Institute of Gene Biology, Russian Academy of Sciences, 34/5 Vavilov Street, 119334 Moscow, Russia.
Moscow Institute of Physics and Technology, 9 Institutskiy Pereulok, 141701 Dolgoprudny, Russia.
Int J Mol Sci. 2021 Jul 8;22(14):7340. doi: 10.3390/ijms22147340.
Blood malignancies often arise from undifferentiated hematopoietic stem cells or partially differentiated stem-like cells. A tight balance of multipotency and differentiation, cell division, and quiescence underlying normal hematopoiesis requires a special program governed by the transcriptional machinery. Acquisition of drug resistance by tumor cells also involves reprogramming of their transcriptional landscape. Limiting tumor cell plasticity by disabling reprogramming of the gene transcription is a promising strategy for improvement of treatment outcomes. Herein, we review the molecular mechanisms of action of transcription-targeted drugs in hematological malignancies (largely in leukemia) with particular respect to the results of clinical trials.
血液恶性肿瘤通常起源于未分化的造血干细胞或部分分化的干细胞样细胞。正常造血需要一个由转录机制控制的特殊程序，以维持多能性和分化、细胞分裂和静止之间的紧密平衡。肿瘤细胞获得耐药性也涉及转录景观的重编程。通过使基因转录的重编程失活来限制肿瘤细胞的可塑性是改善治疗效果的一种有前途的策略。本文综述了转录靶向药物在血液恶性肿瘤（主要是白血病）中的作用机制，并特别关注临床试验结果。
