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Guidelines for the welfare and use of animals in cancer research
New guidelines on the welfare and use of animals in cancer research are provided, including recommendations on all aspects of cancer research, including: study design, statistics and pilot studies; choice of tumour models and humane endpoints.
Combretastatin A-4, an agent that displays potent and selective toxicity toward tumor vasculature.
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.
ZD6126: a novel vascular-targeting agent that causes selective destruction of tumor vasculature.
The synthesis of a water-soluble phosphate prodrug, ZD6126, of the tubulin-binding agent N-acetylcolchinol is reported to be a promising antivascular agent for the treatment of solid tumors.
Mechanisms associated with tumor vascular shut-down induced by combretastatin A-4 phosphate: intravital microscopy and measurement of vascular permeability.
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.
The development of combretastatin A4 phosphate as a vascular targeting agent.
  • D. Chaplin, S. Hill
  • Medicine
    International journal of radiation oncology…
  • 1 December 2002
Results confirm the ability of CA4P to selectively compromise vascular function in experimental tumors, inducing extensive tumor cell death at well-tolerated doses, and offer considerable potential for enhancing the effectiveness of existing and emerging cancer therapies.
Intermittent blood flow in a murine tumor: radiobiological effects.
It is demonstrated that acute hypoxia results from transient changes in blood perfusion in 500-mg SCC VII tumors, using a new fluorescence-activated cell-sorting technique which facilitates isolation of viable tumor cells as a function of their distance from the blood supply.
Combretastatin A-4 phosphate as a tumor vascular-targeting agent: early effects in tumors and normal tissues.
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 and shows that tissue production of nitric oxide protects against the damaging vascular effects of CA- 4-P.
Combretastatin A4 phosphate induces rapid regression of tumor neovessels and growth through interference with vascular endothelial-cadherin signaling.
Combined treatment with anti-VE-cadherin agents in conjunction with microtubule-disrupting agents provides a novel synergistic strategy to selectively disrupt assembly and induce regression of nascent tumor neovessels, with minimal toxicity and without affecting normal stabilized vasculature.
Contribution of granulocyte colony-stimulating factor to the acute mobilization of endothelial precursor cells by vascular disrupting agents.
Following treatment of mice with OXi-4503, a second-generation potent prodrug derivative of combretastatin-A4 phosphate, rapid increases in circulating plasma vascular endothelial growth factor, stromal derived factor-1 (SDF-1), and granulocyte colony-stimulating factor (G-CSF) levels are detected.
Anti-vascular approaches to solid tumour therapy: evaluation of combretastatin A4 phosphate.
The studies confirm combretastatin A4 phosphate as a novel agent which targets and damages tumour vasculature and, moreover, indicate its potential therapeutic usefulness as an adjuvant to conventional cytotoxic approaches.