VEGFA and tumour angiogenesis
2013 (English)In: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 273, no 2, 114-127 p.Article, review/survey (Refereed) Published
In this review we summarize the current understanding of signal transduction downstream of vascular endothelial growth factor A (VEGFA) and its receptor VEGFR2, and the relationship between these signal transduction pathways and the hallmark responses of VEGFA, angiogenesis and vascular permeability. These physiological responses involve a number of effectors, including extracellular signal-regulated kinases (ERKs), Src, phosphoinositide 3 kinase (PI3K)/Akt, focal adhesion kinase (FAK), Rho family GTPases, endothelial NO and p38 mitogen-activated protein kinase (MAPK). Several of these factors are involved in the regulation of both angiogenesis and vascular permeability. Tumour angiogenesis primarily relies on VEGFA-driven responses, which to a large extent result in a dysfunctional vasculature. The reason for this remains unclear, although it appears that certain aspects of the VEGFA-stimulated angiogenic milieu (high level of microvascular density and permeability) promote tumour expansion. The high degree of redundancy and complexity of VEGFA-driven tumour angiogenesis may explain why tumours commonly develop resistance to anti-angiogenic therapy targeting VEGFA signal transduction.
Place, publisher, year, edition, pages
2013. Vol. 273, no 2, 114-127 p.
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:uu:diva-188261DOI: 10.1111/joim.12019ISI: 000313869400003OAI: oai:DiVA.org:uu-188261DiVA: diva2:577024
The definitive version is available at www.blackwell-synergy.com2012-12-142012-12-142013-02-27Bibliographically approved