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Preclinical efficacy of targeting epigenetic mechanisms in AML with 3q26 lesions and EVI1 overexpression. Preclinical efficacy of targeting epigenetic mechanisms in AML with 3q26 lesions and EVI1 overexpression

NIAID Data Ecosystem2026-05-01 收录

急性髓系白血病表观遗传

AMLEVI1过表达

数据链接：

https://www.ncbi.nlm.nih.gov/bioproject/PRJNA1036204 数据链接链接失效反馈

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资源简介：

This SuperSeries is composed of the SubSeries listed below. Overall design: Refer to individual Series

应用场景：

创建时间：

2023-11-06

急性髓系白血病表观遗传

治疗反应预测

BackgroundDNMT3A mutations occur in 20-25% of acute myeloid leukemia (AML) cases and are associated with poor prognosis, yet the epigenetic mechanisms underlying treatment response remain poorly under

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Inhibitors of LSD1 target demethylase-independent activity to induce differentiation in acute myeloid leukemia [anti-H3K9 ac, anti-H3K27, RCOR1, SPI1, and MLL4 ChIP-Seq]. Inhibitors of LSD1 target demethylase-independent activity to induce differentiation in acute myeloid leukemia [anti-H3K9 ac, anti-H3K27, RCOR1, SPI1, and MLL4 ChIP-Seq]

急性髓系白血病表观遗传

LSD1抑制剂

To determine whether changes in histone modifications directly correlate with changes in transcription, THP1 AML cells were treated with a potent and selective LSD1 inhibitor (OG86, 250nM) and then su

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A molecular switch between mammalian MLL complexes dictates response to Menin-MLL inhibition [RNA-seq]. A molecular switch between mammalian MLL complexes dictates response to Menin-MLL inhibition [RNA-seq]

急性髓系白血病表观遗传

Menin-MLL抑制剂响应机制

The chromatin adaptor Menin interacts with oncogenic fusion proteins encoded by MLL1-rearrangements (MLL1-r), and small molecules that disrupt these associations are currently in clinical trials for t

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Mediator kinase inhibition further activates super-enhancer-associated genes in AML

急性髓系白血病表观遗传

增强子靶向治疗

Super-enhancers (SEs), which are composed of large clusters of enhancers densely loaded with the Mediator complex, transcription factors and chromatin regulators, drive high expression of genes implic

NIAID Data Ecosystem80

H3K9 acetylation and di-methylation changes in HL-60 cells following treatment with different compounds. H3K9 acetylation and di-methylation changes in HL-60 cells following treatment with different compounds

急性髓系白血病表观遗传

药物响应蛋白质组学

We investigate the effects of GCN5 and LSD1 inhibition in acute myeloid leukemia. Therefore, we characterized acetylation and di-methylation changes by ChIP-seq in AML cells (AML M2 cell line HL-60) f

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Preclinical efficacy of targeting epigenetic mechanisms in AML with 3q26 lesions and EVI1 overexpression. Preclinical efficacy of targeting epigenetic mechanisms in AML with 3q26 lesions and EVI1 overexpression

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