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本文引用的文献

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Increased dosage of the chromosome 21 ortholog Dyrk1a promotes megakaryoblastic leukemia in a murine model of Down syndrome.染色体 21 同源物 Dyrk1a 剂量增加可促进唐氏综合征小鼠模型中的巨核母细胞白血病。
J Clin Invest. 2012 Mar;122(3):948-62. doi: 10.1172/JCI60455. Epub 2012 Feb 22.
2
The OTT-MAL fusion oncogene activates RBPJ-mediated transcription and induces acute megakaryoblastic leukemia in a knockin mouse model.OTT-MAL融合致癌基因在敲入小鼠模型中激活RBPJ介导的转录并诱发急性巨核细胞白血病。
J Clin Invest. 2009 Apr;119(4):852-64. doi: 10.1172/JCI35901. Epub 2009 Mar 16.
3
Role for MKL1 in megakaryocytic maturation.MKL1在巨核细胞成熟过程中的作用。
Blood. 2009 Mar 19;113(12):2826-34. doi: 10.1182/blood-2008-09-180596. Epub 2009 Jan 9.
4
Deletion of Mtg16, a target of t(16;21), alters hematopoietic progenitor cell proliferation and lineage allocation.t(16;21)的靶点Mtg16的缺失会改变造血祖细胞的增殖和谱系分配。
Mol Cell Biol. 2008 Oct;28(20):6234-47. doi: 10.1128/MCB.00404-08. Epub 2008 Aug 18.
5
BMP4 regulation of human megakaryocytic differentiation is involved in thrombopoietin signaling.骨形态发生蛋白4（BMP4）对人类巨核细胞分化的调控参与血小板生成素信号传导。
Blood. 2008 Oct 15;112(8):3154-63. doi: 10.1182/blood-2008-03-145326. Epub 2008 Jul 29.
6
Prenatal origin of GATA1 mutations may be an initiating step in the development of megakaryocytic leukemia in Down syndrome.GATA1突变的产前起源可能是唐氏综合征中巨核细胞白血病发生发展的起始步骤。
Blood. 2004 Sep 1;104(5):1588-9. doi: 10.1182/blood-2004-04-1563.
7
The role of cytidine deaminase and GATA1 mutations in the increased cytosine arabinoside sensitivity of Down syndrome myeloblasts and leukemia cell lines.胞苷脱氨酶和GATA1突变在唐氏综合征成髓细胞及白血病细胞系对阿糖胞苷敏感性增加中的作用。
Cancer Res. 2004 Jan 15;64(2):728-35. doi: 10.1158/0008-5472.can-03-2456.
8
Origins of chromosome translocations in childhood leukaemia.儿童白血病中染色体易位的起源
Nat Rev Cancer. 2003 Sep;3(9):639-49. doi: 10.1038/nrc1164.
9
Acute megakaryocytic leukemia: the Eastern Cooperative Oncology Group experience.急性巨核细胞白血病：东部肿瘤协作组的经验
Blood. 2000 Oct 1;96(7):2405-11.

BMP 与 AML 的相遇：新型融合基因诱导 BMP 信号转导促进小儿急性白血病。

BMP meets AML: induction of BMP signaling by a novel fusion gene promotes pediatric acute leukemia.

机构信息

Division of Hematology/Oncology, Northwestern University, University of Chicago, Chicago, IL 60637, USA.

出版信息

Cancer Cell. 2012 Nov 13;22(5):567-8. doi: 10.1016/j.ccr.2012.10.008.

DOI:10.1016/j.ccr.2012.10.008
PMID:23153530
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3501979/
Abstract

In this issue of Cancer Cell, Gruber et al. report that a significant proportion of children with acute megakaryoblastic leukemia acquire a translocation that confers enhanced BMP signaling and promotes self-renewal of hematopoietic progenitors. This study presents novel therapeutic targets that may lead to improved therapies for this aggressive leukemia.

摘要

在本期《癌细胞》中，Gruber 等人报告称，相当一部分患有急性巨核细胞白血病的儿童获得了一种易位，该易位赋予了增强的 BMP 信号，并促进了造血祖细胞的自我更新。这项研究提出了新的治疗靶点，可能为这种侵袭性白血病带来更好的治疗方法。