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Nat Rev Cancer. 2016 Jul;16(7):413-30. doi: 10.1038/nrc.2016.51. Epub 2016 Jun 10.

RNA splicing factors as oncoproteins and tumour suppressors.

Author information

1
Computational Biology Program, Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA.
2
Basic Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA.
3
Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
4
Leukemia Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.

Abstract

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.

PMID:
27282250
PMCID:
PMC5094465
DOI:
10.1038/nrc.2016.51
[Indexed for MEDLINE]
Free PMC Article

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