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      Molecular Pathways: Cachexia Signaling—A Targeted Approach to Cancer Treatment

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          Abstract

          Cancer cachexia is a multifactorial syndrome characterized by an ongoing loss of skeletal muscle mass, which negatively impacts quality of life and portends a poor prognosis. Numerous molecular substrates and mechanisms underlie the dysregulation of skeletal muscle synthesis and degradation observed in cancer cachexia, including pro-inflammatory cytokines (TNF-α, IL-1 and IL-6), and the NF-kB, IGF1-AKT-mTOR, and myostatin/activin-SMAD pathways. Recent preclinical and clinical studies have demonstrated that anti-cachexia drugs (such as MABp1 and soluble receptor antagonist of myostatin/activin) not only prevent muscle wasting but may also prolong overall survival. In this review, we focus on the significance of cachexia signalling in cancer patients and highlight promising drugs targeting tumor cachexia in clinical development.

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          Author and article information

          Journal
          9502500
          8794
          Clin Cancer Res
          Clin. Cancer Res.
          Clinical cancer research : an official journal of the American Association for Cancer Research
          1078-0432
          25 June 2016
          23 June 2016
          15 August 2016
          15 February 2017
          : 22
          : 16
          : 3999-4004
          Affiliations
          [1 ]Division of Medical Oncology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, California
          [2 ]Department of Gastroenterological Surgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan
          Author notes
          Corresponding Author: Heinz-Josef Lenz, Division of Medical Oncology, Sharon Carpenter Laboratory, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, 1441 Eastlake Avenue, Los Angeles, CA 90033. Phone: 323-865-3967; Fax: 323-865-0061; lenz@ 123456usc.edu
          Article
          PMC4987228 PMC4987228 4987228 nihpa797269
          10.1158/1078-0432.CCR-16-0495
          4987228
          27340276
          9086b3ed-15df-4a3d-9ad5-4021d5c8d6aa
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