Steri, Veronica, Ellison, Tim S, Gontarczyk, Aleksander Maksym, Weilbaecher, Katherine, Schneider, Jochen G, Edwards, Dylan ORCID: https://orcid.org/0000-0002-3292-2064, Fruttiger, Marcus, Hodivala-Dilke, Kairbaan M and Robinson, Stephen Douglas
ORCID: https://orcid.org/0000-0002-6606-7588
(2014)
Acute depletion of endothelial β3-integrin transiently inhibits tumor growth and angiogenesis in mice.
Circulation Research, 114 (1).
pp. 79-91.
ISSN 0009-7330
Abstract
The dramatic upregulation of αvβ3-integrin that occurs in the vasculature during tumor growth has long suggested that the endothelial expression of this molecule is an ideal target for antiangiogenic therapy to treat cancer. This discovery led to the development of small-molecule inhibitors directed against αvβ3-integrin that are currently in clinical trials. In 2002, we reported that β3-integrin-knockout mice exhibit enhanced tumor growth and angiogenesis. However, as β3-integrin is expressed by a wide variety of cells, endothelial cell-specific contributions to tumor angiogenesis are muddied by the use of a global knockout of β3-integrin function.
Item Type: | Article |
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Uncontrolled Keywords: | animals,cell adhesion,cell line, tumor,cell proliferation,endothelial cells,endothelium, vascular,focal adhesion protein-tyrosine kinases,integrin alphavbeta3,lung,mice,mice, inbred c57bl,neoplasms, experimental,neovascularization, pathologic,sdg 3 - good health and well-being ,/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_being |
Faculty \ School: | Faculty of Science > School of Biological Sciences Faculty of Science |
Depositing User: | Pure Connector |
Date Deposited: | 26 Mar 2014 13:18 |
Last Modified: | 24 Oct 2022 06:14 |
URI: | https://ueaeprints.uea.ac.uk/id/eprint/48287 |
DOI: | 10.1161/CIRCRESAHA.114.301591 |
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