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RUNX1::ETO translocations must precede CSF3R mutations to promote acute myeloid leukemia development.RUNX1::ETO 易位必须先于 CSF3R 突变，以促进急性髓系白血病的发展。
Leukemia. 2023 May;37(5):1141-1146. doi: 10.1038/s41375-023-01862-8. Epub 2023 Mar 9.
2
CSF3R Mutations are frequently associated with abnormalities of RUNX1, CBFB, CEBPA, and NPM1 genes in acute myeloid leukemia.CSF3R 突变常与急性髓系白血病中 RUNX1、CBFB、CEBPA 和 NPM1 基因的异常有关。
Cancer. 2018 Aug;124(16):3329-3338. doi: 10.1002/cncr.31586. Epub 2018 Jun 22.
3
Cooperativity of RUNX1 and CSF3R mutations in severe congenital neutropenia: a unique pathway in myeloid leukemogenesis.RUNX1 和 CSF3R 突变在严重先天性中性粒细胞减少症中的协同作用：髓系白血病发生的独特途径。
Blood. 2014 Apr 3;123(14):2229-37. doi: 10.1182/blood-2013-11-538025. Epub 2014 Feb 12.
4
Effect of the unfolded protein response and oxidative stress on mutagenesis in CSF3R: a model for evolution of severe congenital neutropenia to myelodysplastic syndrome/acute myeloid leukemia.未折叠蛋白反应和氧化应激对 CSF3R 突变的影响：严重先天性中性粒细胞减少症向骨髓增生异常综合征/急性髓系白血病演变的模型。
Mutagenesis. 2020 Dec 1;35(5):381-389. doi: 10.1093/mutage/geaa027.
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Cooperating, congenital neutropenia-associated Csf3r and Runx1 mutations activate pro-inflammatory signaling and inhibit myeloid differentiation of mouse HSPCs.协同作用的，与先天性中性粒细胞减少症相关的 CSF3R 和 RUNX1 突变激活促炎信号，并抑制小鼠 HSPCs 的髓系分化。
Ann Hematol. 2020 Oct;99(10):2329-2338. doi: 10.1007/s00277-020-04194-0. Epub 2020 Aug 3.
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CSF3R and CALR mutations in paediatric myeloid disorders and the association of CSF3R mutations with translocations, including t(8; 21).儿童髓系疾病中的CSF3R和CALR突变以及CSF3R突变与易位（包括t(8;21)）的关联
Br J Haematol. 2015 Aug;170(3):391-7. doi: 10.1111/bjh.13439. Epub 2015 Apr 9.
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Clinical Relevance of RUNX1 and CBFB Alterations in Acute Myeloid Leukemia and Other Hematological Disorders.RUNX1和CBFB改变在急性髓系白血病及其他血液系统疾病中的临床相关性
Adv Exp Med Biol. 2017;962:175-199. doi: 10.1007/978-981-10-3233-2_12.
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Negative effects of GM-CSF signaling in a murine model of t(8;21)-induced leukemia.GM-CSF 信号在 t(8;21)-诱导白血病小鼠模型中的负性作用。
Blood. 2012 Mar 29;119(13):3155-63. doi: 10.1182/blood-2011-04-350694. Epub 2012 Jan 5.
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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.
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[Acute myeloid leukemia (aml) subtype M2 with variation of the t (8;21)translocation and AML1/ETO expression].伴有t(8;21)易位及AML1/ETO表达变异的急性髓系白血病（AML）M2亚型
Rev Peru Med Exp Salud Publica. 2013 Mar;30(1):145-6. doi: 10.1590/s1726-46342013000100029.

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1
Research progress on the mechanisms of CSF3R mutations in leukemogenesis and treatment strategies.CSF3R突变在白血病发生中的机制及治疗策略的研究进展
Cancer Cell Int. 2025 Aug 14;25(1):304. doi: 10.1186/s12935-025-03941-5.
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Distribution of different classes of CSF3R mutations and co-mutational pattern in 360 myeloid neoplasia.360例髓系肿瘤中不同类型CSF3R突变的分布及共突变模式
Ann Hematol. 2025 Jan;104(1):263-274. doi: 10.1007/s00277-025-06232-1. Epub 2025 Feb 5.

本文引用的文献

1
Prognostic impact of CSF3R mutations in favorable risk childhood acute myeloid leukemia.CSF3R突变对低危儿童急性髓系白血病的预后影响
Blood. 2020 Apr 30;135(18):1603-1606. doi: 10.1182/blood.2019004179.
2
Myeloid lineage enhancers drive oncogene synergy in CEBPA/CSF3R mutant acute myeloid leukemia.髓系谱系增强子驱动 CEBPA/CSF3R 突变急性髓系白血病中的癌基因协同作用。
Nat Commun. 2019 Nov 29;10(1):5455. doi: 10.1038/s41467-019-13364-2.
3
CSF3R mutations were associated with an unfavorable prognosis in patients with acute myeloid leukemia with CEBPA double mutations.CSF3R 突变与伴有 CEBPA 双突变的急性髓系白血病患者的不良预后相关。
Ann Hematol. 2019 Jul;98(7):1641-1646. doi: 10.1007/s00277-019-03699-7. Epub 2019 Apr 30.
4
CSF3R Mutations are frequently associated with abnormalities of RUNX1, CBFB, CEBPA, and NPM1 genes in acute myeloid leukemia.CSF3R 突变常与急性髓系白血病中 RUNX1、CBFB、CEBPA 和 NPM1 基因的异常有关。
Cancer. 2018 Aug;124(16):3329-3338. doi: 10.1002/cncr.31586. Epub 2018 Jun 22.
5
Mutational spectrum of acute myeloid leukemia patients with double mutations based on next-generation sequencing and its prognostic significance.基于二代测序的急性髓系白血病双突变患者的突变谱及其预后意义
Oncotarget. 2018 Jan 3;9(38):24970-24979. doi: 10.18632/oncotarget.23873. eCollection 2018 May 18.
6
CSF3R mutations have a high degree of overlap with CEBPA mutations in pediatric AML.在儿童急性髓系白血病中，CSF3R突变与CEBPA突变有高度重叠。
Blood. 2016 Jun 16;127(24):3094-8. doi: 10.1182/blood-2016-04-709899. Epub 2016 May 3.
7
CSF3R and CALR mutations in paediatric myeloid disorders and the association of CSF3R mutations with translocations, including t(8; 21).儿童髓系疾病中的CSF3R和CALR突变以及CSF3R突变与易位（包括t(8;21)）的关联
Br J Haematol. 2015 Aug;170(3):391-7. doi: 10.1111/bjh.13439. Epub 2015 Apr 9.
8
Granulopoiesis requires increased C/EBPα compared to monopoiesis, correlated with elevated Cebpa in immature G-CSF receptor versus M-CSF receptor expressing cells.与单核细胞生成相比，粒细胞生成需要增加的C/EBPα，这与未成熟的表达G-CSF受体的细胞中Cebpa升高相对于表达M-CSF受体的细胞相关。
PLoS One. 2014 Apr 21;9(4):e95784. doi: 10.1371/journal.pone.0095784. eCollection 2014.
9
Oncogenic CSF3R mutations in chronic neutrophilic leukemia and atypical CML.致癌性 CSF3R 突变在慢性中性粒细胞白血病和非典型 CML 中的作用。
N Engl J Med. 2013 May 9;368(19):1781-90. doi: 10.1056/NEJMoa1214514.
10
Runx1 deletion or dominant inhibition reduces Cebpa transcription via conserved promoter and distal enhancer sites to favor monopoiesis over granulopoiesis.Runx1 缺失或显性抑制通过保守的启动子和远端增强子位点减少 Cebpa 转录，有利于单核细胞生成而不是粒细胞生成。
Blood. 2012 May 10;119(19):4408-18. doi: 10.1182/blood-2011-12-397091. Epub 2012 Mar 26.

RUNX1::ETO translocations must precede CSF3R mutations to promote acute myeloid leukemia development.

作者信息

Carratt Sarah A, Kong Garth L, Coblentz Cody, Schonrock Zachary, Maloney Lauren, Weeder Ben, Yashar Will, Callahan Rowan, Blaylock Hunter, Coleman Colin, Coleman Dan, Braun Theodore P, Maxson Julia E

机构信息

Division of Oncologic Sciences, Knight Cancer Institute, Oregon Health & Science University, Portland, OR, 97239, USA.

Division of Hematology & Medical Oncology, Oregon Health & Science University, Portland, OR, 97239, USA.

出版信息

Leukemia. 2023 May;37(5):1141-1146. doi: 10.1038/s41375-023-01862-8. Epub 2023 Mar 9.

DOI:10.1038/s41375-023-01862-8
PMID:36894620
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10544281/
Abstract
摘要