随着时间的推移，人们逐渐认识到表观遗传修饰在一系列癌症的发病机制中的关键作用。组蛋白去乙酰化酶(HDACs)作为众所周知的表观遗传调控因子，在DNA修复、细胞增殖、分化、凋亡和血管生成等过程中发挥重要作用。研究表明，HDACs的异常表达在许多癌症类型中存在。因此，HDACs的抑制提供了一种有希望的替代性治疗方法。自从2006年美国食品药品监督管理局(FDA)首次批准组蛋白去乙酰化酶抑制剂（HDACi）沃瑞诺斯塔治疗皮肤T细胞淋巴瘤(CTCL)以来，HDAC抑制剂与其他分子（如化疗药物）的联合应用在目前的癌症治疗中引起了广泛的关注，特别是在血液恶性肿瘤的治疗中。到目前为止，已经有超过二十种HDAC抑制剂在临床试验中进行了研究，其中五种已经获得了批准。事实上，组蛋白去乙酰化酶抑制剂促进或增强了多种不同的抗癌机制，因此作为潜在的抗白血病药物而备受关注。在本综述中，我们将重点讨论HDAC抑制剂的可能治疗机制以及它们在白血病中的临床应用。版权所有©2023 Elsevier Inc. 保留所有权利。

The essential role of epigenetic modification in the pathogenesis of a series of cancers have gradually been recognized. Histone deacetylase (HDACs), as well-known epigenetic modulators, are responsible for DNA repair, cell proliferation, differentiation, apoptosis and angiogenesis. Studies have shown that aberrant expression of HDACs is found in many cancer types. Thus, inhibition of HDACs has provided a promising therapeutic approach alternative for these patients. Since HDAC inhibitor (HDACi) vorinostat was first approved by the Food and Drug Administration (FDA) for treating cutaneous T-cell lymphoma (CTCL) in 2006, the combination of HDAC inhibitors with other molecules such as chemotherapeutic drugs has drawn much attention in current cancer treatment, especially in hematological malignancies therapy. Up to now, there have been more than twenty HDAC inhibitors investigated in clinic trials with five approvals being achieved. Indeed, Histone deacetylase inhibitors promote or enhance several different anticancer mechanisms and therefore are in evidence as potential antileukemia agents. In this review, we will focus on possible mechanisms by how HDAC inhibitors exert therapeutic benefit and their clinical utility in leukemia.Copyright © 2023 Elsevier Inc. All rights reserved.