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Analysis of global gene expression of a human T-ALL cell lines, comparing GATA3low ETP-ALL (i.e. PER-117) and "typical" T-ALL

ABSTRACT: Cell lines representing human T-ALL were analyzed to compare GATA3low ETP-ALL (i.e. PER-117) with "typical" T-ALL. Moreover, changes in global gene expression were assessed comparing GATA3low ETP-ALL (i.e. PER-117) and GATA3high ETP-ALL (i.e. Loucy) upon treatment with Decitabine, a hypomethylating agent.

ORGANISM(S): Homo sapiens

PROVIDER: GSE78166 | GEO | 2016/02/26

SECONDARY ACCESSION(S): PRJNA313227

REPOSITORIES: GEO

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Analysis of global gene expression of a human T-ALL cell lines, comparing GATA3low ETP-ALL (i.e. PER-117) and "typical" T-ALL

Project description:Cell lines representing human T-ALL were analyzed to compare GATA3low ETP-ALL (i.e. PER-117) with "typical" T-ALL. Moreover, changes in global gene expression were assessed comparing GATA3low ETP-ALL (i.e. PER-117) and GATA3high ETP-ALL (i.e. Loucy) upon treatment with Decitabine, a hypomethylating agent. Analysis of 6 human cell lines representing "typical" T-ALL (BE13, Jurkat, Molt4, RPM18402) and ETP-ALL (Loucy, PER-117). Additionally, global gene expression was assessed before and after treatment of ETP-ALL cell lines with Decitabine

2016-02-26 | E-GEOD-78166 | biostudies-arrayexpress

The spleen as a sanctuary site for residual leukemic cells following ABT-199 monotherapy in ETP-ALL

Project description:Two mice in which luciferase-positive LOUCY ETP-ALL cells were xenografted were treated with either vehicle or ABT-199 (50 mg/kg) for 11 days. Afterwards, single cells suspensions were made from bone marrow and spleen of both mice for 10x Genomics scRNA-seq. Following quality control, a total of 13,681 spleen cells and 11,442 bone marrow cells of the control mouse and 15,955 spleen cells and 9,443 bone marrow cells of the ABT 199 treated mouse were processed for further analysis. Our data show that ABT-199 triggers transcriptional changes in T-cell differentiation genes in leukemic cells obtained from the spleen microenvironment. These results are in line with our previous findings that mature typical T-ALL are resistant to ABT-199.

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Project description:Here we performed low coverage whole genome enzymatic-mehtyl-conversion sequencing (EM-seq) of 11 commercially available T-ALL cell lines to evaluate their global DNA methylation profile. We then proceeded to treat ALL-SIL, SUP-T1, LOUCY and JURKAT with varying concentrations (0-3000 nM) of three different hypomethylating agents, 5-azacytidine (AZA), 5-aza-2′-deoxycytidine (DEC) and GSK3685032 (GSK5032), for 3 and 7 days to evaluate their DNA demethylating ability.

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The Zmiz1-Notch1 interaction induces Myc expression to drive steady state and stress thymopoiesis [ETP and DN3]

Project description:Notch1 signaling ramps up to very high levels in order to drive CD4-CD8- double-negative (DN) thymocytes to the CD4+CD8+ double-positive (DP) stage. During this important phase of T-cell development, which is known as the DN-DP transition, it is unclear whether the Notch1 complex simply strengthens its signal output as an isolated unit or recruits cofactors to amplify its signals. We previously showed that the PIAS-like coactivator Zmiz1 is a direct and context-dependent cofactor of Notch1 in T-cell leukemia. Using conditional knockout mouse models, we show that like inactivation of Notch, inactivation of Zmiz1 impaired the DN-DP transition under steady state and stress conditions. To determine mechanism, we performed RNA-Seq on sorted early T-lineage progenitor (ETP) and DN3 cells that were deprived of Zmiz1 signals either acutely (DeltaTamCre) or chronically (DeltaMxCre). To differentiate Notch1-independent from Notch1-dependent target genes, we also performed RNA-Seq on ETP and DN3 cells that were deprived of Notch1 signals using the anti-NRR Notch1 antibody. Our data suggests that Zmiz1 selectively amplifies a subset of Notch1 target genes in DN3 cells, such as Myc. In contrast, Zmiz1 does not have these functions in ETP cells, thus indicating stage-specific roles of Zmiz1.

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