Research Department of Pathology, Cancer Institute, University College London, London, UK.
Department of Cellular and Molecular Pathology, Royal National Orthopaedic Hospital NHS Trust, Stanmore, UK.
J Pathol. 2022 Jul;257(4):454-465. doi: 10.1002/path.5912. Epub 2022 May 20.
The genome of each cell in the human body is constantly under assault from a plethora of exogenous and endogenous processes that can damage DNA. If not successfully repaired, DNA damage generally becomes permanently imprinted in cells, and all their progenies, as somatic mutations. In most cases, the patterns of these somatic mutations contain the tell-tale signs of the mutagenic processes that have imprinted and are termed mutational signatures. Recent pan-cancer genomic analyses have elucidated the compendium of mutational signatures for all types of small mutational events, including (1) single base substitutions, (2) doublet base substitutions, and (3) small insertions/deletions. In contrast to small mutational events, where, in most cases, DNA damage is a prerequisite, aneuploidy, which refers to the abnormal number of chromosomes in a cell, usually develops from mistakes during DNA replication. Such mistakes include DNA replication stress, mitotic errors caused by faulty microtubule dynamics, or cohesion defects that contribute to chromosomal breakage and can lead to copy number (CN) alterations (CNAs) or even to structural rearrangements. These aberrations also leave behind genomic scars which can be inferred from sequencing as CN signatures and rearrangement signatures. The analyses of mutational signatures of small mutational events have been extensively reviewed, so we will not comprehensively re-examine them here. Rather, our focus will be on summarising the existing knowledge for mutational signatures of CNAs. As studying CN signatures is an emerging field, we briefly summarise the utility that mutational signatures of small mutational events have provided in basic science, cancer treatment, and cancer prevention, and we emphasise the future role that CN signatures may play in each of these fields. © 2022 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.
人体每个细胞的基因组都不断受到大量外源性和内源性过程的攻击,这些过程会损害 DNA。如果不能成功修复,DNA 损伤通常会在细胞及其所有后代中永久留下印记,成为体细胞突变。在大多数情况下,这些体细胞突变模式包含了导致突变的过程的明显特征,并被称为突变特征。最近的泛癌症基因组分析阐明了所有类型小突变事件的突变特征图谱,包括(1)单个碱基替换,(2)双碱基替换,和(3)小插入/缺失。与小突变事件不同,在大多数情况下,DNA 损伤是前提条件,非整倍体是指细胞中染色体数量异常,通常是由于 DNA 复制过程中的错误而发展起来的。这些错误包括 DNA 复制应激、由微管动力学故障引起的有丝分裂错误,或导致染色体断裂的着丝粒缺陷,从而导致拷贝数(CN)改变(CNAs)甚至结构重排。这些异常也会留下基因组痕迹,可以通过测序推断为 CN 特征和重排特征。小突变事件突变特征的分析已经得到了广泛的综述,因此我们在这里不会全面重新检查。相反,我们的重点将放在总结 CNA 突变特征的现有知识上。由于研究 CN 特征是一个新兴领域,我们简要总结了小突变事件突变特征在基础科学、癌症治疗和癌症预防方面提供的实用性,并强调了 CN 特征在这些领域中的未来作用。