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Blood. 2021 Apr 15;137(15):1988-1990. doi: 10.1182/blood.2020010541.
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Formaldehyde exposure and leukemia: critical review and reevaluation of the results from a study that is the focus for evidence of biological plausibility.甲醛暴露与白血病:对一项研究结果的批判性回顾和再评估,该研究是证明生物学合理性的重点。
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G-quadruplexes as a source of vulnerability in BRCA2deficient granule cell progenitors and medulloblastoma.G-四链体作为BRCA2缺陷型颗粒细胞祖细胞和髓母细胞瘤中脆弱性的一个来源。
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ALDH9A1 deficiency as a source of endogenous DNA damage that requires repair by the Fanconi anemia pathway.乙醛脱氢酶9A1缺乏作为内源性DNA损伤的一个来源,这种损伤需要通过范可尼贫血途径进行修复。
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Deficiency of the Fanconi anemia core complex protein FAAP100 results in severe Fanconi anemia.范可尼贫血核心复合物蛋白FAAP100的缺陷会导致严重的范可尼贫血。
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Development. 2022 May 15;149(10). doi: 10.1242/dev.200277. Epub 2022 May 19.

本文引用的文献

1
Analysis of disease model iPSCs derived from patients with a novel Fanconi anemia-like IBMFS ADH5/ALDH2 deficiency.分析来自具有新型范可尼贫血样 IBMFS ADH5/ALDH2 缺陷的患者的疾病模型 iPSCs。
Blood. 2021 Apr 15;137(15):2021-2032. doi: 10.1182/blood.2020009111.
2
Digenic mutations in and impair formaldehyde clearance and cause a multisystem disorder, AMeD syndrome.和中的双基因突变异致甲醛清除障碍,并引发一种多系统疾病——AmeD综合征。
Sci Adv. 2020 Dec 18;6(51). doi: 10.1126/sciadv.abd7197. Print 2020 Dec.
3
A Surge of DNA Damage Links Transcriptional Reprogramming and Hematopoietic Deficit in Fanconi Anemia.DNA 损伤激增将范可尼贫血症中的转录重编程与造血缺陷联系起来。
Mol Cell. 2020 Dec 17;80(6):1013-1024.e6. doi: 10.1016/j.molcel.2020.11.040.
4
Two Aldehyde Clearance Systems Are Essential to Prevent Lethal Formaldehyde Accumulation in Mice and Humans.两种醛清除系统对于防止甲醛在人和小鼠中蓄积致死至关重要。
Mol Cell. 2020 Dec 17;80(6):996-1012.e9. doi: 10.1016/j.molcel.2020.10.012. Epub 2020 Nov 3.
5
Alcohol and endogenous aldehydes damage chromosomes and mutate stem cells.酒精和内源性醛会损伤染色体并使干细胞发生突变。
Nature. 2018 Jan 11;553(7687):171-177. doi: 10.1038/nature25154. Epub 2018 Jan 3.
6
Mammals divert endogenous genotoxic formaldehyde into one-carbon metabolism.哺乳动物将内源性基因毒性甲醛导入一碳代谢。
Nature. 2017 Aug 31;548(7669):549-554. doi: 10.1038/nature23481. Epub 2017 Aug 16.
7
Endogenous Formaldehyde Is a Hematopoietic Stem Cell Genotoxin and Metabolic Carcinogen.内源性甲醛是一种造血干细胞基因毒素和代谢致癌物。
Mol Cell. 2015 Oct 1;60(1):177-88. doi: 10.1016/j.molcel.2015.08.020. Epub 2015 Sep 24.
8
Why does the bone marrow fail in Fanconi anemia?范可尼贫血症患者的骨髓为何会衰竭?
Blood. 2014 Jan 2;123(1):26-34. doi: 10.1182/blood-2013-09-427740. Epub 2013 Nov 7.
9
Variant ALDH2 is associated with accelerated progression of bone marrow failure in Japanese Fanconi anemia patients.变异型 ALDH2 与日本范可尼贫血患者骨髓衰竭的加速进展有关。
Blood. 2013 Oct 31;122(18):3206-9. doi: 10.1182/blood-2013-06-507962. Epub 2013 Sep 13.
10
Fancd2 counteracts the toxic effects of naturally produced aldehydes in mice.Fancd2 可拮抗小鼠体内天然产生的醛类的毒性作用。
Nature. 2011 Jul 6;475(7354):53-8. doi: 10.1038/nature10192.

内源性甲醛会破坏血液干细胞。

Endogenous formaldehyde destroys blood stem cells.

机构信息

The Rockefeller University.

出版信息

Blood. 2021 Apr 15;137(15):1988-1990. doi: 10.1182/blood.2020010541.

DOI:10.1182/blood.2020010541
PMID:33856442
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8057262/
Abstract

In this issue of , Mu et al show that induced pluripotent stem cells (iPSCs) derived from patients with novel inherited bone marrow failure syndrome (IBMFS), alcohol dehydrogenase 5 (ADH5)/aldehyde dehydrogenase 2 (ALDH2) deficiency, fail to produce hematopoietic progenitors.

摘要

本期 杂志中,Mu 等人研究表明,源自新型遗传性骨髓衰竭综合征(IBMFS)、醇脱氢酶 5(ADH5)/醛脱氢酶 2(ALDH2)缺乏症患者的诱导多能干细胞(iPSC)无法生成造血祖细胞。