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首页> 外文期刊>Molecular and Cellular Biology >E2A-Pbx1, the t(1;19) translocation protein of human pre-B-cell acute lymphocytic leukemia, causes acute myeloid leukemia in mice.
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E2A-Pbx1, the t(1;19) translocation protein of human pre-B-cell acute lymphocytic leukemia, causes acute myeloid leukemia in mice.

机译：E2A-Pbx1是人类前B细胞急性淋巴细胞性白血病的t（1; 19）易位蛋白，可引起小鼠急性髓性白血病。

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摘要

One-quarter of pediatric pre-B-cell leukemias contain the t(1;19) chromosomal translocation, which fuses 5' exons encoding the transactivation domain of the E2A transcription factor gene to 3' exons ecoding the putative DNA-binding region of the unusual homeobox gene, PBX1. To test the leukemic potential of this fused gene, a cDNA encoding its major protein product, p85E2A-Pbx1, was incorporated into a retrovirus construct and introduced into normal mouse marrow progenitors by infection. The cells were used in a bone marrow transplantation protocol to reconstitute the hematopoietic compartments of lethally irradiated recipients. After 3 to 8 months, reconstituted mice developed acute myeloid leukemias that expressed high levels of p85E2A-Pbx1 and were readily transmissible to immunocompetent mice. Most acute myeloid leukemias also grew as granulocytic sarcomas and exhibited some neutrophilic differentiation. These results demonstrate a causative role for p85E2A-Pbx1 in human acute leukemia and indicate that the oncogenic potential of Pbx1 is not limited to pre-B-cell malignancies.
机译：四分之一的小儿前B细胞白血病含有t（1; 19）染色体易位，它将编码E2A转录因子基因反式激活域的5'外显子与编码E2A假定的DNA结合区的3'外显子融合。不寻常的同源盒基因PBX1。为了测试该融合基因的白血病潜能，将编码其主要蛋白质产物p85E2A-Pbx1的cDNA整合入逆转录病毒构建体中，并通过感染将其引入正常小鼠骨髓祖细胞中。这些细胞用于骨髓移植方案，以重建经致死性照射的受体的造血区室。 3至8个月后，重组小鼠发展为急性髓细胞性白血病，表达高水平的p85E2A-Pbx1，并易于传染给具有免疫能力的小鼠。大多数急性髓细胞性白血病也以粒细胞肉瘤的形式生长，并表现出中性粒细胞分化。这些结果证明了p85E2A-Pbx1在人类急性白血病中的致病作用，并表明Pbx1的致癌潜能不仅限于前B细胞恶性肿瘤。

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