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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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RNA-Seq analysis of primary AML specimens exposed to AhR modulating agents

ABSTRACT: The goal of the study was to identify genes that are directly or indirectly coregulated by the AhR pathway in primary human AML cells. Patient AML cells were treated for 16 hours with the two indirubin derivatives 6-bromoindirubin-3'oxime (BIO), 1-Methyl-6-bromoindirubin-3'oxime (MeBIO), the AHR-antagonist SR1 (StemReginin1), combinations of BIO+SR1 and MeBIO+SR1 or DMSO alone at indicated concentrations prior to RNA extraction for sequencing. RNA-Seq performed on 5 primary AML samples fresh (t0) and after exposure to AhR-agonists (2), -antagonist (1), and DMSO Contributor: Leucegene Project, IRIC

ORGANISM(S): Homo sapiens

SUBMITTER: Guy Sauvageau

PROVIDER: E-GEOD-48843 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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GPR56 identifies primary human acute myeloid leukemia cells with high repopulating potential in vivo.

Pabst Caroline C Bergeron Anne A Lavallée Vincent-Philippe VP Yeh Jonathan J Gendron Patrick P Norddahl Gudmundur L GL Krosl Jana J Boivin Isabel I Deneault Eric E Simard Jessica J Imren Suzan S Boucher Geneviève G Eppert Kolja K Herold Tobias T Bohlander Stefan K SK Humphries Keith K Lemieux Sébastien S Hébert Josée J Sauvageau Guy G Barabé Frédéric F

Blood 20160201 16

Acute myeloid leukemia (AML) is a genetically heterogeneous hematologic malignancy, which is initiated and driven by a rare fraction of leukemia stem cells (LSCs). Despite the difficulties of identifying a common LSC phenotype, there is increasing evidence that high expression of stem cell gene signatures is associated with poor clinical outcome. Identification of functionally distinct subpopulations in this disease is therefore crucial to dissecting the molecular machinery underlying LSC self-r ...[more]

PMID: 26834243

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RNA-Seq analysis of primary AML specimens exposed to AhR modulating agents

Project description:The goal of the study was to identify genes that are directly or indirectly coregulated by the AhR pathway in primary human AML cells. Patient AML cells were treated for 16 hours with the two indirubin derivatives 6-bromoindirubin-3'oxime (BIO), 1-Methyl-6-bromoindirubin-3'oxime (MeBIO), the AHR-antagonist SR1 (StemReginin1), combinations of BIO+SR1 and MeBIO+SR1 or DMSO alone at indicated concentrations prior to RNA extraction for sequencing.

2016-07-20 | GSE48843 | GEO

Transcriptome data of CD34+ human cord blood-derived cell treated with UM171, SR1 or both

Project description:mRNA profiling of CD34+ human cord blood-derived cell treated with UM171, SR1 or both mRNA profiles of CD34+ human cord blood-derived cell treated with DMSO (control), SR1 [500nM], UM171 [35nM] or combination SR1 [500nM]+ UM171 [35nM] for 30min, 3hr, 12hr, 24hr, 48hr, 72hr were generated by deep sequencing

2014-10-21 | E-GEOD-57299 | biostudies-arrayexpress

RNA expression profiling of human mPB or CB-derived CD34+ cells treated with UM171 at different doses

Project description:RNASeq data for mPB or CB-derived CD34+ exposed to UM171 human mobilized peripheral blood or cord blood-derived CD34(+) cells were cultured for 16 hours with vehicle (DMSO), dose response of UM171 [11.9nM, 19nM, 30.5nM, 48.8nM, 78.1nM and 125nM], SR1 [500nM] and combination of( UM171 [48.8nM]+SR1 [500nM])

2014-10-21 | E-GEOD-57561 | biostudies-arrayexpress

Integrated analysis of MLL-AF9 AML patients and model leukemias highlights RET and other novel therapeutic targets [RNA-Seq_AML]

Project description:Next generation DNA sequencing of acute myeloid leukemia (AML) patient samples has revealed novel recurrent mutations while at the same time highlighting the genetic heterogeneity of the disease. These observations suggest that an extraordinarily large number of combinations of mutations can contribute to leukemogenesis. In order to address the question of the contribution of patient genetic background to AML we have developed a model system to generate multiple human leukemias in a single donorâs genetic background. Stepwise RNA-seq data from this model shows that in the context of AML driven by the MLL-AF9 (MA9) oncogene, the genetic background of the donor does not have a detectable effect. Comparison of these model leukemias from multiple single donors to AML patient samples containing MA9 translocations revealed conserved gene expression patterns not previously highlighted in this genetic sub-type. We further demonstrate that the expression of one of these genes, RET, is essential both in vivo and in vitro growth of MA9 AMLs . Transcriptome of several AML cell lines

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Integrated analysis of MLL-AF9 AML patients and model leukemias highlights RET and other novel therapeutic targets (Leukemia Cell Bank)

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Leucegene: AML sequencing (part 2)

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Integrated analysis of MLL-AF9 AML patients and model leukemias highlights RET and other novel therapeutic targets [RNA-Seq_normal]

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Leucegene: AML sequencing (part 5)

2015-07-09 | E-GEOD-67039 | biostudies-arrayexpress

Leucegene: AML sequencing (part 3)

2015-07-09 | E-GEOD-62190 | biostudies-arrayexpress