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首页> 外文期刊>Clinical epigenetics. >A clinical-molecular update on azanucleoside-based therapy for the treatment of hematologic cancers
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A clinical-molecular update on azanucleoside-based therapy for the treatment of hematologic cancers

机译：基于氮杂核苷的血液疗法治疗的临床分子更新

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The azanucleosides azacitidine and decitabine are currently used for the treatment of acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) in patients not only eligible for intensive chemotherapy but are also being explored in other hematologic and solid cancers. Based on their capacity to interfere with the DNA methylation machinery, these drugs are also referred to as hypomethylating agents (HMAs). As DNA methylation contributes to epigenetic regulation, azanucleosides are further considered to be among the first true “epigenetic drugs” that have reached clinical application. However, intriguing new evidence suggests that DNA hypomethylation is not the only mechanism of action for these drugs. This review summarizes the experience from more than 10?years of clinical practice with azanucleosides and discusses their molecular actions, including several not related to DNA methylation. A particular focus is placed on possible causes of primary and acquired resistances to azanucleoside treatment. We highlight current limitations for the success and durability of azanucleoside-based therapy and illustrate that a better understanding of the molecular determinants of drug response holds great potential to overcome resistance.
机译：氮杂核苷阿扎胞苷和地西他滨目前被用于治疗急性髓样白血病（AML）和骨髓增生异常综合症（MDS）的患者，不仅适合进行强化化疗，而且还在其他血液学和实体癌中进行研究。基于它们干扰DNA甲基化机制的能力，这些药物也称为次甲基化剂（HMA）。由于DNA甲基化有助于表观遗传调控，氮杂核苷被进一步认为是已在临床上应用的首批真正的“表观遗传药物”。但是，有趣的新证据表明，DNA低甲基化并不是这些药物的唯一作用机制。这篇综述总结了十多年的氮杂核苷临床实践经验，并讨论了它们的分子作用，包括几种与DNA甲基化无关的作用。特别关注对氮杂核苷治疗的原发性和获得性耐药的可能原因。我们重点介绍了目前基于氮杂核苷治疗成功和持久性的局限性，并说明对药物反应分子决定因素的更好理解具有克服耐药性的巨大潜力。

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