Combined epigenetic and metabolic treatments overcome differentiation blockade in acute myeloid leukemia [ATAC-Seq]
收藏干细胞与再生医学数据中心2022-02-20 更新2024-03-06 收录
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http://data.iscr.ac.cn/Article?id=35ba57ed46c203ba8e133d53a58d1a8e
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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 such as LSD1 interact with metabolic pathways to support the differentiation blockade, we screened a small molecule library to identify druggable substrates that promote myeloid maturation. We found that differentiation caused by LSD1 inhibition is enhanced by combinatorial perturbation of purine nucleotide salvage and de novo lipogenesis pathways. We used ATAC-seq to determine whether the drug combination induces chromatin changes.
提供机构：
Boston Children's Hospital
创建时间：
2022-02-20
