减数分裂通过产生基因上不同的单倍体配子来增加后代的遗传多样性，这些配子具有重组后的染色体，这个过程需要专门的减数分裂蛋白质，这些蛋白质促进染色体的重组和分离。然而，有机体在有丝分裂中重新表达减数分裂蛋白质可能会产生灾难性的致癌后果，减数分裂蛋白质的异常表达在人体肿瘤中常见。从机理上讲，癌症中减数行为的重新激活促进了起始侵略可能是因为与健康的有丝分裂相反，癌症的动力是遗传不稳定导致肿瘤进化，以及逃避免疫反应和治疗压力。在这篇综述中，我们探讨了减数和癌细胞之间的相似之处，特别关注了癌症中减数基因的致癌激活。我们强调了组蛋白及其修饰，DNA 甲基化，基因组组织，R-环以及远端增强子的可用性的作用。版权所有©Elsevier Inc. 2023年。保留所有权利。

Meiosis increases genetic diversity in offspring by generating genetically unique haploid gametes with reshuffled chromosomes. This process requires a specialized set of meiotic proteins, which facilitate chromosome recombination and segregation. However, re-expression of meiotic proteins in mitosis can have catastrophic oncogenic consequences and aberrant expression of meiotic proteins is a common occurrence in human tumors. Mechanistically, re-activation of meiotic genes in cancer promotes oncogenesis likely because cancers-conversely to healthy mitosis-are fueled by genetic instability which promotes tumor evolution, and evasion of immune response and treatment pressure. In this review, we explore similarities between meiotic and cancer cells with a particular focus on the oncogenic activation of meiotic genes in cancer. We emphasize the role of histones and their modifications, DNA methylation, genome organization, R-loops and the availability of distal enhancers.Copyright © 2023 Elsevier Inc. All rights reserved.