한빛사논문
- 조회2,774
Abstract
Heidi Dvinge1,2*, Eunhee Kim3*, Omar Abdel-Wahab3,4 and Robert K. Bradley1,2
1 Computational Biology Program, Public Health Sciences Division, Fred Hutchinson Cancer Research Center. 2Basic Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. 3Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center. 4Leukemia Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
*These authors contributed equally to this work.
Correspondence to : Robert K. Bradley or Omar Abdel-Wahab
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.
논문정보
- Review Paper
- 2016년 06월 (BRIC 등록일 2016-06-16)
- 국외 연구진
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