Cancer Associated Cachexia; Etiopathogenesis, Molecular Mechanisms and Therapeutic StrategiesMohamed Hassan1,2,3*, Abdelouahid El-khattouiti1, Youssef Haikel2,3 and Mossaad Megahed4
- *Corresponding Author:
- Mohamed Hassan
Cancer Institute, University of Mississippi
Medical Center, Jackson, MS, USA
Tel: +1 601 815 8945
Fax: +1 601 984 2981 E-mail: [email protected]
Received Date: July 10, 2014; Accepted Date: August 21, 2014; Published Date: August 23, 2014
Citation: Hassan M, El-khattouiti A, Haikel Y, Megahed M (2014) Cancer Associated Cachexia; Etiopathogenesis, Molecular Mechanisms and Therapeutic Strategies. J Cytol Histol 5: 271. doi: 10.4172/2157-7099.1000271
Copyright: © 2014 Hassan M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Cachexia is a multifunctional syndrome that is characterized by anorexia and extensive loss of adipose tissue and skeletal muscle, is common in many chronic and advanced diseases. Most of cancer patients show variable patterns of body loss that is known as cancer associated cachexia (CAC). Although CAC share common characteristics, the severity of this disease is variable, and seems to be tumor type, site and stage-dependent. The etiology of cachexia is attributed to abnormal metabolism that is thought to be mediated by tumor- and host-derived cytokines and factors. Although the role of cytokines in the etiology of CAC has been reported, the molecular mechanisms regulating its occurrence in cancer patients are not described in details. This review focuses on the etiopathogenesis of CAC and the underlying mechanisms.