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Abstract
Chronic myelogenous leukemia (CML) is a type of cancer with a series of characteristics that make it particularly suitable for observations on leukemogenesis. Research have exhibited that the occurrence and progression of CML are associated with the dynamic alterations of histone modification (HM) patterns. In this study, we analyze the distribution patterns of 11 HM signals and calculate the signal changes of these HMs in CML cell lines as compared with that in normal cell lines. Meanwhile, the impacts of HM signal changes on expression level changes of CML-related genes are investigated. Based on the alterations of HM signals between CML and normal cell lines, the up- and down-regulated genes are predicted by the random forest algorithm to identify the key HMs and their regulatory regions. Research show that H3K79me2, H3K36me3, and H3K27ac are key HMs to expression level changes of CML-related genes in leukemogenesis. Especially H3K79me2 and H3K36me3 perform their important functions in all 100 bins studied. Our research reveals that H3K79me2 and H3K36me3 may be the core HMs for the clinical treatment of CML.
Highlights
Chronic myelogenous leukemia (CML) is a malignant hematopoietic stem cell disease of the bone marrow and owns a series of characteristics that make it suitable for observations on leukemogenesis (Liu et al, 2015; Radivoyevitch et al, 2020; Wu et al, 2020)
For the up- and down-differential expression genes (DEGs), we calculate the ratios of histone modification (HM) signals/gene expression levels in CML
Cells to that in normal cells, respectively, and the relations between HM signal changes and gene expression changes are implemented through Spearman correlation analysis
Summary
Chronic myelogenous leukemia (CML) is a malignant hematopoietic stem cell disease of the bone marrow and owns a series of characteristics that make it suitable for observations on leukemogenesis (Liu et al, 2015; Radivoyevitch et al, 2020; Wu et al, 2020). It is characterized by the (9:22) translocation and resultant production of the constitutively activated BCR-ABL. Though the application of targeted drugs is expected to overcome CML, the persistence of leukemia stem cells indicates that additional strategies for treating CML need to be researched
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