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Haploinsufficiency of multiple del(5q) genes induce B cell abnormalities in mice.多个5号染色体长臂缺失（del(5q)）基因的单倍剂量不足在小鼠中诱发B细胞异常。
Leuk Res. 2020 Sep;96:106428. doi: 10.1016/j.leukres.2020.106428. Epub 2020 Jul 23.
2
Haploinsufficiency of miR-143 and miR-145 reveal targetable dependencies in resistant del(5q) myelodysplastic neoplasm.miR-143和miR-145单倍剂量不足揭示了难治性del(5q)骨髓增生异常肿瘤中可靶向的依赖性。
Leukemia. 2025 Apr;39(4):917-928. doi: 10.1038/s41375-025-02537-2. Epub 2025 Feb 25.
3
Combined immunophenotyping and FISH identifies the involvement of B-cells in 5q- syndrome.联合免疫表型分析和荧光原位杂交技术可确定5q-综合征中B细胞的受累情况。
Genes Chromosomes Cancer. 2000 Nov;29(3):276-80. doi: 10.1002/1098-2264(2000)9999:9999<::aid-gcc1035>3.0.co;2-l.
4
Deletion 5q MDS: molecular and therapeutic implications.5q 缺失 MDS 的分子与治疗学意义。
Best Pract Res Clin Haematol. 2013 Dec;26(4):365-75. doi: 10.1016/j.beha.2013.10.013. Epub 2013 Oct 16.
5
Myelodysplastic syndrome associated with isolated del (5q) chromosome abnormality ("5q- syndrome").与孤立性5号染色体长臂缺失（“5q-综合征”）相关的骨髓增生异常综合征
Blood. 2007 Dec 1;110(12):3825.
6
Pleiotropic mechanisms of action of lenalidomide efficacy in del(5q) myelodysplastic syndromes.来那度胺在 del(5q) 骨髓增生异常综合征疗效中的多效作用机制。
Expert Rev Anticancer Ther. 2010 Oct;10(10):1663-72. doi: 10.1586/era.10.135.
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Deletion of 5q31 is observed in megakaryocytic cells in patients with myelodysplastic syndromes and a del(5q), including the 5q- syndrome.在骨髓增生异常综合征伴有5号染色体长臂缺失（del(5q)）的患者中，包括5q-综合征患者，在巨核细胞中观察到5q31缺失。
Genes Chromosomes Cancer. 2000 Dec;29(4):350-2. doi: 10.1002/1098-2264(2000)9999:9999<::aid-gcc1041>3.0.co;2-w.
8
Molecular dissection of the 5q deletion in myelodysplastic syndrome.骨髓增生异常综合征中 5q 缺失的分子剖析。
Semin Oncol. 2011 Oct;38(5):621-6. doi: 10.1053/j.seminoncol.2011.04.010.
9
Interphase FISH does not improve the detection of DEL(5q) and DEL(20q) in myelodysplastic syndromes.间期荧光原位杂交不能提高骨髓增生异常综合征中 DEL(5q) 和 DEL(20q) 的检出率。
Anticancer Res. 2011 Mar;31(3):1007-10.
10
Bone marrow morphology in myelodysplastic syndrome associated with isolated del(5q).与孤立性5号染色体长臂缺失相关的骨髓增生异常综合征的骨髓形态学
Am J Hematol. 2010 Aug;85(8):609-10. doi: 10.1002/ajh.21775.

引用本文的文献

1
Cytogenetic and Genetic Abnormalities with Diagnostic Value in Myelodysplastic Syndromes (MDS): Focus on the Pre-Messenger RNA Splicing Process.具有诊断价值的骨髓增生异常综合征（MDS）的细胞遗传学和基因异常：聚焦于信使前体RNA剪接过程
Diagnostics (Basel). 2022 Jul 7;12(7):1658. doi: 10.3390/diagnostics12071658.
2
Toll-like receptor and cytokine expression throughout the bone marrow differs between patients with low- and high-risk myelodysplastic syndromes.低危和高危骨髓增生异常综合征患者骨髓中的 Toll 样受体和细胞因子表达不同。
Exp Hematol. 2022 Jun;110:47-59. doi: 10.1016/j.exphem.2022.03.011. Epub 2022 Apr 1.
3
RBM22, a Key Player of Pre-mRNA Splicing and Gene Expression Regulation, Is Altered in Cancer.RBM22是前体mRNA剪接和基因表达调控的关键因子，在癌症中发生改变。
Cancers (Basel). 2022 Jan 27;14(3):643. doi: 10.3390/cancers14030643.
4
Mutant U2AF1-induced alternative splicing of H2afy (macroH2A1) regulates B-lymphopoiesis in mice.突变 U2AF1 诱导 H2afy（macroH2A1）的可变剪接调控小鼠的 B 淋巴细胞发生。
Cell Rep. 2021 Aug 31;36(9):109626. doi: 10.1016/j.celrep.2021.109626.

本文引用的文献

1
Rps14, Csnk1a1 and miRNA145/miRNA146a deficiency cooperate in the clinical phenotype and activation of the innate immune system in the 5q- syndrome.Rps14、Csnk1a1 和 miRNA145/miRNA146a 缺失在 5q- 综合征的临床表型和固有免疫系统激活中协同作用。
Leukemia. 2019 Jul;33(7):1759-1772. doi: 10.1038/s41375-018-0350-3. Epub 2019 Jan 16.
2
-initiating mutations in MDS-RSs target lymphomyeloid hematopoietic stem cells.骨髓增生异常综合征伴环形铁粒幼细胞（MDS-RS）中的起始突变靶向淋巴髓系造血干细胞。
Blood. 2017 Aug 17;130(7):881-890. doi: 10.1182/blood-2017-03-776070. Epub 2017 Jun 20.
3
Knockdown of HSPA9 induces TP53-dependent apoptosis in human hematopoietic progenitor cells.HSPA9基因敲低可诱导人造血祖细胞中依赖TP53的细胞凋亡。
PLoS One. 2017 Feb 8;12(2):e0170470. doi: 10.1371/journal.pone.0170470. eCollection 2017.
4
CD74 is a novel transcription regulator.CD74是一种新型转录调节因子。
Proc Natl Acad Sci U S A. 2017 Jan 17;114(3):562-567. doi: 10.1073/pnas.1612195114. Epub 2016 Dec 28.
5
Rps14 haploinsufficiency causes a block in erythroid differentiation mediated by S100A8 and S100A9.核糖体蛋白S14单倍体不足导致由S100A8和S100A9介导的红系分化受阻。
Nat Med. 2016 Mar;22(3):288-97. doi: 10.1038/nm.4047. Epub 2016 Feb 15.
6
Combining gene mutation with gene expression data improves outcome prediction in myelodysplastic syndromes.将基因突变与基因表达数据相结合可改善骨髓增生异常综合征的预后预测。
Nat Commun. 2015 Jan 9;6:5901. doi: 10.1038/ncomms6901.
7
Reduced levels of Hspa9 attenuate Stat5 activation in mouse B cells.热休克蛋白9（Hspa9）水平降低会减弱小鼠B细胞中信号转导和转录激活因子5（Stat5）的激活。
Exp Hematol. 2015 Apr;43(4):319-30.e10. doi: 10.1016/j.exphem.2014.12.005. Epub 2014 Dec 27.
8
Haploinsufficiency of del(5q) genes, Egr1 and Apc, cooperate with Tp53 loss to induce acute myeloid leukemia in mice.del(5q) 基因、Egr1 和 Apc 的单倍不足与 Tp53 缺失协同作用诱导小鼠急性髓系白血病。
Blood. 2014 Feb 13;123(7):1069-78. doi: 10.1182/blood-2013-07-517953. Epub 2013 Dec 31.
9
Knockdown of Hspa9, a del(5q31.2) gene, results in a decrease in hematopoietic progenitors in mice.Hspa9 基因敲除导致小鼠造血祖细胞减少，该基因位于 del(5q31.2)。
Blood. 2011 Feb 3;117(5):1530-9. doi: 10.1182/blood-2010-06-293167. Epub 2010 Dec 1.
10
Deregulated gene expression pathways in myelodysplastic syndrome hematopoietic stem cells.骨髓增生异常综合征造血干细胞中失调的基因表达途径。
Leukemia. 2010 Apr;24(4):756-64. doi: 10.1038/leu.2010.31. Epub 2010 Mar 11.

Haploinsufficiency of multiple del(5q) genes induce B cell abnormalities in mice.

作者信息

Liu Tuoen, Ahmed Tanzir, Krysiak Kilannin, Shirai Cara Lunn, Shao Jin, Nunley Ryan, Bucala Richard, McKenzie Andrew, Ndonwi Matthew, Walter Matthew J

机构信息

Department of Medicine, Division of Oncology, Washington University School of Medicine, St. Louis, Missouri, United States; Department of Biomedical Sciences, West Virginia School of Osteopathic Medicine, 400 Lee Street North, Lewisburg, West Virginia, United States.

Department of Medicine, Division of Oncology, Washington University School of Medicine, St. Louis, Missouri, United States.

出版信息

Leuk Res. 2020 Sep;96:106428. doi: 10.1016/j.leukres.2020.106428. Epub 2020 Jul 23.

DOI:10.1016/j.leukres.2020.106428
PMID:32739655
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7768807/
Abstract
摘要