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Cancer cachexia: an unmet need in cancer treatment


Cachexia is one of the most distressing and devastating experiences for cancer patients. It is now considered a complex, multifactorial metabolic syndrome characterized by anorexia, progressive and uncontrollable weight loss, fatigue, progressive depletion of adipose tissue and skeletal muscle, systemic inflammation, insulin resistance, abnormalities in the metabolism of carbohydrate, protein and lipid, as well as impaired immune function [1–3]. Within recent years substantial progress has been made in unraveling the underlying mechanisms of cancer cachexia [3–6]. Numerous cytokines including TNFα, IL1, IL6 and IFNγ have been postulated to play an important role in cachexia development [3–6]. These cytokines have been directly or indirectly implicated in cancer-induced muscle wasting by activating the ATP–ubiquitin–proteasome-dependent proteolytic pathway and profound anorexia by mimicking leptin signaling and suppressing orexigenic ghrelin and neuropeptide Y signaling [3–6].

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