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Acute depletion of endothelial β3-integrin transiently inhibits tumor growth and angiogenesis in mice

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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.

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Original languageEnglish
Pages (from-to)79-91
Number of pages13
JournalCirculation Research
Volume114
Issue number1
DOIs
StatePublished - 3 Jan 2014
Peer-reviewedYes

Keywords

    Research areas

  • 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

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