Abstract

The physiology of microvessels limits the growth and development of tumours. Tumours gain nutrients and excrete waste through growth-associated microvessels. New anticancer therapies target this microvasculature by inhibiting vascular endothelial growth factor A (VEGF-A) splice isoforms that promote microvessel growth. However, certain VEGF-A splice isoforms in normal tissues inhibit growth of microvessels. Thus, it is the VEGF-A isoform balance, which is controlled by mRNA splicing, that orchestrates angiogenesis. Here, we highlight the functional differences between the pro-angiogenic and the anti-angiogenic VEGF-A isoform families and the potential to harness the synthetic capacity of cancer cells to produce factors that inhibit, rather than aid, cancer growth.

Author affiliations

1. Steven J. Harper and David O. Bates are at the Microvascular Research Laboratories, Department of Physiology & Pharmacology, Bristol Heart Institute, School of Veterinary Science, University of Bristol, Southwell Street, Bristol BS2 8EJ, UK.

Correspondence to: Steven J. Harper¹ Email: s.harper@bristol.ac.uk

Published online 16 October 2008

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