Department of Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Department of Biological Sciences and Fralin Life Sciences Institute, Virginia Tech, Blacksburg, VA 24061, USA.
Genes (Basel). 2021 Apr 12;12(4):558. doi: 10.3390/genes12040558.
Cancer is a disease of cellular evolution. For this cellular evolution to take place, a population of cells must contain functional heterogeneity and an assessment of this heterogeneity in the form of natural selection. Cancer cells from advanced malignancies are genomically and functionally very different compared to the healthy cells from which they evolved. Genomic alterations include aneuploidy (numerical and structural changes in chromosome content) and polyploidy (e.g., whole genome doubling), which can have considerable effects on cell physiology and phenotype. Likewise, conditions in the tumor microenvironment are spatially heterogeneous and vastly different than in healthy tissues, resulting in a number of environmental niches that play important roles in driving the evolution of tumor cells. While a number of studies have documented abnormal conditions of the tumor microenvironment and the cellular consequences of aneuploidy and polyploidy, a thorough overview of the interplay between karyotypically abnormal cells and the tissue and tumor microenvironments is not available. Here, we examine the evidence for how this interaction may unfold during tumor evolution. We describe a bidirectional interplay in which aneuploid and polyploid cells alter and shape the microenvironment in which they and their progeny reside; in turn, this microenvironment modulates the rate of genesis for new karyotype aberrations and selects for cells that are most fit under a given condition. We conclude by discussing the importance of this interaction for tumor evolution and the possibility of leveraging our understanding of this interplay for cancer therapy.
癌症是一种细胞进化的疾病。为了发生这种细胞进化,细胞群体必须包含功能异质性,并以自然选择的形式评估这种异质性。与它们进化而来的健康细胞相比,晚期恶性肿瘤的癌细胞在基因组和功能上有很大的不同。基因组改变包括非整倍体(染色体内容的数值和结构变化)和多倍体(例如,全基因组加倍),这会对细胞生理学和表型产生相当大的影响。同样,肿瘤微环境中的条件在空间上是异质的,与健康组织有很大的不同,导致许多环境小生境在驱动肿瘤细胞进化中起着重要作用。虽然许多研究已经记录了肿瘤微环境的异常情况以及非整倍体和多倍体的细胞后果,但尚不清楚染色体异常细胞与组织和肿瘤微环境之间相互作用的全面概述。在这里,我们研究了这种相互作用在肿瘤进化过程中是如何展开的。我们描述了一种双向相互作用,其中非整倍体和多倍体细胞改变和塑造它们及其后代所在的微环境;反过来,这种微环境调节新的核型异常发生的速度,并选择在给定条件下最适应的细胞。最后,我们讨论了这种相互作用对肿瘤进化的重要性,以及利用我们对这种相互作用的理解为癌症治疗提供可能性。