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Cited by 514

The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

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

Open access
Harper, Steven J., Bates, David O.·2008·Nature Reviews Cancer

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.

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Crossref · 10.1038/nrc2505

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Metadata

Authors
Harper, S. J., & Bates, D. O.
Venue
Nature Reviews Cancer
Published
2008-10-16
Volume
8
Issue
11
Pages
880-887
ISSN
  • 1474-175X (ISSN-L)
  • 1474-1768
OpenAlex
W1976221241
Cited by
514
References
4
FWCI
1.74
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: VEGF-A splicing: the key to anti-angiogenic therapeutics? https://app.cochat.ai/papers/10.1038/nrc2505
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Harper, S. J., & Bates, D. O. (2008). VEGF-A splicing: the key to anti-angiogenic therapeutics? Nature Reviews Cancer. https://doi.org/10.1038/nrc2505

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.