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Maintenance of Leukemic Cell Identity by the Activity of the Polycomb Complex PRC1 (ChIP-seq)

ABSTRACT: These data include the genome wide occupancy of H2AUbq by ChIP sequencing in Cdkn2a-/- Lin- HSC cells non-transduced or transduced with MLL-AF9, HOXA9 and PML-RARa. Immuno-precipitation of formaldehyde cross-linked chromatin prepared from Cdkn2a-/- Lin- HSC cells non-transduced or transduced with MLL-AF9, HOXA9 and PML-RARa using H2AK119Ubq antibody.

ORGANISM(S): Mus musculus

SUBMITTER: Sri Ganesh Jammula

PROVIDER: E-GEOD-67498 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Maintenance of leukemic cell identity by the activity of the Polycomb complex PRC1 in mice.

Rossi Alessandra A Ferrari Karin J KJ Piunti Andrea A Jammula SriGanesh S Chiacchiera Fulvio F Mazzarella Luca L Scelfo Andrea A Pelicci Pier Giuseppe PG Pasini Diego D

Science advances 20161007 10

Leukemia is a complex heterogeneous disease often driven by the expression of oncogenic fusion proteins with different molecular and biochemical properties. Whereas several fusion proteins induce leukemogenesis by activating <i>Hox</i> gene expression (Hox-activating fusions), others impinge on different pathways that do not involve the activation of <i>Hox</i> genes (non-Hox-activating fusions). It has been postulated that one of the main oncogenic properties of the HOXA9 transcription factor i ...[more]

PMID: 27730210

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Maintenance of Leukemic Cell Identity by the Activity of the Polycomb Complex PRC1 (RNA-seq)

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Maintenance of Leukemic Cell Identity by the Activity of the Polycomb Complex PRC1 (ChIP-seq)

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Maintenance of Leukemic Cell Identity by the Activity of the Polycomb Complex PRC1 (RNA-seq)

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PML-RARA fusion gene requires Dnmt3a to induce acute promyelocytic leukemia in mice

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KrasG12D partially compensates for the loss of beta-catenin in MLL-AF9 AML

Project description:The Wnt/beta-catenin pathway is required for the development of leukemia stem cells in MLL-AF9 AML. We evaluated the dependance on beta-catenin for KrasG12DMLL-AF9 leukemia. Lin-Kit+ bone marrow cells obtained from mice transplanted with primary MLL-AF9 leukemia cells and KRasG12DMLL-AF9 leukemia cells were assessed for gene expression in the presence or absence of beta-catenin

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Gene expression regulated by miR-101 in murine MLL-AF9-transduced LSK cells

Project description:miR-101 has been reported as a tumor suppressor in several types of cancer. However, its role in AML is still unknown. In this study, we restored the expression of miR-101 in MLL-AF9 transduced LSK cells by introducing a retroviral miR-101 expression vector. To identify miR-101-regulated gene expression, we performed genome-wide gene expression analysis on GFP+ MLL-AF9-transduced LSK cells overexpressing miR-101 versus control vector. Our gene expression analysis and subsequent functional studies demonstrate that enforced expression of miR-101 has antitumor effects on the development of MLL-rearranged AML. Each group has 3 samples.

2019-07-03 | E-MTAB-7344 | biostudies-arrayexpress

Expression and function of PML-RARA in the multipotent hematopoietic progenitor cells of Ctsg-PML-RARA mice

Project description:Because PML-RARA-positive acute promyelocytic leukemia (APL) is a morphologically differentiated leukemia, much speculation has been made about whether its leukemic cell of origin might be committed myeloid precursor (e.g., a promyelocyte) vs. a hematopoietic stem/progenitor cell (HSPC). We originally targeted PML-RARA expression with CTSG regulatory elements, based on the early observation that this gene was maximally expressed in cells with promyelocyte morphology. Here, we show that both Ctsg and PML-RARA targeted to the Ctsg locus (in Ctsg-PML-RARA mice) are detected in the purified KLS cells of these mice (Kit+Lin-Sca+ cells, which are highly enriched for HSPCs), and this expression results in biological effects in multi-lineage competitive repopulation assays. Although PML-RARA is indeed expressed at high levels in the promyelocytes of Ctsg-PML-RARA mice, it does not significantly alter the transcriptional signature of these cells, or induce their self-renewal. In sum, these results suggest that in murine models, PML-RARA acts primarily to affect the function of multi-potent progenitor cells, rather than promyelocytes. Since PML/Pml is normally expressed in the HSPCs of both humans and mice, and since some human APL samples contain TCR rearrangements and express T lineage genes, we suggest that the very early hematopoietic expression of PML-RARA in our mouse model may closely mimic the physiologic expression pattern of PML-RARA in human APL patients.

2012-08-14 | GSE40022 | GEO

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