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编码粒细胞集落刺激因子受体的基因是前B细胞急性淋巴细胞白血病中t(1;19)特异性癌蛋白E2A-Pbx1导致失调的一个靶点。

The gene encoding the granulocyte colony-stimulating factor receptor is a target for deregulation in pre-B ALL by the t(1;19)-specific oncoprotein E2A-Pbx1.

作者信息

de Lau W B, Hurenkamp J, Berendes P, Touw I P, Clevers H C, van Dijk M A

机构信息

Academic Hospital Utrecht, Department of Immunology, The Netherlands.

出版信息

Oncogene. 1998 Jul 30;17(4):503-10. doi: 10.1038/sj.onc.1201967.

Abstract

Approximately 25-30% of childhood pre-B cell acute lymphoblastic leukemias (pre-B ALL) is characterized by the presence of a (1;19)(q23;p13.3) translocation. The presence of this translocation is generally accompanied by a poor prognosis. The chimeric gene resulting from this chromosomal rearrangement encodes a hybrid transcription factor, E2A-Pbx1. In an attempt to delineate the genetic cascade initiated by E2A-Pbx1, we sought to identify genes that are deregulated by this transcription factor in t(1;19) pre-B ALL. We show here that the gene encoding the granulocyte colony-stimulating factor receptor (G-CSFr) is specifically upregulated in pre-B cells expressing E2A-Pbx1. G-CSFr is also expressed in cell lines established from t(1;19) pre-B cell leukemia and on primary t(1;19) tumor cells, but not on control cells. These data indicate that G-CSFr gene is a target for deregulation by E2A-Pbx1.

摘要

大约25% - 30%的儿童前B细胞急性淋巴细胞白血病(前B - ALL)的特征是存在(1;19)(q23;p13.3)易位。这种易位的存在通常伴随着不良预后。由这种染色体重排产生的嵌合基因编码一种混合转录因子E2A - Pbx1。为了描绘由E2A - Pbx1引发的遗传级联反应,我们试图鉴定在t(1;19)前B - ALL中受该转录因子失调调控的基因。我们在此表明,编码粒细胞集落刺激因子受体(G - CSFr)的基因在表达E2A - Pbx1的前B细胞中特异性上调。G - CSFr也在由t(1;19)前B细胞白血病建立的细胞系以及原发性t(1;19)肿瘤细胞中表达,但在对照细胞中不表达。这些数据表明G - CSFr基因是E2A - Pbx1失调调控的一个靶点。

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