AML1-ETO driven acute leukemia: insights into pathogenesis and potential therapeutic approaches.
AML1-ETO driven acute leukemia: insights into pathogenesis and potential therapeutic approaches.
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DOI：
10.1007/s11684-012-0206-6
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发表时间：
2012-09-01
影响因子：
8.1
通讯作者：
Nimer, Stephen D
中科院分区：
文献类型：
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作者：
Hatlen, Megan A;Wang, Lan;Nimer, Stephen D
AML1-ETO融合转录因子是由t(8；21)易位产生的，它存在于大约4%-12%的成人和12%-30%的儿童急性髓系白血病(AML)患者中。人类和小鼠的AML模型都表明，在没有继发性事件的情况下，AML1-ETO对于白血病的发生是不够的。在这篇综述中，我们讨论了在活体中识别与AML1-ETO协同诱发AML的各种事件所获得的致病见解。我们还讨论了针对t(8；21)阳性AML的潜在治疗策略，包括靶向融合蛋白本身、与融合蛋白结合的蛋白或融合蛋白调节的基因。最近发表的研究表明，针对t(8；21)阳性AML的靶向治疗是可行的，可能很快就会到来。
The AML1-ETO fusion transcription factor is generated by the t(8;21) translocation, which is present in approximately 4%-12% of adult and 12%-30% of pediatric acute myeloid leukemia (AML) patients. Both human and mouse models of AML have demonstrated that AML1-ETO is insufficient for leukemogenesis in the absence of secondary events. In this review, we discuss the pathogenetic insights that have been gained from identifying the various events that can cooperate with AML1-ETO to induce AML in vivo. We also discuss potential therapeutic strategies for t(8;21) positive AML that involve targeting the fusion protein itself, the proteins that bind to it, or the genes that it regulates. Recently published studies suggest that a targeted therapy for t(8;21) positive AML is feasible and may be coming sometime soon.