Tumor angiogenesis inhibition by prostaglandin synthetase inhibitors.
The release of prostaglandins from tumor cells seems to play an important role in tumor angiogenesis, in which platelet-derived factors may be also included. Administration of prostaglandin synthetase inhibitors reduces the growth of both experimental and human malignant tumors. One explanation may be reduced tumor vascularization, as observed in microangiographic studies of experimental transplantable tumors. A similar effect was observed after induced thrombocytopenia. A number of angiogenesis stimulating factors have been isolated from tumors during recent years. Factors released from host cells in the tumor area (e.g., mast cells, macrophages) with similar properties may also contribute to tumor vascularization. This seems to make stimulation of tumor angiogenesis to a rather complicated cascade of events, about which more must be learned before efficient inhibition of tumor vascularization can be attained. The target cell for angiogenesis stimulation, the endothelial cell, seems increasingly important as an object for future studies.
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Peterson
D000818:Animals; D001792:Blood Platelets / Q000502:physiology; D016861:Cyclooxygenase Inhibitors; D004727:Endothelium / Q000502:physiology; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D009374:Neoplasms, Experimental / Q000098:blood supply*; D009389:Neovascularization, Pathologic; D011453:Prostaglandins / Q000502:physiology; D011817:Rabbits; D013921:Thrombocytopenia / Q000503:physiopathology
D016861:Cyclooxygenase Inhibitors; D011453:Prostaglandins; D007213:Indomethacin