title: Modeling human cancer cachexia in colon 26 tumor-bearing adult mice.
abstract: BACKGROUND
  Muscle wasting is a profound side effect of advanced cancer. Cancer-induced cachexia decreases patient quality of life and is associated with poor patient survival. Currently, no clinical therapies exist to treat cancer-induced muscle wasting. Although cancers commonly associated with cachexia occur in older individuals, the standard animal models used to elucidate the causes of cachexia rely on juvenile mice.
  
  
  METHODS
  In an effort to better model human cancer cachexia, we determined whether cachectic features seen in young mice could be achieved in adult, pre-sarcopenic mice following colon 26 (C-26) tumor cell inoculation.
  
  
  RESULTS
  Both young and adult mice developed similar-sized tumors and progressed to cachexia with similar kinetics, as evidenced by losses in body mass, and adipose and skeletal muscle tissues. Proteolytic signaling, including proteasome and autophagy genes, was also increased in muscles from both young and adult tumor-bearing animals. Furthermore, tumor-associated muscle damage and activation of Pax7 progenitor cells was induced in both young and adult mice.
  
  
  CONCLUSIONS
  Although cancer cachexia generally occurs in older individuals, these data suggest that the phenotype and underlying mechanisms can be effectively modeled using the currently accepted protocol in juvenile mice.
authors.affiliation: Department of Molecular Virology, Immunology, and Medical Genetics, Human Cancer Genetics Program, and the Arthur G. James Comprehensive Cancer Center, The Ohio State University College of Medicine, 460 W. 12th Avenue, Columbus, OH, 43210, USA, erin.talbert@osumc.edu.
authors.forename: Erin E
authors.initials: EE
authors.lastname: Talbert
authors.forename: Gregory A
authors.initials: GA
authors.lastname: Metzger
authors.forename: Wei A
authors.initials: WA
authors.lastname: He
authors.forename: Denis C
authors.initials: DC
authors.lastname: Guttridge