Cancer anorexia-cachexia syndrome: Cytokines and neuropeptides

Eduardo J.B. Ramos, Susumu Suzuki, Daniel Marks, Akio Inui, Akihiro Asakawa, Michael M. Meguid

Research output: Contribution to journalReview article

143 Scopus citations

Abstract

Purpose of review: 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. Recent findings: 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 α; and Interferon γ). It is likely that close interrelation among these mediators exists in the hypothalamus, decreasing food intake and leading to cachexia. Summary: 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.

Original languageEnglish (US)
Pages (from-to)427-434
Number of pages8
JournalCurrent Opinion in Clinical Nutrition and Metabolic Care
Volume7
Issue number4
DOIs
StatePublished - Jul 1 2004

Keywords

  • Anorexia
  • Cachexia
  • Cytokine
  • Neuropeptide

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Nutrition and Dietetics

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