title: Cancer anorexia-cachexia syndrome: cytokines and neuropeptides.
abstract: OBJECTIVE
  Cancer anorexia-cachexia syndrome is observed in 80% of patients in the advanced stages of cancer and is a strong independent risk factor for mortality. Numerous cytokines produced by tumor and immune cells, interacting with the neuropeptidergic system, mediate the cachectic effect of cancer. Since there is currently no effective pharmacological treatment and the anorexia-cachexia syndrome continues to be defined biochemically, we review the role of cytokines and neuropeptides in this process.
  
  
  RESULTS
  Currently data suggest that cancer anorexia-cachexia syndrome results from a multifactorial process involving many mediators, including hormones (e.g. leptin), neuropeptides (e.g. neuropeptide Y, melanocortin, melanin-concentrating hormone and orexin) and cytokines (e.g. interleukin 1, interleukin 6, tumor necrosis factor alpha and interferon gamma). It is likely that close interrelation among these mediators exists in the hypothalamus, decreasing food intake and leading to cachexia.
  
  
  CONCLUSIONS
  In the pathogenesis of cancer anorexia, cytokines play a pivotal role influencing the imbalance of orexigenic and anorexigenic circuits that regulate the homeostatic loop of body-weight regulation, leading to cachexia. Interfering pharmacologically with cytokine expression or neural transduction of cytokine signals can be an effective therapeutic strategy in anorectic patients before they develop cancer anorexia-cachexia syndrome.
authors.affiliation: Surgical Metabolism and Nutrition Laboratory, Neuroscience Program, Department of Surgery, University Hospital, Upstate Medical University, Syracuse, NY 13210, USA.
authors.forename: Eduardo J B
authors.initials: EJ
authors.lastname: Ramos
authors.forename: Susumu
authors.initials: S
authors.lastname: Suzuki
authors.forename: Daniel
authors.initials: D
authors.lastname: Marks
authors.forename: Akio
authors.initials: A
authors.lastname: Inui
authors.forename: Akihiro
authors.initials: A
authors.lastname: Asakawa
authors.forename: Michael M
authors.initials: MM
authors.lastname: Meguid
mesh_terms: D000818:Animals; D000855:Anorexia / Q000209:etiology / Q000503:physiopathology*; D002100:Cachexia / Q000209:etiology / Q000503:physiopathology*; D016207:Cytokines / Q000378:metabolism / Q000502:physiology*; D054439:Ghrelin; D006801:Humans; D020738:Leptin / Q000378:metabolism / Q000502:physiology; D009369:Neoplasms / Q000150:complications / Q000503:physiopathology*; D009479:Neuropeptides / Q000378:metabolism / Q000502:physiology*; D036361:Peptide Hormones / Q000378:metabolism / Q000502:physiology; D013577:Syndrome
chemical_list: D016207:Cytokines; D054439:Ghrelin; D020738:Leptin; D009479:Neuropeptides; D036361:Peptide Hormones