@article {CORONELLA2243, author = {JULIA CORONELLA and LINGNA LI and KIMBERLY JOHNSON and STEVEN PIRIE-SHEPHERD and GIOVANNI ROXAS and NANCY LEVIN}, title = {Selective Activity Against Proliferating Tumor Endothelial Cells by CVX-22, A Thrombospondin-1 Mimetic CovX-Body{\texttrademark}}, volume = {29}, number = {6}, pages = {2243--2252}, year = {2009}, publisher = {International Institute of Anticancer Research}, abstract = {CVX-22 is a CovX-Body{\texttrademark}, produced by covalently attaching a thrombospondin-1 (TSP-1) type 1 repeat peptide mimetic to a humanized IgG1 molecule. To dissect the antiangiogenic mechanism of CVX-22, the numbers and proliferative status of defined tumor endothelial cell (TEC) subsets from the B16 and C32 melanoma models were examined. CVX-22 treatment reduced the numbers of activated, vascular endothelial growth factor receptor 2 (VEGFR2)-positive TECs. Because the vast majority of mitotically active TECs reside in the VEGFR2 subset, a reduction in numbers of this compartment resulted in an 82\% overall decrease in BrdU labeling of TEC. However, the rate of proliferation and VEGFR2 receptor density of this VEGFR2-positive subpopulation were unaffected. Instead, CVX-22 induced endothelial cell apoptosis both in vitro and in vivo, indicating that CVX-22 acts by selective deletion of activated, VEGFR2-positive TEC. The overrepresentation of activated cells in sites of tumor angiogenesis may confer a unique specificity of CVX-22 for tumor vasculature.}, issn = {0250-7005}, URL = {https://ar.iiarjournals.org/content/29/6/2243}, eprint = {https://ar.iiarjournals.org/content/29/6/2243.full.pdf}, journal = {Anticancer Research} }