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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Promotion and maintenance of leukemia by ERG No.1

ABSTRACT: Thymocytes without mutation in Notch1 in mice transplanted with ERG-transduced BM cells were compared with thymocytes in mice transplanted with GFP control-transduced bone marrow cells.

ORGANISM(S): Mus musculus

SUBMITTER: Shinobu Tsuzuki

PROVIDER: E-MEXP-2986 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Promotion and maintenance of leukemia by ERG.

Tsuzuki Shinobu S Taguchi Osamu O Seto Masao M

Blood 20110214 14

The Ets-related gene (ERG) located on human chromosome 21 encodes a transcription factor and is thought to be causally related to Down syndrome-associated acute megakaryocytic leukemia in childhood. In clinical adult leukemia, however, increased expression of ERG is indicative of poor prognosis in T-cell acute lymphoblastic leukemia and cytogenetically normal acute myeloid leukemia, although the involvement of ERG in the development of adult leukemia remains elusive. Here, we show that forced ex ...[more]

PMID: 21321361

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ERG promotes the maintenance of hematopoietic stem cells by restricting their differentiation

Project description:To investigate the role of the transcription factor ERG in hematopoiesis we generated Erg heterozygous knockout and conditional Erg knockout mice. We found that several hematopoietic cell types were decreased in these mice. To define Erg downstream target genes in hematopoietic stem cells, we sorted Lineage-, Sca-1+, c-kit+, CD150+, CD48- cells from Erg +/- mice for gene expression analysis. To define Erg downstream target genes in hematopoietic progenitors, we sorted multipotent progenitors (Lineage-, Sca-1+, c-kit+, CD150-) from Erg -/- mice for gene expression analysis. We generated Erg heterozygous knockout mice and provide 3 replicates for wild type (Erg +/+) populations of stem cells (HSC) and 3 replicates for Erg +/- mices. We also generated a conditional Erg knockout mice. We provide 3 replicates for Erg fl/fl and 3 replicates for Erg (-/-) mice.

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ERG promotes the maintenance of hematopoietic stem cells by restricting their differentiation

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Project description:ERG is an Ets-transcription factor required for normal blood stem cell development. High ERG expression in acute myeloid leukemia (AML) and acute T-cell lymphoblastic leukemia (T-ALL) is associated with a stem cell signature and poor prognosis. In murine over-expression models, human ERG is a potent oncogene that induces both T-ALL and AML. However the functional and molecular consequences of high ERG expression in normal hematopoietic stem/progenitors (HSPCs), and how this contributes to leukemia development, are unknown. Here we show that retroviral transduction of ERG into human CD34+ cells and maintenance of ERG at levels present in high ERG AML results in altered myeloid and T cell differentiation and an increase in the self-renewal capacity of transduced progenitors but not the more primitive stem cell compartment. Integrated analysis of genome-wide expression in high ERG CD34+ and ERG binding profiles in HSPCs revealed that these functional characteristics were accompanied by an expression signature that was enriched in normal HSCs, high ERG AMLs, early T-cell precursor (ETP)-ALLs and leukemic stem cell signatures associated with poor clinical outcome. The proliferative advantage of high ERG progenitors may provide a cellular context for the acquisition and propagation of mutations that contribute to the pathogenesis of leukaemia. RNA sequencing in ERG overexpressing human CD34+ cells

2014-10-31 | E-GEOD-53665 | biostudies-arrayexpress

Expression data of leukemia samples taken from transgenic ERG mice

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Project description:Here we show that pan-haematopoietic ERG expression driven by the Vav promoter induces an early progenitor myeloid leukemia in transgenic mice. Integrated genome-scale analysis of gene expression and ERG binding profiles revealed that ERG activates a transcriptional program similar to human AML stem/progenitor cells and human AML with high ERG expression. We further show that ERG induces expression of the Pim1 kinase oncogene through a novel enhancer element validated in transgenic mice, and Pim1 inhibition disrupts growth and induces apoptosis of ERG-driven leukemic cells. In addition, ERG indirectly induces the RAS pathway and direct RAS inhibition by a RAS inhibitor blocks growth of leukemia cells in vitro and in vivo. Thus, integrative genomic analysis of transgenic ERG leukemias reveals mechanisms and potential therapeutic targets of high ERG expressing AML.

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