Metabolic dysfunction contributes to the clinical deterioration observed in advanced cancer patients and is characterized by weight loss, skeletal muscle wasting, and atrophy of the adipose tissue. This systemic syndrome, termed cancer-associated cachexia (CAC), is a major cause of morbidity and mortality. While once attributed solely to decreased food intake, the present description of cancer cachexia is a disorder of multiorgan energy imbalance. Here we review the molecules and pathways responsible for metabolic dysfunction in CAC and the ideas that led to the current understanding.EFW is supported by a grant from the Spanish Ministry of Economy (BFU2012-40230) and a European Research Council Advanced Grant (ERC FCK/2008/37).This is the author accepted manuscript. It is currently embargoed pending publication
