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Flt3-ITD mutations in a mouse model of radiation-induced acute myeloid leukaemia.

作者信息

Finnon R, Brown N, Moody J, Badie C, Olme C-H, Huiskamp R, Meijne E, Sutmuller M, Rosemann M, Bouffler S D

出版信息

Leukemia. 2012 Jun;26(6):1445-6. doi: 10.1038/leu.2011.377. Epub 2012 Jan 6.

DOI:10.1038/leu.2011.377
PMID:22289922
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3377996/
Abstract
摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a76/3377996/51ae1cdb38a6/leu2011377f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a76/3377996/51ae1cdb38a6/leu2011377f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a76/3377996/51ae1cdb38a6/leu2011377f1.jpg

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本文引用的文献

1
Sfpi1/PU.1 mutations in mouse radiation-induced acute myeloid leukaemias affect mRNA and protein abundance and associate with disrupted transcription.Sfpi1/PU.1 突变在小鼠辐射诱导的急性髓系白血病中影响 mRNA 和蛋白质丰度,并与转录失调相关。
Leuk Res. 2011 Jan;35(1):126-32. doi: 10.1016/j.leukres.2010.06.015. Epub 2010 Jul 17.
2
Radiation leukemogenesis in mice: loss of PU.1 on chromosome 2 in CBA and C57BL/6 mice after irradiation with 1 GeV/nucleon 56Fe ions, X rays or gamma rays. Part I. Experimental observations.小鼠辐射诱发白血病:用1 GeV/核子的56Fe离子、X射线或γ射线照射后,CBA和C57BL/6小鼠2号染色体上PU.1的缺失。第一部分。实验观察。
Radiat Res. 2009 Apr;171(4):474-83. doi: 10.1667/RR1547.1.
3
R235C点突变使小鼠对辐射诱导的急性髓系白血病敏感。
iScience. 2023 Aug 3;26(9):107530. doi: 10.1016/j.isci.2023.107530. eCollection 2023 Sep 15.
4
Leukemic stem cells and advances in hematopoietic stem cell transplantation for acute myeloid leukemia: a narrative review of clinical trials.白血病干细胞与急性髓系白血病造血干细胞移植的进展:临床试验的叙述性综述
Stem Cell Investig. 2022 Dec 5;9:10. doi: 10.21037/sci-2022-044. eCollection 2022.
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Hyper-radiosensitivity affects low-dose acute myeloid leukemia incidence in a mathematical model.超敏感性会影响低剂量急性髓性白血病发病的数学模型。
Radiat Environ Biophys. 2022 Aug;61(3):361-373. doi: 10.1007/s00411-022-00981-7. Epub 2022 Jul 21.
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Small tandem DNA duplications result from CST-guided Pol α-primase action at DNA break termini.小串联 DNA 重复序列是由 CST 引导的 Pol α-引发酶在 DNA 断裂末端的作用产生的。
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Tracking preleukemic cells in vivo to reveal the sequence of molecular events in radiation leukemogenesis.在体内追踪白血病前体细胞,以揭示辐射性白血病发生过程中分子事件的顺序。
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FLT3 mutations: biology and treatment.
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Hematology Am Soc Hematol Educ Program. 2006:178-84. doi: 10.1182/asheducation-2006.1.178.
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Mutations of the PU.1 Ets domain are specifically associated with murine radiation-induced, but not human therapy-related, acute myeloid leukaemia.PU.1 Ets结构域的突变与小鼠辐射诱导的急性髓系白血病特异性相关,但与人类治疗相关的急性髓系白血病无关。
Oncogene. 2005 May 19;24(22):3678-83. doi: 10.1038/sj.onc.1208422.
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The roles of FLT3 in hematopoiesis and leukemia.FLT3在造血作用和白血病中的作用。
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Molecular mapping of chromosome 2 deletions in murine radiation-induced AML localizes a putative tumor suppressor gene to a 1.0 cM region homologous to human chromosome segment 11p11-12.小鼠辐射诱导急性髓系白血病中2号染色体缺失的分子定位将一个假定的肿瘤抑制基因定位于与人类染色体11p11 - 12区段同源的1.0 cM区域。
Genes Chromosomes Cancer. 1999 Feb;24(2):95-104.
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Internal tandem duplication of the FLT3 gene is a novel modality of elongation mutation which causes constitutive activation of the product.
Leukemia. 1998 Sep;12(9):1333-7. doi: 10.1038/sj.leu.2401130.