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Cbfb/Runx1-repression independent blockage of differentiation and accumulation of Csf2rb expressing cells by Cbfb-MYH11

ChEBI2010-04-12 更新2026-07-21 收录

急性髓系白血病

造血分化阻滞

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-19194 数据链接链接失效反馈

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资源简介：

Cbfb/Runx1-repression independent blockage of differentiation and accumulation of Csf2rb expressing cells by Cbfb-MYH11

应用场景：

创建时间：

2010-04-12

急性髓系白血病

耐药性机制

Targeting the MYST acetyltransferases are an exciting therapeutic opportunity in acute myeloid leukaemia (AML). Here we define the individual and combined contribution of KAT6A, KAT6B and KAT7, in ran

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Combined epigenetic and metabolic treatments overcome differentiation blockade in acute myeloid leukemia [RNA-Seq]

急性髓系白血病

基因表达分析

A hallmark of acute myeloid leukemia (AML) is the inability of self-renewing malignant cells to mature into a non-dividing terminally differentiated state. To better understand how chromatin factors s

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Data supporting the publication: Transcriptomic analysis of glycolytic regulation by lncRNAs in acute myeloid leukemia

急性髓系白血病

长链非编码RNA

Acute myeloid leukemia (AML), a high-mortality malignancy, limits the efficacy of traditional therapies due to high heterogeneity. Glycolysis drives AML progression via the tumor microenvironment, but

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Aberrant expression of T cell activation markers and upregulation of Tregs in bone marrow and peripheral blood in acute myeloid leukemia patients

急性髓系白血病

免疫学

T cells’ function and activation and the immunosuppressive effect of regulatory T cells (Tregs) play a pivotal role in the occurrence and progression of acute myeloid leukemia (AML). In this study, we

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CARM1/PRMT4 is essential for myeloid leukemogenesis but dispensable for normal hematopoiesis

急性髓系白血病

RNA-seq转录组学

We investigated the role of PRMT4 in normal and malignant hematopoiesis. We found that knockdown of PRMT4 impairs cell cycle progression, induces apoptosis, and downgretulateds E2F target genes in leu

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Cbfb/Runx1-repression independent blockage of differentiation and accumulation of Csf2rb expressing cells by Cbfb-MYH11

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