PDF(Pubmed)
Abstract：
Polyploidization and depolyploidization are critical processes in the normal development and tissue homeostasis of diploid organisms. Recent investigations have revealed that polyaneuploid cancer cells (PACCs) exploit this ploidy variation as a survival strategy against anticancer treatment and for the repopulation of tumors. Unscheduled polyploidization and chromosomal instability in PACCs enhance malignancy and treatment resistance. However, their inability to undergo mitosis causes catastrophic cellular death in most PACCs. Adaptive ploid reversal mechanisms, such as multipolar mitosis, centrosome clustering, meiosis-like division, and amitosis, counteract this lethal outcome and drive cancer relapse. The purpose of this work is to focus on PACCs induced by cytotoxic therapy, highlighting the latest discoveries in ploidy dynamics in physiological and pathological contexts. Specifically, by emphasizing the role of \"poly-depolyploidization\" in tumor progression, the aim is to identify novel therapeutic targets or paradigms for combating diseases associated with aberrant ploidies.
摘要：
多倍体化和去多倍体化是二倍体生物正常发育和组织稳态的关键过程。最近的研究表明，多非整倍体癌细胞（PACCs）利用这种倍性变异作为对抗抗癌治疗和肿瘤再增殖的生存策略。PACCs中的计划外多倍体化和染色体不稳定性增强恶性和治疗抗性。然而,它们不能进行有丝分裂会在大多数PACCs中导致灾难性的细胞死亡。适应性倍体逆转机制，如多极有丝分裂，中心体聚类，减数分裂样分裂,和无丝分裂，抵消这种致命的结果和驱动癌症复发。这项工作的目的是专注于细胞毒性治疗诱导的PACCs，强调生理和病理环境中倍性动力学的最新发现。具体来说,通过强调“多倍化”在肿瘤进展中的作用，目的是确定新的治疗靶点或范例，以对抗与异常倍性相关的疾病。
