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.
| Original language | English |
|---|---|
| Pages (from-to) | 79-91 |
| Number of pages | 13 |
| Journal | Circulation Research |
| Volume | 114 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 3 Jan 2014 |
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
Access to Document
Profiles
-
Dylan Edwards
- Norwich Medical School - Emeritus Professor
- Norwich Institute for Healthy Aging - Member
- Cancer Studies - Member
Person: Honorary, Research Group Member, Research Centre Member
-
Stephen Robinson
- School of Biological Sciences - Research Leader
- Norwich Institute for Healthy Aging - Member
- Cells and Tissues - Member
Person: Research Group Member, Research Centre Member, Academic, Teaching & Research