Journal
NATURE REVIEWS CANCER
Volume 16, Issue 7, Pages 413-430Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nrc.2016.51
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Funding
- US Department of Defense Breast Cancer Research Program [W81XWH-14-1-0044]
- Worldwide Cancer Research Fund
- Edward P. Evans Foundation
- Department of Defense Bone Marrow Failure Research Program [BM150092]
- National Institutes of Health/National Heart, Lung and Blood Institute (NIH/NHLBI) [R01 HL128239]
- NIH K08 Clinical Investigator Award [1K08CA160647-01]
- US Department of Defense Postdoctoral Fellow Award in Bone Marrow Failure Research [W81XWH-12-1-0041]
- Starr Cancer Consortium [I8-A8-075]
- Josie Robertson Investigator Program
- Evans Foundation
- Mr William H. Goodwin and Mrs Alice Goodwin Commonwealth Foundation for Cancer Research
- Experimental Therapeutics Center of Memorial Sloan Kettering Cancer Center
- Ellison Medical Foundation [AG-NS-1030-13]
- NIH/National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) [R01 DK103854]
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The recent genomic characterization of cancers has revealed recurrent somatic point mutations and copy number changes affecting genes encoding RNA splicing factors. Initial studies of these 'spliceosomal mutations' suggest that the proteins bearing these mutations exhibit altered splice site and/or exon recognition preferences relative to their wild-type counterparts, resulting in cancer-specific mis-splicing. Such changes in the splicing machinery may create novel vulnerabilities in cancer cells that can be therapeutically exploited using compounds that can influence the splicing process. Further studies to dissect the biochemical, genomic and biological effects of spliceosomal mutations are crucial for the development of cancer therapies targeted at these mutations.
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