Wang K, Baldwin GS, Nikfarjam M, He H. p21-activated kinase signalling in pancreatic cancer: New insights into tumour biology and immune modulation. World J Gastroenterol 2018; 24(33): 3709-3723 [PMID: 30197477 DOI: 10.3748/wjg.v24.i33.3709]
Corresponding Author of This Article
Hong He, MD, PhD, Senior Research Fellow, Department of Surgery, University of Melbourne, Austin Health, 145 Studley Rd., Heidelberg 3084, Victoria, Australia. hong.he@unimelb.edu.au
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Review
Open-Access Policy of This Article
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/
World J Gastroenterol. Sep 7, 2018; 24(33): 3709-3723 Published online Sep 7, 2018. doi: 10.3748/wjg.v24.i33.3709
p21-activated kinase signalling in pancreatic cancer: New insights into tumour biology and immune modulation
Kai Wang, Graham S Baldwin, Mehrdad Nikfarjam, Hong He
Kai Wang, Graham S Baldwin, Mehrdad Nikfarjam, Hong He, Department of Surgery, University of Melbourne, Melbourne 3084, Australia
Author contributions: Wang K reviewed the literature and drafted the manuscript; He H, Baldwin GS and Nikfarjam M revised the manuscript; all authors approved the final version of this review.
Conflict-of-interest statement: No potential 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: Hong He, MD, PhD, Senior Research Fellow, Department of Surgery, University of Melbourne, Austin Health, 145 Studley Rd., Heidelberg 3084, Victoria, Australia. hong.he@unimelb.edu.au
Telephone: +61-3-94965468
Received: May 22, 2018 Peer-review started: May 23, 2018 First decision: June 11, 2018 Revised: June 22, 2018 Accepted: June 27, 2018 Article in press: June 27, 2018 Published online: September 7, 2018 Processing time: 106 Days and 20 Hours
Core Tip
Core tip: Pancreatic cancer is still one of the most lethal malignancies, with a five-year survival of less than 8%. The dismal prognosis is largely the result of reprogramming of the tumour microenvironment, which leads to chemo-resistance and high aggressiveness. So far, combination chemotherapies can only marginally improve patients’ survival, but with high toxicity. Therefore, alternative treatment targeting protein kinase signalling has been proposed. As downstream effectors of Kras signalling, p21-activated kinases (PAKs) are positioned at the nexus of multiple oncogenic signalling pathways. Here, the importance of PAKs as therapeutic targets in Kras signalling is discussed, and their essential role in tumour biology and immune modulation within the tumour microenvironment is highlighted.
