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Expression data from human hematopoietic stem and progenitor compartments from patients with acute myeloid leukemia with complex karyotype

ABSTRACT: Expression data from human hematopoietic stem and progenitor compartments from patients with acute myeloid leukemia with complex karyotype

PROVIDER: PRJNA473980 | ENA |

REPOSITORIES: ENA

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Expression data from human hematopoietic stem and progenitor compartments from patients with acute myeloid leukemia with complex karyotype

Project description:We applied transcriptional analysis of multiple, highly fractionated stem and progenitor populations from patients with acute myeloid leukemia (AML) with complex karyotype. We isolated phenotypic long-term HSC (LT-HSC), short-term HSC (ST-HSC), and committed granulocyte-monocyte progenitors (GMP) from individual patients, and measured gene expression profiles of each population, and in comparison to their phenotypic counterparts from age-matched healthy controls. In this dataset, we include the expression data obtained from sorted hematopoietic stem and progenitor cells from patients with AML with complex karyotype.

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Expression data from human hematopoietic stem and progenitor compartments from patients with acute myeloid leukemia with normal karyotype and healthy controls

Project description:We applied a novel approach of parallel transcriptional analysis of multiple, highly fractionated stem and progenitor populations from patients with acute myeloid leukemia (AML) and a normal karyotype. We isolated phenotypic long-term HSC (LT-HSC), short-term HSC (ST-HSC), and committed granulocyte-monocyte progenitors (GMP) from individual patients, and measured gene expression profiles of each population, and in comparison to their phenotypic counterparts from age-matched healthy controls. Bone marrow samples from AML patients with normal karyotype and age-matched healthy controls were used in this study. Hematopoietic stem and progenitor compartments were purified by multiparameter-high speed fluorescence-activated cell sorting (FACS) from CD34+ enriched bone marrow to isolate LT-HSC (Lin-/CD34+/CD38-/CD90+), ST-HSC (Lin-/CD34+/CD38-/CD90-), and GMP (Lin-/CD34+/CD38+/CD123+/CD45R+).

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Project description:We applied a novel approach of parallel transcriptional analysis of multiple, highly fractionated stem and progenitor populations in a genetically defined subset of AML (AML with monosomy 7). We isolated phenotypic long-term HSC (LT-HSC), short-term HSC (ST-HSC), and committed granulocyte-monocyte progenitors (GMP) from individual patients with AML, and measured gene expression profiles of each population, and in comparison to their phenotypic counterparts from age-matched healthy controls. Bone marrow samples from AML patients bearing monosomy 7 and age-matched healthy controls were used in this study. Hematopoietic stem and progenitor compartments were purified by multiparameter-high speed fluorescence-activated cell sorting (FACS) from CD34+ enriched bone marrow to isolate LT-HSC (Lin-/CD34+/CD38-/CD90+), ST-HSC (Lin-/CD34+/CD38-/CD90-), and GMP (Lin-/CD34+/CD38+/CD123+/CD45R+).

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Project description:Quantitative proteomic analysis of mouse fetal and adult hematopoietic progenitor cells using TMT6plex and an SPS-MS3 method.

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Differential expression of proteins in hematopoietic stem/progenitor cells lacking the Cullin-5 protein

Project description:Cullin proteins are scaffolds that coordinate assembly of cullin-RING E3 ubiquitin (Ub) ligases (CRL), complexes that control post-translational ubiquitin modification and degradation of cellular proteins. Cullin-5 (Cul5) coordinates assembly of CRL complexes containing the RING E3 ligase Rbx1/2, the adapter proteins Elongins B and C, and a Suppressor of Cytokine Signalling (SOCS) box-containing substrate recognition protein. To explore potential roles for Cul5, we generated mice lacking Cul5 in the in hematopoietic system. Analyses included biological and molecular studies including proteomic analysis of differential expression of proteins in primary purified hematopoietic stem/progenitor (LSK) cells lacking Cul5.

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Affymetrix SNP array data for acute myeloid leukemia (AML) samples with complex karyotype

Project description:AML with complex karyotype (CK-AML) is characterized by a high frequency of TP53 alteration (loss and/or mutation). TP53-altered CK-AML were characterized by a higher degree of genomic complexity (aberrations per case, 14.30 vs. 6.16; P<.0001), and by a higher frequency of specific copy number alterations, such as -5/5q-, -7/7q-, -16/16q-, -18/18q-, +1/+1p, and +11/+11q/amp11q13~25; among CK-AML, TP53-altered more frequently exhibited a monosomal karyotype (MK). Patients with TP53 alterations were older and had significantly lower complete remission rates, inferior event-free, relapse-free, and overall survival. In multivariable analysis for overall survival, TP53 alterations, white blood cell counts, and age were the only significant factors. In conclusion, TP53 is the most frequently known altered gene in CK-AML. TP53 alterations are associated with older age, genomic complexity, specific DNA copy number alterations, MK, and dismal outcome. In multivariable analysis, TP53 alteration is the most important prognostic factor in CK-AML, outweighing all other variables, including the MK category.

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Effect of depletion of the transcriptional factor FoxP1 on gene expression in mouse normal adult hematopoietic stem and progenitor cells.

Project description:Transcription factor Forkhead box P1 (FOXP1) is a key regulator of various immune cell functions, including monocyte differentiation, B cell terminal differentiation and CD4+ or CD8+ T cell quiescence. In previous studies, we have shown that FOXP1 contributes to human hematopoietic stem progenitor cell (HSPC) and acute myeloid leukemia (AML) cell growth. Here we investigated the in vivo role of Foxp1 in early adult murine hematopoiesis. We showed that hematopoietic-speciﬁc loss of Foxp1 expression leads to attrition of the medullar HSC/Multipotent progenitor (MPP)-1 compartment in parallel with an enhancement of the myeloid-biased MPP3 compartment, without impact on MPP2 or MPP4 compartments. Foxp1-deﬁcient HSCs exhibited a reduced self-renewal capacity in competitive hematopoietic reconstitution assays, and HSC and all MPP compartments showed enhanced proliferation with a G0 phase reduction. To further investigate the role of Foxp1 in the regulation of HSC and MPP compartments, we performed gene expression profiling analysis of HSC/MPP1 and MPP3 compartments from WT and Foxp1-deficient mice using data obtained from RNASeq of 3 different cell populations.

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