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Platelet aggregation

Specific proteins expressed on the surface of platelets enable the platelets to adhere to their receptors exposed in areas of vascular damage. The process of adhesion activates the platelets to aggregate, leading to the formation of a platelet plug in the vessel wall. Activated platelets also induce the formation of a fibrin clot by carrying coagulation factors (i.e., Fibrinogen, Factor V, etc.) and providing a catalytic surface for the major interactions of the coagulation cascade. Interactions between tumor cells and platelets have been considered to facilitate tumor cell cluster arrest in the microvasculature, with the subsequent formation of experimental metastasis. Platelets appear to enhance the development of arrested tumor emboli into a secondary metastatic colony. Purified Aggrus/gp44 itself could induce platelet aggregation with no need for plasma components. C–type lectin–like receptor 2 (CLEC-2) expressed on platelets was a counterpart of Aggrus. When CLEC-2 binds to Aggrus expressed on tumor cells, it generates activation signals, including Src, Syk and PLCgamma2 in platelets, and eventually induces platelets to degranulate. Small molecule inhibitors or antibodies against the platelet–aggregating factors could be a therapeutic strategy for inhibiting tumor metastasis and for enhancing cancer patient survival.