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Tumor necrosis factor a (TNF) is a potent, pleiotropic, proinflammatory cytokine that is produced by macrophages, neutrophils, fibroblasts, keratinocytes, NK, T-and B-cells and also by tumor cells. TNF binds to either of two receptors, TNF-R1 or TNF-R2, expressed on virtually all mammalian cell types. TNF was named because of its ability, when administered in pharmacologic doses, to cause necrosis of tumors in experimental models. Recombinant TNF is approved in Europe to be given locoregionally as a therapy for sarcoma. TNF produced by the body mediates host responses in acute and chronic inflammatory conditions and aids in host protection from infection and malignancy. The biology of the TNF/TNF-receptor system was reviewed by Palladino et al. 2003 (1). [ABSTRACT FROM AUTHOR]

Cachexia is characterised by accelerated loss of adipose tissue and skeletal muscle in the context of a chronic inflammatory response [1] [3]. It is a common complication of advanced cancer [4]. About half of all cancer patients suffer from this syndrome, which is among the most debilitating and life-threatening complications [5]. The key feature of this syndrome is weight loss, but other symptoms, such as anorexia, fatigue, vomiting and anaemia, and accelerated malnutrition with depletion of whole-body lipid and protein stores are frequently observed. Cancer cachexia contributes to immobility, a propensity to infection, shortened duration of survival, and overall decreased quality of life [6]. [ABSTRACT FROM AUTHOR]