As collagen I is found to be overexpressed in tumor versus normal tissue of the breast [29,30], and is itself a substrate for attachment of integrins that can profoundly influence endothelial function [33-37], we therefore examined the ability of three known angiostatic molecules, TSP-1, IP-10 and endostatin to inhibit endothelial cell proliferation, induce endothelial cell apoptosis on both plastic and collagen I coated surfaces in vitro and to inhibit VEGF-induced endothelial cell tube formation in collagen I gels in vitro. Here, CXCL10 is linked to neoplasm.