Endothelial injury caused by antineoplastic agents.
The vascular lining of the blood vessels to normal organs and malignant tissues would be expected to reflect the functional demands placed upon it. These functional requirements may be accomplished by specific biochemical macromolecules, some of which are localized on the plasma membrane of the endothelium. Considerable evidence exists that toxicity to at least some normal organs caused by antineoplastic agents is heralded by endothelial damage. This endothelial damage may reflect a specific drug-endothelium interaction, the mechanism and basis of which are not yet understood. The possibility also exists that destruction of solid tumors by currently employed antitumor agents is mediated in part by local loss of essential vasculature. Selective destruction of the tumor endothelium could be a rational and novel target to which drugs could be designed.
D000818:Animals; D000970:Antineoplastic Agents; D001761:Bleomycin; D001808:Blood Vessels / Q000187:drug effects* / Q000528:radiation effects; D003520:Cyclophosphamide; D004727:Endothelium / Q000187:drug effects / Q000502:physiology / Q000648:ultrastructure; D006801:Humans; D007365:Intercellular Junctions; D009369:Neoplasms / Q000098:blood supply; D009607:Nitrosourea Compounds
D000970:Antineoplastic Agents; D009607:Nitrosourea Compounds; D001761:Bleomycin; D003520:Cyclophosphamide