ABSTRACT
Platelets in plasma can be aggregated by a wide variety of low molecular weight agonists such as Adenosine diphosphate and epinephrine, or by protein agonists such as thrombin and collagen. In 1878, Billroth stated that the spread of tumors could be brought about by the circulation of thrombi containing tumor cells. The adherence of the platelet-tumor cell emboli was observed post-mortem in a variety of animal model systems and by the use of microcinematography to study the time sequence of the interactions. Using homologous human systems, the chapter examines the aggregation of platelets and tumor cells, their attachment as mixed thrombi at the vessel wall, and individual susceptibilities to tumor cells among different donors. The perfusion studies with microvesicles showed that they were capable of stimulating platelet interaction with subendothelium in a manner similar to that observed with intact cells.
