Given the differences in the human tumor matrix microenvironment, and our results that "tumor-associated" matrices such as collagen I and tenascin C may enhance the resistance of endothelial cells to certain anti-angiogenic agents, it is imperative that we gain a clearer understanding of the mechanism of inhibition of angiogenesis by these molecules and how this may be affected by differences in the tumor microenvironment. This evidence concerns the gene TNC and neoplasm.