[Cancer blood-borne metastasis and platelets].
Platelet aggregation plays an important role in the phase of arrest of tumor cells in the microcirculation of the metastatic site in blood-borne metastasis. Hyper-aggregability of platelets, hypercoagulability and suppression of fibrinolysis accelerate the adhesion of tumor cells in the microcirculation of the target organ, but it may be inhibited by suppression of platelet aggregation, biosynthesis of thromboxane A2 and the coagulation system. Platelet aggregation is induced by not only metabolites of arachidonic acid but also factors released from tumor cells. Thromboxane A2 and prostaglandin I2 may play a role in blood-borne metastasis.
D000818:Animals; D001792:Blood Platelets / Q000502:physiology*; D011464:Epoprostenol / Q000502:physiology; D005342:Fibrinolysis; D008175:Lung Neoplasms / Q000097:blood / Q000473:pathology; D008297:Male; D008545:Melanoma / Q000097:blood / Q000473:pathology; D051379:Mice; D008819:Mice, Nude; D009374:Neoplasms, Experimental / Q000097:blood / Q000473:pathology*; D009360:Neoplastic Cells, Circulating; D010974:Platelet Aggregation; D051381:Rats; D013928:Thromboxane A2 / Q000502:physiology
D013928:Thromboxane A2; D011464:Epoprostenol