Laboratory of Structural and Functional Organization of Chromosomes, Institute of Gene Biology RAS, 34/5 Vavilova Street, 119334 Moscow, Russia.
Gene. 2012 Dec 1;510(2):142-6. doi: 10.1016/j.gene.2012.09.028. Epub 2012 Sep 17.
Chromosomal translocation t (8;21)(q22;22) is one of the most frequent cytogenetic abnormalities found in acute myeloid leukaemia (AML). It generates the AML1/ETO fusion gene, which itself supports human haematopoietic stem cell self-renewal. However, the mechanism guiding transcription of this chimeric gene remains unclear. In our work, we attempted to shed light on this essential issue. We investigated the promoter from which transcription of the AML1/ETO gene is initiated and defined the three-dimensional structure of the whole rearranged locus.
8;21(q22;22)染色体易位是急性髓系白血病（AML）中最常见的细胞遗传学异常之一。它产生 AML1/ETO 融合基因，该基因本身支持人类造血干细胞自我更新。然而，指导这个嵌合基因转录的机制尚不清楚。在我们的工作中，我们试图阐明这个重要问题。我们研究了 AML1/ETO 基因转录起始的启动子，并定义了整个重排基因座的三维结构。
