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Extrachromosomal DNA: Biogenesis and Functions in Cancer

Cancer Biology 1000年第1期8卷 135-153页

作者： Ellis J. Curtis John C. Rose Paul S. Mischel Howard Y. Chang 2Medical Scientist Training Program University of California San Diego La Jolla California USA 1Department of Pathology Stanford University School of Medicine Stanford California USA email: pmischel@stanford.edu 3Center for Personal Dynamic Regulomes Stanford University Stanford California USA email: howchang@stanford.edu 4Sarafan Chemistry Engineering and Medicine for Human Health (Sarafan ChEM-H) Stanford University Stanford California USA 5Howard Hughes Medical Institute Stanford California USA

In cancer, oncogenes can untether themselves from chromosomes onto circular, extrachromosomal DNA (ecDNA) particles. ecDNA are common in many of the most aggressive forms of cancer of women and men and of adults and children, and they contribute to treatment resistance and shorter survival for patients. Hiding in plain sight and missing from cancer genome maps, ecDNA was not, until recently, widely recognized to be an important feature of cancer pathogenesis. However, extensive new data demonstrate that ecDNA is a frequent and potent driver of aggressive cancer growth and treatment failure that can arise early or late in the course of the disease. The non-Mendelian genetics of ecDNA lies at the heart of the problem. By untethering themselves from chromosomes, ecDNA are randomly distributed to daughter cells during cell division, promoting high oncogene copy number, intratumoral genetic heterogeneity, accelerated tumor evolution, and treatment resistance due to rapid genome change. Further, the circular shape of ecDNA, and its high level of chromatin accessibility, promotes oncogene transcription and generates unique enhancer–promoter interactions in cis, as well as cooperative regulatory interactions between ecDNA particles in trans. In this review, we discuss the state of the field and its implications for patients with oncogene-amplified cancers.

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