Josep Carreras Leukaemia Research Institute, School of Medicine, University of Barcelona, Barcelona, Spain; Centro de investigación Biomédica en Red de Cáncer (CIBER-ONC), Instituto de Salud Carlos III (ISCIII), Barcelona, Spain.
Wellcome Center for Cell Biology, University of Edinburgh, Edinburgh, Scotland, UK.
Trends Cancer. 2021 Jan;7(1):37-47. doi: 10.1016/j.trecan.2020.08.008. Epub 2020 Sep 17.
Aneuploidy, the gain or loss of chromosomes in a cell, is a hallmark of cancer. Although our understanding of the contribution of aneuploidy to cancer initiation and progression is incomplete, significant progress has been made in uncovering the cellular consequences of aneuploidy and how aneuploid cancer cells self-adapt to promote tumorigenesis. Aneuploidy is physiologically associated with significant cellular stress but, paradoxically, it favors tumor progression. Although more common in solid tumors, different forms of aneuploidy represent the initiating oncogenic lesion in patients with B cell acute lymphoblastic leukemia (B-ALL), making B-ALL an excellent model for studying the role of aneuploidy in tumorigenesis. We review the molecular mechanisms underlying aneuploidy and discuss its contributions to B-ALL initiation and progression.
非整倍体，即细胞内染色体的增益或丢失，是癌症的一个标志。尽管我们对非整倍体在癌症起始和进展中的作用的理解还不完全，但在揭示非整倍体的细胞后果以及非整倍体癌细胞如何自我适应以促进肿瘤发生方面已经取得了重大进展。非整倍体在生理上与显著的细胞应激有关，但矛盾的是，它有利于肿瘤的进展。虽然在实体瘤中更为常见，但不同形式的非整倍体代表了 B 细胞急性淋巴细胞白血病（B-ALL）患者的起始致癌病变，使 B-ALL 成为研究非整倍体在肿瘤发生中的作用的理想模型。我们综述了非整倍体的分子机制，并讨论了它对 B-ALL 起始和进展的贡献。
