C
Chryso Kanthou
Researcher at University of Sheffield
Publications - 72
Citations - 3939
Chryso Kanthou is an academic researcher from University of Sheffield. The author has contributed to research in topics: Vascular smooth muscle & Combretastatin. The author has an hindex of 30, co-authored 71 publications receiving 3741 citations. Previous affiliations of Chryso Kanthou include Royal Hallamshire Hospital & Max Planck Society.
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Disrupting tumour blood vessels
TL;DR: A full understanding of the action of tubulin-binding combretastatins and other VDAs will provide insights into mechanisms that control tumour blood flow and will be the basis for the development of new therapeutic drugs for targeting the established tumour vasculature for therapy.
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The biology of the combretastatins as tumour vascular targeting agents
TL;DR: The current understanding of the mechanism of action of the combretastatins and their therapeutic potential is reviewed.
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The tumor vascular targeting agent combretastatin A-4-phosphate induces reorganization of the actin cytoskeleton and early membrane blebbing in human endothelial cells.
Chryso Kanthou,Gillian M. Tozer +1 more
TL;DR: It is demonstrated that within minutes of endothelial cell exposure to CA-4-P, myosin light chain (MLC) was phosphorylated, leading to actinomyosin contractility, assembly of actin stress fibers, and formation of focal adhesions, and a Rho-dependent increase in monolayer permeability to dextrans.
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Expression of vascular endothelial growth factor receptors in smooth muscle cells
Atsushi Ishida,Jacqueline Murray,Yuji Saito,Chryso Kanthou,Omar Benzakour,Masabumi Shibuya,Errol S. Wijelath +6 more
TL;DR: The studies demonstrate the presence of VEGF receptors on VSMCs that are functional and indicate that in vivo, V EGF may play a role in modulating the response of VSMC's.
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Microtubule depolymerizing vascular disrupting agents: novel therapeutic agents for oncology and other pathologies.
Chryso Kanthou,Gillian M. Tozer +1 more
TL;DR: Despite causing profound damage to tumours, VDAs fail to halt tumour growth unless used together with conventional treatments, and the focus is now to understand mechanisms of susceptibility and resistance to identify novel molecular targets and develop strategies that are more effective.