underlying angiogenesis, particularly from the study of mice lacking some of the signalling systems involved, has greatly improved, and may suggest new approaches for treating conditions such as cancer that depend onAngiogenesis.

TL;DR: It is reported that formation of blood vessels was abnormal, but not abolished, in heterozygous VEGF-deficient (VEGF+/-) embryos, generated by aggregation of embryonic stem (ES) cells with tetraploid embryos (T-ES)16,17, and even more impaired in homozygous D1-VEGF- deficient (VDGF-/-) T-ES embryos, resulting in death at mid-gestation.

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: Investigation of flk-1 receptor tyrosine kinase mRNA expression by in situ hybridization analysis revealed specific association with endothelial cells at all stages of mouse development, suggesting a major role of this ligand-receptor signaling system in vasculogenesis and angiogenesis.

TL;DR: In vivo analyses of embryos deficient in Tie-2 showed that it is important in angiogen-esis, particularly for vascular network formation in endothelial cells, which contrasts with previous reports on Tie-1 function in vasculogenesis and/or endothelial cell survival.