Although we are just beginning to understand the mechanisms that regulate the epigenome, aberrant epigenetic programming has already emerged as a hallmark of hematologic malignancies including acute myeloid leukemia (AML) and B-cell lymphomas. Although these diseases arise from the hematopoietic system, the epigenetic mechanisms that drive these malignancies are quite different. Yet, in all of these tumors, somatic mutations in transcription factors and epigenetic modifiers are the most commonly mutated set of genes and result in multilayered disruption of the epigenome. Myeloid and lymphoid neoplasms generally manifest epigenetic allele diversity, which contributes to tumor cell population fitness regardless of the underlying genetics. Epigenetic therapies are emerging as one of the most promising new approaches for these patients. However, effective targeting of the epigenome must consider the need to restore the various layers of epigenetic marks, appropriate biological end points, and specificity of therapeutic agents to truly realize the potential of this modality.

中文翻译：

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白血病和淋巴瘤的表观遗传机制

尽管我们才刚刚开始了解调节表观基因组的机制，但异常的表观遗传程序已成为血液系统恶性肿瘤的标志，包括急性髓细胞性白血病（AML）和B细胞淋巴瘤。尽管这些疾病来自造血系统，但驱动这些恶性肿瘤的表观遗传机制却大不相同。然而，在所有这些肿瘤中，转录因子和表观遗传修饰剂中的体细胞突变是最常见的基因突变集，并导致表观基因组的多层破坏。髓样和淋巴样肿瘤通常表现出表观遗传等位基因多样性，无论潜在的遗传学如何，都有助于肿瘤细胞群体的适应性。表观遗传疗法正在成为这些患者最有希望的新方法之一。然而，