Cancer cachexia: mediators, signaling, and metabolic pathways.
Cancer cachexia is characterized by a significant reduction in body weight resulting predominantly from loss of adipose tissue and skeletal muscle. Cachexia causes reduced cancer treatment tolerance and reduced quality and length of life, and remains an unmet medical need. Therapeutic progress has been impeded, in part, by the marked heterogeneity of mediators, signaling, and metabolic pathways both within and between model systems and the clinical syndrome. Recent progress in understanding conserved, molecular mechanisms of skeletal muscle atrophy/hypertrophy has provided a downstream platform for circumventing the variations and redundancy in upstream mediators and may ultimately translate into new targeted therapies.
Clinical Surgery, School of Clinical Sciences and Community Health, University of Edinburgh, Royal Infirmary, Edinburgh EH16 4SA, UK. k.fearon@ed.ac.uk
Kenneth C H
KC
Fearon
David J
DJ
Glass
Denis C
DC
Guttridge
D028341:Activins / Q000378:metabolism; D002100:Cachexia / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy; D006801:Humans; D015850:Interleukin-6 / Q000378:metabolism; D008066:Lipolysis / Q000502:physiology*; D053858:Metabolic Networks and Pathways / Q000502:physiology*; D008954:Models, Biological; D009133:Muscular Atrophy / Q000378:metabolism / Q000503:physiopathology*; D055435:Myostatin / Q000378:metabolism; D009369:Neoplasms / Q000150:complications*; D015398:Signal Transduction / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D015850:Interleukin-6; D055435:Myostatin; D014409:Tumor Necrosis Factor-alpha; D028341:Activins