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World J Gastrointest Surg. Dec 27, 2018; 10(9): 95-106
Published online Dec 27, 2018. doi: 10.4240/wjgs.v10.i9.95
Molecular therapeutic strategies targeting pancreatic cancer induced cachexia
Anastasiya Yakovenko, Miles Cameron, Jose Gilberto Trevino
Anastasiya Yakovenko, Miles Cameron, University of Florida College of Medicine, Gainesville, Florida 32610, United States
Jose Gilberto Trevino, Department of Surgery, University of Florida Health Sciences Center, Gainesville, Florida 32610, United States
Author contributions: Yakovenko A and Trevino JG designed research; Yakovenko A performed research; Yakovenko A, Cameron M, and Trevino JG analyzed data; Yakovenko A critically interpreted the data; Yakovenko A and Cameron M wrote the manuscript; Yakovenko A, Cameron M and Trevino JG performed critical revisions.
Conflict-of-interest statement: The authors declare that there is no conflict of interest regarding the publication of this paper.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Corresponding author: Jose Gilberto Trevino, MD, Assistant Professor, Department of Surgery, University of Florida College of Medicine, 1600 SW Archer Road, PO Box 100109, Gainesville, FL32610, United States. jose.trevino@surgery.ufl.edu
Telephone: +1-352-2650761
Received: August 9, 2018
Peer-review started: August 9, 2018
First decision: October 22, 2018
Revised: November 1, 2018
Accepted: November 27, 2018
Article in press: November 27, 2018
Published online: December 27, 2018
Core Tip

Core tip: Pancreatic cancer (PC) induced cachexia is a complex metabolic syndrome associated with increased morbidity, mortality and reduced quality of life. The complex pathophysiology of cachexia involves muscle wasting, systemic inflammation, and metabolic alterations. Molecular signaling pathways responsible for muscle wasting include TGF-β, myostatin/activin, IGF-1/PI3K/Akt, and JAK-STAT. IL-6, TNF-α, and INF-γ are the most well studied pro-cachectic cytokines that promote systemic inflammation. Metabolic alterations such as increased energy expenditure and glycolytic pathway dysfunction could be potentially improved with ketonemia, silibinin, and ω3-polyunsaturated fatty acids. Targeting molecular signaling pathways in PC induced cachexia could lead to discovery of effective therapies.