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Expression data from isogenic Pten WT mouse T-ALLs infected with MSCV Myr-AKT-IRES-mCherry or empty vector, treated with DBZ or DMSO

ABSTRACT: To explore the mechanisms downstream of NOTCH1 and PTEN in the control of leukemia cell growth, we performed expression profiling on NOTCH1 induced and Pten-positive T-ALL tumor cells infected with constitutively active AKT (myristoylated-AKT). Constitutive activation of AKT rescues the transcriptional programs induced by NOTCH1 inhibition in Pten-positive T-ALL cells

ORGANISM(S): Mus musculus

PROVIDER: GSE71089 | GEO | 2015/08/31

SECONDARY ACCESSION(S): PRJNA290331

REPOSITORIES: GEO

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Expression data from isogenic Pten WT mouse T-ALLs infected with MSCV Myr-AKT-IRES-mCherry or empty vector, treated with DBZ or DMSO

Project description:To explore the mechanisms downstream of NOTCH1 and PTEN in the control of leukemia cell growth, we performed expression profiling on NOTCH1 induced and Pten-positive T-ALL tumor cells infected with constitutively active AKT (myristoylated-AKT). Constitutive activation of AKT rescues the transcriptional programs induced by NOTCH1 inhibition in Pten-positive T-ALL cells We performed microarray gene expression analysis of GSI treatment in Pten WT NOTCH1 induced leukemias infected with constitutively active AKT (myristoylated-AKT) or empty vector.

2015-08-31 | E-GEOD-71089 | biostudies-arrayexpress

Expression data from isogenic Pten WT or KO mouse T-ALLs treated with DBZ or DMSO

Project description:To investigate the underlying mechanisms mediating resistance to NOTCH inhibition in Pten-null T-ALL tumor cells we performed gene expression profiling of isogenic Pten-positive and Pten-deleted leukemia lymphoblasts after acute treatment with DBZ in vivo. This analysis revealed that, while direct NOTCH1 target genes (such as Hes1, Dtx1, PtcrA, HeyL and Notch3) are effectively downregulated in both Pten-positive and Pten-deleted tumors, genetic ablation of Pten elicits a global reversal of much of the transcriptional effects of NOTCH inhibition. We performed microarray gene expression analysis of GSI treatment in isogenic Pten KO or WT NOTCH1 induced leukemias

2015-08-31 | E-GEOD-71087 | biostudies-arrayexpress

Expression data from isogenic Pten WT or KO mouse T-ALLs treated with DBZ or DMSO

2015-08-31 | GSE71087 | GEO

RNAseq in Pten enhancer wild-type or deleted mouse T-ALLs

Project description:C57BL6 mice harboring Pten enhancer (PE) conditional knockout NOTCH1-induced leukemias were treated with vehicle (control) or tamoxifen to induce isogenic deletion of PE. Here we report the gene expression profile of leukemic blasts obtained from the spleen from control- or tamoxifen-treated leukemic mice. GSEA analysis show a significant enrichment of Pten signature genes, consistent with a role of PE in regulating Pten expression.

2020-12-17 | GSE150894 | GEO

Gene expression analysis of gamma-secretase inhibitor-sensitive and -resistant T-ALL cell lines

2007-09-01 | GSE5682 | GEO

Transcription profiling of human gamma-secretase inhibitor-sensitive and -resistant T-ALL cell lines

Project description:Gain-of-function mutations in NOTCH1 are common in T-cell lymphoblastic leukemias making this receptor a promising target for drugs such as gamma-secretase inhibitors, which block a proteolytic cleavage required for NOTCH1 activation. However, the enthusiasm for these therapies has been tempered by tumor resistance and the paucity of information on the oncogenic programs regulated by oncogenic NOTCH1. Here we show that NOTCH1 regulates PTEN expression and the activity of the PI3K-AKT signaling pathway in normal and leukemic T cells. Notch signaling and the PI3K-AKT pathway synergize in vivo in a Drosophila model of Notch-induced tumorigenesis, and mutational loss of PTEN is associated with increased glycolysis and resistance to NOTCH1 inhibition in human T-ALL. These findings identify the transcriptional regulation of PTEN and the control of cellular metabolism as key elements of the oncogenic program activated by NOTCH1 and provide the basis for the design of new therapeutic strategies for T-ALL. Experiment Overall Design: Samples for microarray analysis were prepared and hybridized in Affymetrix Human U133 Plus 2.0 arrays according to the manufacturerâs instructions and as previously described. RNA was extracted from duplicate cultures of GSI-sensitive (ALL-SIL, CUTLL1, DND41, HPB-ALL, KOPTK1) and GSI-resistant (CCRF-CEM, MOLT3, P12 ICHIKAWA, PF382 and RPMI8402) T-ALL cell lines treated for 24 h with vehicle (DMSO) or 500 nM CompE. Interarray intensity differences were normalized with Dchip

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ATAC-seq in NOTCH1-induced mouse T-ALLs

Project description:Here we report the genome-wide open chormatin profile (ATACseq) of a NOTCH1-induced mouse T-cell Acute Lymphoblastic Leukemia

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Human AsPC1-CFP and AsPC1-AKT PDAC orthotopic tumors: Lean vs Obese

Project description:Transcriptional profiling comparing human AsPC1 PDA cells transduced with either CFP control or myristoylated-AKT orthotopically grown in pancreata of lean vs obese Rag1-/- immunodeficient mice for 5 weeks (100,000 cells/pancreas). The Goal was to determine the transcriptional deregulation of Obesity-driven and AKT-driven tumors.

2017-05-26 | GSE99289 | GEO

Expression Data from Pten mutant epithelial cells

Project description:PTEN imparts tumor suppression in mice by cell autonomous and non-autonomous mechanisms. Whether these two tumor suppressor roles are mediated through similar or distinct signaling pathways is not known. Here we generated and analyzed knockin mice that express a series of human cancer-derived mutant alleles of PTEN in either stromal or tumor cell compartments of mammary glands. We find that cell non-autonomous tumor suppression by Pten in stromal fibroblasts strictly requires activation of P-Akt signaling, whereas cell autonomous tumor suppression in epithelial tumor cells is independent of overt canonical pathway activation These findings expose distinct Akt-dependent and independent tumor suppressor functions of PTEN in stromal fibroblasts and tumor cells, respectively, that can be used to guide clinical care of breast cancer patients Wild type. PtenF341V, PtenWT/null, and Pten null CDH1 positive epithelials cells of mammary ducts from 8 week old female mice were isolated by FACS, RNA was extracted and Affymetrix gene expression arrays were performed.

2014-12-19 | E-GEOD-64303 | biostudies-arrayexpress

Differentially expressed genes between oncogene-transformed and non-transformed fetal liver progenitor cells

Project description:The activation of different oncogenic signals may primarily contribute to the heterogeneity of cancer cells. However, the exact mechanisms underlying different oncogenic transformation are still unclear. We used the c-Myc, H-Ras and Akt transformed liver cell model to define mRNA expression profiles in the non-transformed and the three types of oncogene-transformed cells Purified p53-/- mouse fetal liver progenitor cells were transformed by three oncogenic genetic factors, c-Myc, H-RasV12 and myristoylated-AKT1(myr-Akt). The gene expression profilings of transformed cells and control cells were analyzed through microarray.

2013-02-02 | E-GEOD-43991 | biostudies-arrayexpress

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