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©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Aug 21, 2016; 22(31): 7046-7057
Published online Aug 21, 2016. doi: 10.3748/wjg.v22.i31.7046
Published online Aug 21, 2016. doi: 10.3748/wjg.v22.i31.7046
Therapeutic potential of targeting acinar cell reprogramming in pancreatic cancer
Chi-Hin Wong, You-Jia Li, Yang-Chao Chen, School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China
Yang-Chao Chen, Shenzhen Research Institute, The Chinese University of Hong Kong, Shenzhen 518172, Guangdong Province, China
Author contributions: Wong CH, Li YJ and Chen YC wrote the paper.
Supported by the General Research Fund, Research Grants Council of Hong Kong , No. CUHK462211 , No. CUHK462713 and No. 14102714 ; and the National Natural Science Foundation of China , No. 81101888 and No. 8142730 .
Conflict-of-interest statement: The authors have no conflicts of interest.
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/
Correspondence to: Yang-Chao Chen, PhD, Associate Professor, School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, NT, Hong Kong, China. b110796@mailserv.cuhk.edu.hk
Telephone: +852-394-31100 Fax: +852-260-35123
Received: April 9, 2016
Peer-review started: April 10, 2016
First decision: May 12, 2016
Revised: June 10, 2016
Accepted: June 28, 2016
Article in press: June 28, 2016
Published online: August 21, 2016
Peer-review started: April 10, 2016
First decision: May 12, 2016
Revised: June 10, 2016
Accepted: June 28, 2016
Article in press: June 28, 2016
Published online: August 21, 2016
Core Tip
Core tip: Treating pancreatic ductal adenocarcinoma (PDAC) remains challenging due to the lack of effective therapeutics. Apart from pancreatic duct cells, acinar cells may also be the origin of PDAC. During pancreatitis or combined with activating KRasG12D mutation, acinar cells undergo a transdifferentiation process called acinar-to-ductal-metaplasia (ADM), forming duct cells which may then be transformed into PanIN and eventually PDAC. This process involves MAPK, Wnt, Notch and PI3K/Akt signaling. Since ADM may be a reversible process, switching PDAC back to normal cells may also be achieved and developed as a novel therapy.