Mechanisms of tandem duplication in the cancer genome

IF 3 3区 生物学 Q2 GENETICS & HEREDITY
Ralph Scully , Dominik Glodzik , Francesca Menghi , Edison T. Liu , Cheng-Zhong Zhang
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引用次数: 0

Abstract

Tandem duplications (TD) are among the most frequent type of structural variant (SV) in the cancer genome. They are characterized by a single breakpoint junction that defines the boundaries and the size of the duplicated segment. Cancer-associated TDs often increase oncogene copy number or disrupt tumor suppressor gene function, and thus have important roles in tumor evolution. TDs in cancer genomes fall into three classes, defined by the size of duplications, and are associated with distinct genetic drivers. In this review, we survey key features of cancer-related TDs and consider possible underlying mechanisms in relation to stressed DNA replication and the 3D organization of the S phase genome.
癌症基因组串联复制的机制。
串联重复(TD)是癌症基因组中最常见的结构变异(SV)类型之一。它们的特点是一个单一的断点连接,定义了边界和重复段的大小。癌症相关的TDs通常会增加癌基因拷贝数或破坏肿瘤抑制基因功能,因此在肿瘤进化中具有重要作用。癌症基因组中的TDs分为三类,由重复的大小定义,并与不同的遗传驱动因素相关。在这篇综述中,我们调查了癌症相关TDs的关键特征,并考虑了与应激DNA复制和S期基因组三维组织相关的可能潜在机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
DNA Repair
DNA Repair 生物-毒理学
CiteScore
7.60
自引率
5.30%
发文量
91
审稿时长
59 days
期刊介绍: DNA Repair provides a forum for the comprehensive coverage of DNA repair and cellular responses to DNA damage. The journal publishes original observations on genetic, cellular, biochemical, structural and molecular aspects of DNA repair, mutagenesis, cell cycle regulation, apoptosis and other biological responses in cells exposed to genomic insult, as well as their relationship to human disease. DNA Repair publishes full-length research articles, brief reports on research, and reviews. The journal welcomes articles describing databases, methods and new technologies supporting research on DNA repair and responses to DNA damage. Letters to the Editor, hot topics and classics in DNA repair, historical reflections, book reviews and meeting reports also will be considered for publication.
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