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Title: Anti-Angiogenesis in Breast Cancer: an Essential Treatment Strategy: Presented at IBCEF

"Anti-Angiogenesis in Breast Cancer: an Essential Treatment Strategy: Presented at IBCEF"

By Chris Berrie VIENNA, AUSTRIA -- February 21, 2006 -- The targeting of vascular endothelial growth factor (VEGF) is a rational approach for treatment of breast cancer as it is a key mediator of tumour angiogenesis and as VEGF expression has been associated with poor clinical outcomes in breast cancer, according to an overview therapy presented here at the International Breast Cancer Expert Forum: Milestones in Management, Confidence and Care (IBCEF). Angiogenesis is the process of creating new blood vessels from pre-existing blood vessels, and as Peter Carmeliet, MD/PhD, Professor of Medicine and Adjunct Director, Centre for Transgene Technology and Gene Therapy, Flanders Interuniversity Institute for Biotechnology, University of Leuven, Belgium, detailed in his presentation on February 11[^th, angiogenesis itself is known to contribute to more than 70 human disorders.

This process is tightly regulated by the balanced expression of many pro-angiogenic and anti-angiogenic factors. Although VEGF is only one of about ten well-described pro-angiogenic factors, its importance can be seen by the embryonic lethality that arises from the inactivation of a single VEGF allele. It is therefore one of the key modulators of angiogenesis.

In its stimulation of the growth of endothelial cells, VEGF has a number of roles throughout tumour formation, growth and metastasis, and particularly in the switch from an avascular tumour to a vascularised and growing tumour. At the same time, as VEGF has a limited role in healthy adults, this would imply that anti-VEGF therapies should have minimal physiological effects, Dr. Carmeliet indicated.

Bevacizumab (Avastin(R)) is a recombinant humanised monoclonal anti-VEGF antibody, and which recognises all the major isoforms of human VEGF. Following on from the potent anti-angiogenic effects that have been demonstrated, bevacizumab is thought to inhibit VEGF actions on tumour growth and development through several different mechanisms.

Dr. Carmeliet detailed three main ways in which bevacizumab may act -- as an early benefit in the regression of the existing microvasculature, in the normalisation of the mature vasculature, and as a continued benefit in the inhibition of the production of new vasculature through vessel regrowth and neovascularisation.

This potential for anti-VEGF therapy with bevacizumab demonstrates that the targeting of VEGF in this way has the potential to be an effective therapy for breast cancer, Dr. Carmeliet said.

This conference was sponsored by Roche.

[Presentation title: Anti-angiogenesis in Breast Cancer: an Essential Treatment Strategy.]

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