Dennison Jessica L, Al-Ali Hassan, Volmar Claude-Henry, Brothers Shaun, Watts Justin, Wahlestedt Claes, Lohse Ines
Center for Therapeutic Innovation, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.
Department of Psychiatry and Behavioral Sciences, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.
Cancers (Basel). 2022 Aug 24;14(17):4094. doi: 10.3390/cancers14174094.
The use of inhibitors of epigenetic modifiers in the treatment of acute myeloid leukemia (AML) has become increasingly appealing due to the highly epigenetic nature of the disease. We evaluated a library of 164 epigenetic compounds in a cohort of 9 heterogeneous AML patients using an ex vivo drug screen. AML blasts were isolated from bone marrow biopsies according to established protocols and treatment response to the epigenetic library was evaluated. We find that 11 histone deacetylase (HDAC) inhibitors, which act upon mechanisms of cell cycle arrest and apoptotic pathways through inhibition of zinc-dependent classes of HDACs, showed efficacy in all patient-derived samples. Other compounds, including bromodomain and extraterminal domain (BET) protein inhibitors, showed efficacy in most samples. Specifically, HDAC inhibitors are already clinically available and can be repurposed for use in AML. Results in this cohort of AML patient-derived samples reveal several epigenetic compounds with high anti-blast activity in all samples, despite the molecular diversity of the disease. These results further enforce the notion that AML is a predominantly epigenetic disease and that similar epigenetic mechanisms may underlie disease development and progression in all patients, despite differences in genetic mutations.
由于急性髓系白血病(AML)具有高度表观遗传的特性,使用表观遗传修饰抑制剂来治疗该疾病已变得越来越具有吸引力。我们使用体外药物筛选,在一组9名异质性AML患者中评估了一个包含164种表观遗传化合物的文库。根据既定方案从骨髓活检中分离出AML原始细胞,并评估对表观遗传文库的治疗反应。我们发现,11种组蛋白去乙酰化酶(HDAC)抑制剂通过抑制锌依赖性HDAC类别,作用于细胞周期停滞和凋亡途径机制,在所有患者来源的样本中均显示出疗效。其他化合物,包括溴结构域和额外末端结构域(BET)蛋白抑制剂,在大多数样本中显示出疗效。具体而言,HDAC抑制剂已在临床上可用,可重新用于AML治疗。在这组AML患者来源样本中的结果显示,尽管该疾病存在分子多样性,但有几种表观遗传化合物在所有样本中均具有高抗原始细胞活性。这些结果进一步强化了这样一种观念,即AML主要是一种表观遗传疾病,并且尽管基因突变存在差异,但相似的表观遗传机制可能是所有患者疾病发生和进展的基础。