Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/12678
Title: The role of p21-activated kinases in pancreatic cancer.
Austin Authors: Yeo, Dannel;He, Hong ;Baldwin, Graham S;Nikfarjam, Mehrdad 
Affiliation: From the Department of Surgery, University of Melbourne, Austin Health, Heidelberg, Melbourne, Victoria, Australia
Issue Date: 1-Apr-2015
Publication information: Pancreas; 44(3): 363-9
Abstract: Pancreatic cancer is an aggressive cancer with a poor prognosis and an overall 5-year survival rate of less than 5%. Management has not improved significantly over the last 30 years, and a better understanding of the genetic and molecular changes that occur is urgently required. Many of these changes appear to involve the p21-activated kinases (PAKs). The PAK family consists of 6 isoforms, 2 of which, PAK1 and PAK4, are up-regulated and/or hyperactivated in pancreatic cancer. p21-Activated kinases can mediate many different cellular processes especially those contributing to cancer development and progression. These processes include the regulation of cytoskeletal dynamics and cell adhesion, the evasion of apoptosis, and the promotion of cell survival, proliferation, migration, and invasion. p21-Activated kinases may also be involved in characteristics unique to pancreatic tumors, such as interplay with the pancreatic stroma, the re-emergence of embryonic pathways, and the involvement of a subset of microRNAs and heat shock proteins. This review highlights the potential role of PAKs in pancreatic cancer and provides a foundation for more effective therapeutics to improve our current treatment of pancreatic cancer.
Gov't Doc #: 25760284
URI: https://ahro.austin.org.au/austinjspui/handle/1/12678
DOI: 10.1097/MPA.0000000000000276
Journal: Pancreas
URL: https://pubmed.ncbi.nlm.nih.gov/25760284
Type: Journal Article
Appears in Collections:Journal articles

Show full item record

Page view(s)

4
checked on Mar 28, 2024

Google ScholarTM

Check


Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.