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©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Clin Oncol. Oct 10, 2015; 6(5): 92-95
Published online Oct 10, 2015. doi: 10.5306/wjco.v6.i5.92
Published online Oct 10, 2015. doi: 10.5306/wjco.v6.i5.92
Modulators of alternative splicing as novel therapeutics in cancer
Sebastian Oltean, School of Physiology and Pharmacology, University of Bristol, Bristol BS1 3NY, United Kingdom
Author contributions: Oltean S solely contributed to this work.
Supported by BBSRC (Biotechnology and Biological Sciences Research Council) United Kingdom and Richard Bright VEGF Research Trust.
Conflict-of-interest statement: The author has no conflict of interests.
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: Sebastian Oltean, MD, PhD, School of Physiology and Pharmacology, University of Bristol, Dorothy Hodgkin Building, Whitson Street, Bristol BS1 3NY, United Kingdom. sebastian.oltean@bristol.ac.uk
Telephone: +44-117-3313165 Fax: +44-117-3313169
Received: May 26, 2015
Peer-review started: May 29, 2015
First decision: June 18, 2015
Revised: July 8, 2015
Accepted: July 29, 2015
Article in press: August 3, 2015
Published online: October 10, 2015
Processing time: 139 Days and 15.3 Hours
Peer-review started: May 29, 2015
First decision: June 18, 2015
Revised: July 8, 2015
Accepted: July 29, 2015
Article in press: August 3, 2015
Published online: October 10, 2015
Processing time: 139 Days and 15.3 Hours
Core Tip
Core tip: Genome-wide studies have recently shown that more than 90% of genes are alternatively spliced in humans. This makes alternative splicing (AS) one of the main drivers of proteomic diversity. Numerous splice isoforms have been described to be associated with cancer. Additionally several splice factors have been shown to have oncogene or tumour suppressors activities. Beside the implications for cancer pathogenesis, de-regulated AS is recognized as one of the novel areas of cell biology where therapeutic manipulations may be designed. This editorial discusses the possibilities of manipulation of AS for therapeutic benefit in cancer.