Mechanisms of metabolic dysfunction in cancer-associated cachexia

  1. Erwin F. Wagner2
  1. 1Department of Oncology, The Medical Research Council Cancer Unit, University of Cambridge, Addenbrooke's Hospital, Cambridge CB2 0QQ, United Kingdon;
  2. 2Genes, Development, and Disease Group, Cancer Cell Biology Programme, Centro Nacional de Investigaciones Oncológicas, Madrid 28029, Spain
  1. Corresponding authors: ewagner{at}cnio.es, mp753{at}cam.ac.uk

Abstract

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.

Keywords

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

| Table of Contents

Life Science Alliance