中文摘要：

基因变化被认为驾驶尖锐 myeloid 的发展白血病(AML ).With 在定序技术的快速的进步，周期性地在 AML 被变异的许多最新报导的基因被发现了管理 AML 的开始和恶化。这些调查结果建议需要区分司机变化，特别最原始的单个变化，从随后的旅客变化。关于 DNA methyltransferase 3A (DNMT3A ) 的最近的研究变化在 AML 病人在 preleukemic 干细胞(最低有效字符前) 的鉴定上提供第一 proof-of-principle 调查。尽管没有引起全面白血病， DNMT3A 变化可以仅仅独自把造血的干细胞转变成最低有效字符前，这个驱动程序变化的函数看起来从 AML 坚持开始直到恶化。因此，识别并且指向 preleukemic 变化，在 AML，例如 DNMT3A 变化是为恶化风险的治疗和减小的有希望的策略。

英文摘要：

Genetic mutations are considered to drive the development of acute myeloid leukemia （AML）. With the rapid progress in sequencing technologies, many newly reported genes that are recurrently mutated in AML have been found to govern the initiation and relapse of AML. These findings suggest the need to distinguish the driver mutations, especially the most primitive single mutation, from the subsequent passenger mutations. Recent research on DNA methyltransferase 3A （DNMT3A） mutations provides the first proof-of-principle investigation on the identification of preleukemic stem cells （pre-LSCs） in AML patients. Although DNMT3A mutations alone may only transform hematopoietic stem cells into pre-LSCs without causing the full-blown leukemia, the function of this driver mutation appear to persist from AML initiation up to relapse. Therefore, identifying and targeting preleukemic mutations, such as DNMT3A mutations, in AML is a promising strategy for treatment and reduction of relapse risk.