Basic and clinical studies over the past half-century have left little doubt that elements within the coagulation mechanism are capable of regulating malignant growth. The information base on this subject has now been expanded by remarkable new data reported by Kozlowski et al. [1] in this issue of the journal. P-selectin-mediated interactions between platelets, leukocytes, endothelial cells and tumor cells are described that illustrate the interplay between the coagulation mechanism and cancer, and the potential for the development of novel cancer treatments. Dermatan sulfates (DSs) from two species of ascidians, tiny sessile marine invertebrates commonly called sea squirts because they squirt water when disturbed, inhibited P-selec-tin-mediated inflammatory cell recruitment in a mouse model of thioglycollate-induced peritonitis. The DSs also inhibited human and mouse colon cancer cell and mouse melanoma cell adhesion to immobilized P-selectin, as well as metastasis in mice. The data cited strongly implicate P-selectin in cancer-associated thrombosis.
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