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Tumor suppressor IKZF1 mediates glucocorticoid resistance in B-cell precursor acute lymphoblastic leukemia.

作者信息

Marke R, Havinga J, Cloos J, Demkes M, Poelmans G, Yuniati L, van Ingen Schenau D, Sonneveld E, Waanders E, Pieters R, Kuiper R P, Hoogerbrugge P M, Kaspers G J L, van Leeuwen F N, Scheijen B

机构信息

Laboratory of Pediatric Oncology, Radboud University Medical Center, Nijmegen, The Netherlands.

Department of Pediatric Oncology/Hematology, VU University Medical Center, Amsterdam, The Netherlands.

出版信息

Leukemia. 2016 Jul;30(7):1599-603. doi: 10.1038/leu.2015.359. Epub 2015 Dec 29.

DOI:10.1038/leu.2015.359
PMID:26713593
Abstract
摘要

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Redefining ALL classification: toward detecting high-risk ALL and implementing precision medicine.重新定义急性淋巴细胞白血病分类:迈向检测高危急性淋巴细胞白血病并实施精准医学
Blood. 2015 Jun 25;125(26):3977-87. doi: 10.1182/blood-2015-02-580043. Epub 2015 May 21.
2
NALP3 inflammasome upregulation and CASP1 cleavage of the glucocorticoid receptor cause glucocorticoid resistance in leukemia cells.NALP3炎性小体上调以及糖皮质激素受体的半胱天冬酶-1切割导致白血病细胞产生糖皮质激素抵抗。
Nat Genet. 2015 Jun;47(6):607-14. doi: 10.1038/ng.3283. Epub 2015 May 4.
3
Ikaros deletions in BCR-ABL-negative childhood acute lymphoblastic leukemia are associated with a distinct gene expression signature but do not result in intrinsic chemoresistance.
通过高通量药物筛选确定组蛋白去乙酰化酶抑制剂吉维司他(ITF2357)在CRLF2重排的儿童B细胞前体急性淋巴细胞白血病中的协同药物相互作用。
Heliyon. 2024 Jul 3;10(13):e34033. doi: 10.1016/j.heliyon.2024.e34033. eCollection 2024 Jul 15.
4
Multifaceted roles of gene, perspectives from bench to bedside.基因的多方面作用:从实验室到临床的视角
Front Oncol. 2024 Jun 24;14:1383419. doi: 10.3389/fonc.2024.1383419. eCollection 2024.
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Glucocorticoid Therapy in Acute Lymphoblastic Leukemia: Navigating Short-Term and Long-Term Effects and Optimal Regimen Selection.糖皮质激素治疗急性淋巴细胞白血病:短期和长期效应的探讨以及最佳方案的选择。
Curr Hematol Malig Rep. 2024 Aug;19(4):175-185. doi: 10.1007/s11899-024-00735-w. Epub 2024 Jun 13.
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gene deletions drive resistance to cytarabine in B-cell precursor acute lymphoblastic leukemia.基因缺失导致B细胞前体急性淋巴细胞白血病对阿糖胞苷产生耐药性。
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Front Oncol. 2022 Sep 2;12:905665. doi: 10.3389/fonc.2022.905665. eCollection 2022.
Ikaros 缺失与 BCR-ABL 阴性儿童急性淋巴细胞白血病的独特基因表达特征相关,但不会导致内在的化疗耐药性。
Pediatr Blood Cancer. 2014 Oct;61(10):1779-85. doi: 10.1002/pbc.25119. Epub 2014 Jun 29.
4
Loss of TBL1XR1 disrupts glucocorticoid receptor recruitment to chromatin and results in glucocorticoid resistance in a B-lymphoblastic leukemia model.TBL1XR1 的缺失会破坏糖皮质激素受体向染色质的募集,从而导致 B 淋巴细胞白血病模型中的糖皮质激素抵抗。
J Biol Chem. 2014 Jul 25;289(30):20502-15. doi: 10.1074/jbc.M114.569889.
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Loss of Ikaros DNA-binding function confers integrin-dependent survival on pre-B cells and progression to acute lymphoblastic leukemia.Ikaros 基因结合功能丧失赋予前 B 细胞整合素依赖性生存能力并促进急性淋巴细胞白血病进展。
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Direct reversal of glucocorticoid resistance by AKT inhibition in acute lymphoblastic leukemia.AKT 抑制可直接逆转急性淋巴细胞白血病的糖皮质激素抵抗。
Cancer Cell. 2013 Dec 9;24(6):766-76. doi: 10.1016/j.ccr.2013.10.022. Epub 2013 Nov 27.
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Genome-wide identification of Ikaros targets elucidates its contribution to mouse B-cell lineage specification and pre-B-cell differentiation.全基因组鉴定 Ikaros 靶标阐明了其对小鼠 B 细胞谱系特异性和前 B 细胞分化的贡献。
Blood. 2013 Mar 7;121(10):1769-82. doi: 10.1182/blood-2012-08-450114. Epub 2013 Jan 9.
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CREBBP mutations in relapsed acute lymphoblastic leukaemia.复发急性淋巴细胞白血病中的 CREBBP 突变。
Nature. 2011 Mar 10;471(7337):235-9. doi: 10.1038/nature09727.
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Blood. 2010 Oct 21;116(16):3013-22. doi: 10.1182/blood-2010-05-284968. Epub 2010 Jul 20.
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IKZF1 deletions predict relapse in uniformly treated pediatric precursor B-ALL.IKZF1 缺失可预测经统一治疗的儿童前体 B-ALL 的复发。
Leukemia. 2010 Jul;24(7):1258-64. doi: 10.1038/leu.2010.87. Epub 2010 May 6.