한빛사논문
- 조회1,114
Eunhee Yi 1,8, Rocío Chamorro González 2,3,4,8, Anton G. Henssen 2,3,4,5,6,* and Roel G. W. Verhaak 1,7,*
1The Jackson Laboratory for Genomic Medicine, Farmington, CT, USA.
2Department of Paediatric Oncology/Hematology, Charité-Universitätsmedizin Berlin, Berlin, Germany.
3Experimental and Clinical Research Center (ECRC) of the MDC and Charité Berlin, Berlin, Germany.
4Max-Delbrück-Centrum für Molekulare Medizin (BIMSB/BIH), Berlin, Germany.
5Berlin Institute of Health, Berlin, Germany.
6German Cancer Consortium (DKTK), partner site Berlin and German Cancer Research Center (DKFZ), Heidelberg, Germany.
7Department of Neurosurgery, Amsterdam UMC, Amsterdam, the Netherlands.
8These authors contributed equally: Eunhee Yi, Rocío Chamorro González.
*Corresponding author.
Abstract
Extrachromosomal DNA (ecDNA) amplification is an important driver alteration in cancer. It has been observed in most cancer types and is associated with worse patient outcome. The functional impact of ecDNA has been linked to its unique properties, such as its circular structure that is associated with altered chromatinization and epigenetic regulatory landscape, as well as its ability to randomly segregate during cell division, which fuels intercellular copy number heterogeneity. Recent investigations suggest that ecDNA is structurally more complex than previously anticipated and that it localizes to specialized nuclear bodies (hubs) and can act in trans as an enhancer for genes on other ecDNAs or chromosomes. In this Review, we synthesize what is currently known about how ecDNA is generated and how its genetic and epigenetic architecture affects proto-oncogene deregulation in cancer. We discuss how recently identified ecDNA functions may impact oncogenesis but also serve as new therapeutic vulnerabilities in cancer.
논문정보
- Review Paper
- 2022년 08월 (BRIC 등록일 2022-08-12)
- 국외 연구진
- 의약학 > 종양의학
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