title: Fn14: a new player in cancer-induced cachexia.
abstract: Although cancer cachexia is a very significant condition that is present in up to 80% of cancer cases, the cause of the condition has remained a puzzle. Cancer cachexia is a condition which is mainly characterised by muscle wasting, mobilization of fat reserves, and overall metabolic disturbance. This review aims to highlight some of the recent findings in cancer cachexia research.
  
  
  
  It has been recently demonstrated that the expression of a single receptor, fibroblast growth factor-inducible 14, on a tumour can initiate cachexia and that this can be completely ablated by treatment with an antibody against this receptor. Also recently described was the role of parathyroid hormone receptor-binding proteins in causing cachexia through a mechanism where white adipose tissue is replaced with brown adipose tissue. In parallel, work done in drosophila suggests that the impaired insulin signalling is a direct cause of cancer cachexia through the release of an insulin growth factor binding protein that inhibits insulin and insulin-like growth factor 1 signalling.
  
  
  
  Successful therapies are urgently needed to combat cancer cachexia in the clinic. Recent research is making progress toward discovering the underlying molecular causes of the condition, which could lead to new therapeutic approaches and in the future contribute to more positive clinical outcomes for cancer sufferers.
authors.affiliation: Department of Biochemistry and Genetics, La Trobe Institute for Molecular Science, La Trobe University, Melbourne, Victoria 3086, Australia.
authors.forename: Amelia J
authors.initials: AJ
authors.lastname: Johnston
authors.forename: Nicholas J
authors.initials: NJ
authors.lastname: Hoogenraad
mesh_terms: D050156:Adipogenesis / Q000187:drug effects; D002001:Adipose Tissue, Brown / Q000187:drug effects / Q000378:metabolism; D052436:Adipose Tissue, White / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D000970:Antineoplastic Agents / Q000627:therapeutic use; D002100:Cachexia / Q000209:etiology* / Q000378:metabolism / Q000517:prevention & control; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D006801:Humans; D009363:Neoplasm Proteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D009369:Neoplasms / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D000074050:TWEAK Receptor / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*
chemical_list: D000970:Antineoplastic Agents; D009363:Neoplasm Proteins; C000613297:TNFRSF12A protein, human; D000074050:TWEAK Receptor