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GFI1 is required for positive acute myeloid leukemia.

作者信息

Marneth Anna E, Botezatu Lacramioara, Hönes Judith M, Israël Jimmy C L, Schütte Judith, Vassen Lothar, Lams Robert F, Bergevoet Saskia M, Groothuis Laura, Mandoli Amit, Martens Joost H A, Huls Gerwin, Jansen Joop H, Dührsen Ulrich, Berg Tobias, Möröy Tarik, Wichmann Christian, Lo Mia-Chia, Zhang Dong-Er, van der Reijden Bert A, Khandanpour Cyrus

机构信息

Department of Laboratory Medicine, Laboratory of Hematology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Centre, Nijmegen, The Netherlands.

Department of Hematology, West German Cancer Center, University Hospital Essen, University of Duisburg-Essen, Germany.

出版信息

Haematologica. 2018 Sep;103(9):e395-e399. doi: 10.3324/haematol.2017.180844. Epub 2018 Apr 19.

DOI:10.3324/haematol.2017.180844
PMID:29674496
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6119136/
Abstract
摘要

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本文引用的文献

1
A FOXO1-induced oncogenic network defines the AML1-ETO preleukemic program.一个由FOXO1诱导的致癌网络定义了AML1-ETO白血病前期程序。
Blood. 2017 Sep 7;130(10):1213-1222. doi: 10.1182/blood-2016-11-750976. Epub 2017 Jul 14.
2
Core-binding factor acute myeloid leukemia in first relapse: a retrospective study from the French AML Intergroup.初发复发时的核心结合因子急性髓系白血病:法国 AML 协作组的一项回顾性研究。
Blood. 2014 Aug 21;124(8):1312-9. doi: 10.1182/blood-2014-01-549212. Epub 2014 Jul 8.
3
Genomic and epigenomic landscapes of adult de novo acute myeloid leukemia.成人新发急性髓系白血病的基因组和表观基因组图谱。
N Engl J Med. 2013 May 30;368(22):2059-74. doi: 10.1056/NEJMoa1301689. Epub 2013 May 1.
4
Growth factor independence 1 antagonizes a p53-induced DNA damage response pathway in lymphoblastic leukemia.生长因子独立性 1 拮抗淋巴母细胞白血病中 p53 诱导的 DNA 损伤反应途径。
Cancer Cell. 2013 Feb 11;23(2):200-14. doi: 10.1016/j.ccr.2013.01.011.
5
ERG and FLI1 binding sites demarcate targets for aberrant epigenetic regulation by AML1-ETO in acute myeloid leukemia.ERG 和 FLI1 结合位点标志着 AML1-ETO 在急性髓系白血病中异常表观遗传调控的靶标。
Blood. 2012 Nov 8;120(19):4038-48. doi: 10.1182/blood-2012-05-429050. Epub 2012 Sep 14.
6
Depletion of RUNX1/ETO in t(8;21) AML cells leads to genome-wide changes in chromatin structure and transcription factor binding.t(8;21)AML 细胞中 RUNX1/ETO 的耗竭导致染色质结构和转录因子结合的全基因组变化。
Leukemia. 2012 Aug;26(8):1829-41. doi: 10.1038/leu.2012.49. Epub 2012 Feb 20.
7
Gfi1-cells and circuits: unraveling transcriptional networks of development and disease.Gfi1 细胞和回路:揭示发育和疾病的转录网络。
Curr Opin Hematol. 2010 Jul;17(4):300-7. doi: 10.1097/MOH.0b013e32833a06f8.
8
Dimer-tetramer transition controls RUNX1/ETO leukemogenic activity.二聚体-四聚体转变控制 RUNX1/ETO 白血病发病机制。
Blood. 2010 Jul 29;116(4):603-13. doi: 10.1182/blood-2009-10-248047. Epub 2010 Apr 29.
9
Gfi1 integrates progenitor versus granulocytic transcriptional programming.Gfi1整合祖细胞与粒细胞转录程序。
Blood. 2009 May 28;113(22):5466-75. doi: 10.1182/blood-2008-09-179747. Epub 2009 Apr 3.
10
Double CEBPA mutations, but not single CEBPA mutations, define a subgroup of acute myeloid leukemia with a distinctive gene expression profile that is uniquely associated with a favorable outcome.双CEBPA突变而非单CEBPA突变定义了急性髓系白血病的一个亚组,该亚组具有独特的基因表达谱,且与良好预后唯一相关。
Blood. 2009 Mar 26;113(13):3088-91. doi: 10.1182/blood-2008-09-179895. Epub 2009 Jan 26.