We suggest that the activity of the MLL complex might be regulated through this interplay.
研究者认为，MLL复合物的活性可能受到这些相互作用的调控。
The genetic change, known as a partial tandem duplication, is located in a gene called MLL (for mixed-lineage leukemia).
该基因改变，即所谓的部分串联复制，位于MLL(混合血系白血病)基因上。
The one of most interesting issues is how leukemia cells with MLL rearrangement acquire a unique feature of TRAIL-resistance.
非常有意思的问题之一是有MLL重排的白血病细胞怎样获得抵抗TRAIL的唯一特征。
Inhibition of GSK3 in a preclinical murine model of MLL leukaemia provides promising evidence of efficacy and earmarks GSK3 as a candidate cancer drug target.
在MLL白血病一个临床前鼠模型中，抑制GSK3可提供有效性的令人鼓舞的证据，并标记了GSK3作为候选的癌症药物靶点。
Conclusions Genotypes defined by the mutational status of NPM1, FLT3, CEBPA, and MLL are associated with the outcome of treatment for patients with cytogenetically normal AML.
结论：由npm 1,FLT3,CEBPA，和MLL基因的突变状态所界定的基因型与细胞遗传学正常的急性髓细胞白血病患者的临床治疗结局之间存在相关性。
In normal cells, MLL combines with four proteins that comprise the W-RAD group to create a molecular switch that controls DNA packaging events required to form white blood cells.
在正常细胞中，MLL与其他四种蛋白联合组成了W-RAD复合体，从而形成了在白细胞形成中所需的一种控制DNA组合的分子开关。
In normal cells, MLL combines with four proteins that comprise the W-RAD group to create a molecular switch that controls DNA packaging events required to form white blood cells.
在正常细胞中，MLL与其他四种蛋白联合组成了W-RAD复合体，从而形成了在白细胞形成中所需的一种控制DNA组合的分子开关。
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