Project description:We report the gene expression of human chronic myelomonocytic leukemia by performing whole transcriptome shotgun sequencing of bone marrow mononuclear cells of patients with chronic myelomonocytic leukemia.
Project description:We report the chromatin characteristics of human chronic myelomonocytic leukemia by performing chromatin immunoprecipitation sequencing of histone modifications (ChIP-seq), immunoprecipitation sequencing of (hydroxy-)methylated residues (DIP-seq), and transposase accessibility sequencing (ATAC-seq) of bone marrow mononuclear cells of patients with chronic myelomonocytic leukemia.
Project description:We report the gene expression of human chronic myelomonocytic leukemia by performing whole transcriptome shotgun sequencing of peripheral blood mononuclear cells of patients with chronic myelomonocytic leukemia.
Project description:In this study, institutional IRB approval was obtained and peripheral blood and bone marrow samples on patients with chronic myelomonocytic leukemia were collected. On the samples, we performed chromatin immuno-precipitation and next generation sequencing to assess histone modifications and epigenetic changes associated with proliferative and dysplastic phenotypes.
Project description:RNA-seq of bone marrow samples of chronic myelomonocytic leukemia (CMML) patients and healthy donors to identify the molecular DNA repair pathways involved in CMML pathogenic
Project description:Chronic myelomonocytic leukemia is an aggressive hematological malignancy with dismal outcomes, with the pCMML subtype in particular having median OS of <2 years and high rates of AML transformation (Patnaik et al., 2014). Given limited therapeutic options for affected patients, we carried out this study to define the genetic and epigenetic landscape of pCMML and identify therapies that could modify disease biology.
Project description:BACKGROUND: Our previous studies showed that RUNX1 and ASXL1 mutations were frequently co-existed in chronic myelomonocytic leukemia (CMML) and clonal evolution of RUNX1 and/or ASXL1 occurred most frequently in chronic myeloid leukemia (CML) with myeloid blastic crisis. The molecular pathogenesis of cooperation of RUNX1 and ASXL1 mutations has not been reported yet. METHODS: Lentiviral-mediated stable transduction of RUNX1-WT/MT (R135T) in K562 cells which harboring ASXL1-MT (Y591X). RNA was extracted from stable cell line and used for gene-expression microarray analysis. RESULTS: For in vitro study, we overexpressed RUNX1-WT/MT (R135T) in K562 cells which harboring ASXL1-MT (Y591X). We found that RUNX1-MT augmented cell proliferation, colony formation, HOXA gene expression and inhibited megakaryocytic differentiation in ASXL1-MT K562 cells compared to RUNX1-WT or empty vector control. We performed gene expression profile of K562 cells overexpressed with EV, RUNX1-WT and RUNX1-R135T mutation. Gene expression microarray data revealed that 147 genes upregulated more than 2-fold in RUNX1-R135T expressing K562 cells compared to EV control cells. From gene expression data analysis, we found that inhibitor of DNA binding 1 (ID1), a key transcriptional regulator of hematopoietic stem cell (HSC) lineage commitment, is upregulated in RUNX1-R135T-transduced K562 cells compared to EV and RUNX1-WT-expressing cells.