急性髓系白血病 (AML) 会导致造血分化过程中断。 AML 的新治疗策略已经取得了重要进展。然而，诱导化疗仍然是大多数 AML 患者的主要选择。表观遗传失调在 AML 发病机制中发挥着核心作用，支持白血病发生和白血病干细胞的维持。在这里，我们概述了 AML 发展中表观遗传机制改变的复杂相互作用，包括 DNA 甲基化、组蛋白修饰和染色质重塑。我们探索表观遗传调节因子（例如 DNMT、HMT、KDM 和 HDAC）在介导基因表达模式推动白血病细胞转化中的作用。此外，我们讨论了细胞遗传学损伤对表观基因组重塑的影响以及针对表观遗传脆弱性作为治疗策略的潜力。了解 AML 的表观遗传景观可以深入了解新的治疗途径，包括表观遗传修饰剂，特别是它们在联合疗法中的应用，以改善治疗结果并克服耐药性。版权所有 © 2024。由 Elsevier Inc. 出版。

Acute myeloid leukemia (AML) results in disruption of the hematopoietic differentiation process. Crucial progress has been made, and new therapeutic strategies for AML have been developed. Induction chemotherapy, however, remains the main option for the majority of AML patients. Epigenetic dysregulation plays a central role in AML pathogenesis, supporting leukemogenesis and maintenance of leukemic stem cells. Here, we provide an overview of the intricate interplay of altered epigenetic mechanisms, including DNA methylation, histone modifications, and chromatin remodeling, in AML development. We explore the role of epigenetic regulators, such as DNMTs, HMTs, KDMs, and HDACs, in mediating gene expression patterns pushing towards leukemic cell transformation. Additionally, we discuss the impact of cytogenetic lesions on epigenomic remodeling and the potential of targeting epigenetic vulnerabilities as a therapeutic strategy. Understanding the epigenetic landscape of AML offers insights into novel therapeutic avenues, including epigenetic modifiers and particularly their use in combination therapies, to improve treatment outcomes and overcome drug resistance.Copyright © 2024. Published by Elsevier Inc.