TY - JOUR
T1 - Cancer anorexia-cachexia syndrome
T2 - Cytokines and neuropeptides
AU - Ramos, Eduardo J.B.
AU - Suzuki, Susumu
AU - Marks, Daniel
AU - Inui, Akio
AU - Asakawa, Akihiro
AU - Meguid, Michael M.
PY - 2004/7
Y1 - 2004/7
N2 - 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.
AB - 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.
KW - Anorexia
KW - Cachexia
KW - Cytokine
KW - Neuropeptide
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U2 - 10.1097/01.mco.0000134363.53782.cb
DO - 10.1097/01.mco.0000134363.53782.cb
M3 - Review article
C2 - 15192446
AN - SCOPUS:14844320127
SN - 1363-1950
VL - 7
SP - 427
EP - 434
JO - Current Opinion in Clinical Nutrition and Metabolic Care
JF - Current Opinion in Clinical Nutrition and Metabolic Care
IS - 4
ER -