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©2014 Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Aug 21, 2014; 20(31): 10752-10757
Published online Aug 21, 2014. doi: 10.3748/wjg.v20.i31.10752
Published online Aug 21, 2014. doi: 10.3748/wjg.v20.i31.10752
Emerging role of the KRAS-PDK1 axis in pancreatic cancer
Riccardo Ferro, Marco Falasca, Queen Mary University of London, Barts and The London School of Medicine and Dentistry, Blizard Institute, Inositide Signalling Group, United Kingdom
Author contributions: Ferro R and Falasca M solely contributed to this paper
Supported by Pancreatic Cancer Research Fund
Correspondence to: Marco Falasca, Professor, Queen Mary University of London, Barts and The London School of Medicine and Dentistry, Blizard Institute, Inositide Signalling Group, 4 Newark Street, London E1 2AT, United Kingdom. m.falasca@qmul.ac.uk
Telephone: +44-20-78828243 Fax: +44-20-78822186
Received: November 29, 2013
Revised: March 11, 2014
Accepted: March 19, 2014
Published online: August 21, 2014
Processing time: 263 Days and 22.3 Hours
Revised: March 11, 2014
Accepted: March 19, 2014
Published online: August 21, 2014
Processing time: 263 Days and 22.3 Hours
Core Tip
Core tip: Recent evidence suggests that protein kinase 1 (PDK1) is a key oncogenic driver in pancreatic cancer. Furthermore, PDK1 appears to be activated downstream the main pancreatic cancer oncogene KRAS that is mutated in nearly all pancreatic adenocarcinomas. This evidence suggests that PDK1 could represent a novel target in the treatment of pancreatic cancer.