VEGF-A splicing: the key to anti-angiogenic therapeutics?

SJ Harper, DO Bates

Research output: Contribution to journalArticle (Academic Journal)peer-review

359 Citations (Scopus)


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.
Translated title of the contributionVEGF-A splicing: the key to anti-angiogenic therapeutics?
Original languageEnglish
Pages (from-to)880 - 887
Number of pages7
JournalNature Reviews Cancer
Publication statusPublished - Nov 2008


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