TUMOUR NECROSIS FACTOR ALPHA AND CANCER

Pragya Srivastava, Taniya* and Vaishali Bhagwani

ABSTRACT

Tumour necrosis factor-alpha (TNF-α, cachectin) is a member of the TNF superfamily. It was the first cytokine (cell signalling protein) to be evaluated for cancer biotherapy and its development. It is a multifunctional cytokine assuming a main job in apoptosis and cell survival just as in irritation and resistance. Still, the medical use of TNF-α is strictly limited by its noxiousness. Now, TNF-α is administered merely by locoregional drug delivery systems like isolated hepatic perfusion (IHP) and isolated limb perfusion (ILP). Meanwhile both of these processes are strictly challenging which require surgical procedure, they are chiefly used for the treatment of locally advanced sarcomas (solid tumours) like in-transit melanoma metastases, primary or metastatic unresectable liver carcinoma and limb- threatening soft tissue sarcomas. To decrease the toxicity in body of TNF-α, a number of schemes have been explored over the previous numerous decades. It has been exhibited in the detached appendage perfusion sitting that TNF-α acts synergistically with cytostatic drugs. The collaboration of TNF-α with TNF receptor 1 (TNFR-1) and TNF receptor 2 (TNFR-2) actuates a few flag transduction pathways, prompting the assorted elements of TNF-α. Tumour necrosis factor alpha produced mainly by activated macrophages, also it can be produced by many other cell types like mast cells (basophils), NK cells (natural killer cell), eosinophils (acidophils), CD4+ lymphocytes, neurons and neutrophils (polymorphs). It is involved in host defense and tissue homeostasis process. The biological effect of tumour necrosis factor alpha may ultimately beneficial or injurious to the host, depending on its period of tissue exposure, concentration and the existence of other mediators in the cellular environment. It shows antitumor activity and causes carcinoma, chronic inflammation, pulmonary, metabolic, cardiovascular, autoimmune and neurologic diseases.

Keywords: Interleukin, apoptosis, carcinoma, transferrin, tumour necrosis factor alpha.