Dr. Olivier Feron and his team from the University of Louvain Medical School in Brussels have turned the whole concept of targeting tumour blood vessels on its head. Instead of the conventional approach of trying to starve tumour cells of the blood supply they need to grow, they are doing the opposite opening up the tumour blood supply to allow better access for cancer drugs and more effective radiotherapy.

The potential for exploiting tumour blood vessels has been made possible by their discovery in a study in mice that the arterioles (blood vessels less than 0.5mm in diameter) that feed tumours have the ability to contract in response to increases in pressure within their lumen (the space within the blood vessels). Equivalent sized blood vessels in healthy tissue can't do this.

"What this means is that we may have the potential to use drugs to selectively exploit these blood vessels against the tumour instead of, or before, killing them. Exploiting tumour blood vessels instead of destroying them by anti-angiogenic drugs constitutes a paradigm shift in approach to angiogenesis," Dr. Feron told a news briefing today (Thursday 30 September) at the EORTC-NCI-AACR[2] Symposium on Molecular Targets and Cancer Therapeutics.

The key to the ability of tumour arterioles to contract lies with endothelin-1 (ET-1) a peptide released in large amounts by many tumour cells, which stimulates their proliferation.

"The effect of ET-1 in tumours has been underestimated up to now," Dr. Feron said. "ET-1 has been known for years in cardiology as a very potent blood vessel constrictor. Here, we found that the myogenic tone (mechanical force) with which the tumour blood vessels contract and expand is exquisitely dependent on the endothelin pathway.

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Contact: Margaret Willson
m.willson@mwcommunications.org.uk
41-227-612-211
European Organisation for Research and Treatment of Cancer
30-Sep-2004