[Inhibition of metastasis by anti-platelet agents-prostaglandins].
The role of platelets in the development of blood-borne metastasis is overviewed, referring to our own experimental data. Platelets interact with tumor cells in circulation or in capillary beds to form tumor thrombi which accelerate the lodging process of metastasis. This interaction is mediated by platelet aggregating substances, such as ADP, thrombin-forming substance and certain membrane proteins from tumor cells. The aggregation of platelets is followed by secretion of various growth factors including PDGF, EGF and TGF-beta although the implication of these factors in growth promotion of metastatic foci is presently uncertain. Certain antiplatelet agents, particularly prostacyclin and prostaglandin E1 inhibit pulmonary metastasis in animal models and thus appear to be potentially useful in the prophylaxis of metastasis.
D000818:Animals; D001792:Blood Platelets / Q000502:physiology*; D004317:Doxorubicin / Q000494:pharmacology; D011464:Epoprostenol / Q000494:pharmacology*; D006801:Humans; D008114:Liver Neoplasms, Experimental / Q000097:blood / Q000473:pathology; D051379:Mice; D009362:Neoplasm Metastasis / Q000473:pathology*; D009374:Neoplasms, Experimental / Q000097:blood / Q000473:pathology*; D009360:Neoplastic Cells, Circulating; D010974:Platelet Aggregation; D011458:Prostaglandins E / Q000494:pharmacology*; D051381:Rats
D011458:Prostaglandins E; D004317:Doxorubicin; D011464:Epoprostenol