Herbert A. Weich

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: The results presented here suggest that monocyte chemotaxis in response to VEGF and most likely to Placenta growth factor is mediated by flt-1 and thus show a possible function for the V EGF-receptor flT-1.

TL;DR: Findings strongly suggest Flt-1 as a functional receptor for VEGF and PlGF in monocytes and endothelial cells and identify this receptor as a mediator of monocyte recruitment and procoagulant activity.

TL;DR: The results suggest that VEGF-C secreted by the intraductal carcinoma cells acts predominantly as an angiogenic growth factor for blood vessels, although this paracrine signaling network between the cancer cells and the endothelium may also be involved in modifying the permeabilities of both blood and lymphatic vessels and metastasis formation.

TL;DR: Both the regular pattern and the typical structure of these lymphatics suggest that CAM is a suitable site to study the in vivo effects of potential lymphangiogenic factors.