Biologic Effects of Tumor Necrosis Factors Alpha and Beta
As early as 1891, clinical reports suggested that major components of the cell wall of gram-negative bacteria such as endotoxins were associated with antitumor activities; Bruns (1) and Coley (2) described the regression of tumors in patients with tumors who were deliberately injected with mixtures of killed bacterial toxins. Gratia and Linz (3) and Shear et al. (4) subsequently demonstrated that bacterial filtrates or endotoxins were capable of inducing hemorrhagic necrosis of specific transplanted tumors. A significant advance in distinguishing the effects of endotoxin from a specific “tumor necrosis factor” was reported in 1975 by Carswell et al. (5). They were impressed with the observations and hypothesis of Algire (6), who suggested that hemorrhagic necrosis of tumors might be secondary to endotoxin-induced hypotension resulting in circulatory stasis and ischemia of the tumor. They argued, however, that rather than an indirect action, endotoxin probably caused the host to release a factor that was directly toxic to the tumor. This hypothesis led Carswell et al. (5) to the discovery of an endotoxin-induced serum factor, which caused necrosis of tumors and which they termed tumor necrosis factor (TNF-like).
KeywordsToxicity Ischemia Leukemia Lipase Superoxide
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