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TNF-α in Cancer Treatment


Tumor necrosis factor alpha (TNF-α) is a multifunctional cytokine playing a key role in apoptosis and cell survival as well as in inflammation and immunity. Although named for its antitumor properties, TNF has been implicated in a wide spectrum of other diseases. The current use of TNF in cancer is in the regional treatment of locally advanced soft tissue sarcomas and metastatic melanomas and other irresectable tumors of any histology to avoid amputation of the limb. It has been demonstrated in the isolated limb perfusion setting that TNF-α acts synergistically with cytostatic drugs. 


ELISA(enzyme-linked immunosorbent assay) is a method for detecting the concentration of some kind antigen or antibody,such as TNF-α, using the characteristic of specific binding between antigen-antibody. The method is suitable for determination of cell culture supernatant, serum, plasma,tissue fluid, and urine samples. Meretciel provide high quality ELISA kits for R&D,can study the role of TNF-α in cancer.

The interaction of TNF-α with TNF receptor 1 and receptor 2 (TNFR-1, TNFR-2) activates several signal transduction pathways, leading to the diverse functions of TNF-α. The signaling molecules of TNFR-1 have been elucidated quite well, but regulation of the signaling remains unclear. Besides extravasation of erythrocytes and lymphocytes, leading to hemorrhagic necrosis, TNF-α targets the tumor-associated vasculature (TAV) by inducing hyperpermeability and destruction of the vascular lining. This results in an immediate effect of selective accumulation of cytostatic drugs inside the tumor and a late effect of destruction of the tumor vasculature. 

It is widely known that TNF-α induces hemorrhagic necrosis in a certain set of tumor types. To investigate the underlying mechanisms of TNF-α action during ILP of solid tumors in humans, scientists set up perfusion models in rats and reported that hemorrhagic necrosis was much greater in tumors treated with TNF-α and chemotherapeutic drugs. In addition, we showed a synergistic antitumor effect of the combination treatment with TNF-α and chemotherapeutic drugs. In contrast, TNF-α alone induced only a mild central necrosis, and there was no objective tumor response observed. 

These observations are comprehensible clues that mechanisms underlying the TNF-α effect during solid tumor treatment cannot be caused by a direct cytotoxic or cytostatic effect of TNF-α toward the tumor cells. It was suggested that, rather than tumor cells themselves, cells of the tumor stroma may be responsible for the observed antitumor effect of TNF-α in patients. This hypothesis was confirmed by data from mice experiments revealing that TNF-α had a cytotoxic effect on tumor vasculature.
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