期刊
ANNUAL REVIEW OF PATHOLOGY-MECHANISMS OF DISEASE
卷 17, 期 -, 页码 367-386出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev-pathmechdis-051821-114223
关键词
extrachromosomal DNA; ecDNA; gene amplification; cancer genomics; tumor evolution; non-Mendelian inheritance
类别
资金
- Cancer Prevention and Research Institute of Texas [RR210034, R35-CA209919, U24CA264379, R01GM114362, RO1-CA238249]
This review discusses the formation and function of circular, extrachromosomal pieces of DNA (ecDNA) found in cancer, as well as their contribution to tumor pathogenesis, drug resistance, and accelerated cancer evolution.
Human genes are arranged on 23 pairs of chromosomes, but in cancer, tumor-promoting genes and regulatory elements can free themselves from chromosomes and relocate to circular, extrachromosomal pieces of DNA (ecDNA). ecDNA, because of its nonchromosomal inheritance, drives high-copy-number oncogene amplification and enables tumors to evolve their genomes rapidly. Furthermore, the circular ecDNA architecture fundamentally alters gene regulation and transcription, and the higher-order organization of ecDNA contributes to tumor pathogenesis. Consequently, patients whose cancers harbor ecDNA have significantly shorter survival. Although ecDNA was first observed more than 50 years ago, its critical importance has only recently come to light. In this review, we discuss the current state of understanding of how ecDNAs form and function as well as how they contribute to drug resistance and accelerated cancer evolution.
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