RNA splicing factors as oncoproteins and tumor suppressors
By H. Dvinge, Eunhee Kim, O. Abdel-Wahab, Robert K. Bradley. Nature Reviews. Cancer, 2016
612 citations recorded by the source corpus.
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.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/7b0776f964195d84f22f8801c3bf17623663f771
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In Molecular Biology
Citations in the corpus
- Anticancer sulfonamides target splicing by inducing RBM39 degradation via recruitment to DCAF15 (2017, background): “Many of the proteins important for pre-mRNA splicing have no enzymatic activity, however, and are thus challenging to target with small molecules (2).”