Vivien E. Prise

TL;DR: Vascular shutdown, within experimental and human breast cancer models in vivo following systemic drug administration, was demonstrated with a reduction in functional vascular volume of 93% at 6 h following drug administration and persisted over the next 12 h, with corresponding histology consistent with hemorrhagic necrosis resulting from vascular damage.

TL;DR: The potential for tumor vascular-targeting by using the tubulin destabilizing agent disodium combretastatin A-4 3-0-phosphate (CA-4-P) was assessed in a rat system as mentioned in this paper.

TL;DR: The tumor vascular effects of the tubulin destabilizing agent disodium combretastatinA-4 3-O-phosphate (CA-4-P) were investigated in the rat P22 tumor growing in a dorsal skin flap window chamber implanted into BD9 rats, and results suggest a mechanism of action of CA- 4-P in vivo.

TL;DR: Intravital microscopy of tumours growing in 'window chambers' in animal models provides a means of directly investigating tumour angiogenesis and vascular response to treatment, in terms of both the morphology of blood vessel networks and the function of individual vessels.

TL;DR: Ktrans values for Gd‐DTPA uptake into tumours could be a useful non‐invasive indicator of blood flow changes induced by anti‐vascular agents such as combretastatin.