In the present study, we make use of different glycosaminoglycan derivatives (RO-heparin, 2-O-desulfated heparin, hexasaccharide and decasaccharide heparin fragments, and UFH) as tools to delineate that the platelet adhesion molecule P-selectin is responsible for the interaction between platelets and tumor cells [10]. The gene discussed is SELP; the disease is neoplasm.