FLT3突变对急性髓性白血病发展的影响。

Leukemia Research and Treatment Pub Date : 2013-01-01 Epub Date: 2013-07-09 DOI:10.1155/2013/275760
Ugo Testa, Elvira Pelosi
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引用次数: 21

摘要

急性髓性白血病(AMLs)遗传学研究的发展导致了一些复发性遗传异常的识别。他们的发现不仅对更好地了解aml的分子发病机制,而且对确定新的治疗靶点具有重要意义。在这种情况下,确定aml相关的“驱动”突变是至关重要的,它在白血病发生中起着致病作用。近年来积累的证据表明,在约20%的AMLs中检测到的激活FLT3内部串联重复突变(FLT3- itd)是AMLs的驱动突变和有效的治疗靶点。此外,FLT3-ITD突变的筛选也大大有助于提高更准确的预后标准的确定和患者的治疗选择。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Impact of FLT3 Mutations on the Development of Acute Myeloid Leukemias.

The development of the genetic studies on acute myeloid leukemias (AMLs) has led to the identification of some recurrent genetic abnormalities. Their discovery was of fundamental importance not only for a better understanding of the molecular pathogenesis of AMLs, but also for the identification of new therapeutic targets. In this context, it is essential to identify AML-associated "driver" mutations, which have a causative role in leukemogenesis. Evidences accumulated during the last years indicate that activating internal tandem duplication mutations in FLT3 (FLT3-ITD), detected in about 20% of AMLs, represents driver mutations and valid therapeutic targets in AMLs. Furthermore, the screening of FLT3-ITD mutations has also considerably helped to improve the identification of more accurate prognostic criteria and of the therapeutic selection of patients.

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