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Links from GEO DataSets

Items: 20

1.
Full record GDS5613

All-trans retinoic acid effect on U937 myeloid cells overexpressing ecotropic virus integration site 1

Analysis of EVI1-overexpressing U937 myeloid cells treated with ATRA. EVI1 overexpression is associated with poor prognosis in myeloid leukemias; ATRA is a myeloid differentiation inducing agent. Results provide insight into the potential interplay between EVI1 and ATRA in myeloid cells.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 2 agent, 2 genotype/variation sets
Platform:
GPL570
Series:
GSE66854
12 Samples
Download data: CEL
2.

The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid [U937]

(Submitter supplied) The product of the ecotropic virus integration site 1 (EVI1) gene, whose overexpression is associated with a poor prognosis in myeloid leukemias and some epithelial tumors, regulates gene transcription both through direct DNA binding and through modulation of the activity of other sequence specific transcription factors. Previous results from our laboratory have shown that EVI1 influenced transcription regulation in response to the myeloid differentiation inducing agent, all-trans retinoic acid (ATRA), in a dual manner: it enhanced ATRA induced transcription of the RARb gene, but repressed the ATRA induction of the EVI1 gene itself. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS5613
Platform:
GPL570
12 Samples
Download data: CEL
Series
Accession:
GSE66854
ID:
200066854
3.

Transcriptional regulation by EVI1 in the absence or presence of TPA

(Submitter supplied) To investigate whether and how expression of the oncogenic transcription factor EVI1 influences gene regulation by phorbol esters and vice versa, the human myeloid cell line U937 was transduced with an EVI1 expression vector or empty vector as a control. Cells were treated with 12-Otetradecanoylphorbol 13-acetate (TPA) or its solvent ethanol as a control. RNA was extracted and subjected to gene expression microarray analysis.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
12 Samples
Download data: CEL
Series
Accession:
GSE66853
ID:
200066853
4.

The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid [HL60]

(Submitter supplied) The product of the ecotropic virus integration site 1 (EVI1) gene, whose overexpression is associated with a poor prognosis in myeloid leukemias and some epithelial tumors, regulates gene transcription both through direct DNA binding and through modulation of the activity of other sequence specific transcription factors. Previous results from our laboratory have shown that EVI1 influenced transcription regulation in response to the myeloid differentiation inducing agent, all-trans retinoic acid (ATRA), in a dual manner: it enhanced ATRA induced transcription of the RARb gene, but repressed the ATRA induction of the EVI1 gene itself. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS5614
Platform:
GPL570
12 Samples
Download data: CEL
Series
Accession:
GSE66837
ID:
200066837
5.
Full record GDS5614

All-trans retinoic acid effect on HL60 myeloid cells overexpressing ecotropic virus integration site 1

Analysis of EVI1-overexpressing HL60 myeloid cells treated with ATRA. EVI1 overexpression is associated with poor prognosis in myeloid leukemias; ATRA is a myeloid differentiation inducing agent. Results provide insight into the potential interplay between EVI1 and ATRA in myeloid cells.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 2 agent, 2 genotype/variation sets
Platform:
GPL570
Series:
GSE66837
12 Samples
Download data: CEL
6.

EVI1 promotes tumor growth via transcriptional repression of MS4A3

(Submitter supplied) Background: The transcription factor EVI1 regulates cellular proliferation, differentiation, and apoptosis, and contributes to an aggressive course of disease in myeloid leukemias and other malignancies. Notwithstanding, knowledge about the target genes mediating its biological and pathological functions remains limited. We therefore aimed to identify and characterize novel EVI1 target genes in human myeloid cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
20 Samples
Download data: CEL
Series
Accession:
GSE60100
ID:
200060100
7.

All-trans retinoic acid enhances, and a pan-RAR antagonist counteracts, the stem cell promoting activity of EVI1 in acute myeloid leukemia

(Submitter supplied) Ecotropic virus integration site 1 (EVI1), whose overexpression characterizes a particularly aggressive subtype of acute myeloid leukemia (AML), enhanced anti-leukemic activities of all-trans retinoic acid (atRA) in cell lines and patient samples. However, the drivers of leukemia formation, therapy resistance, and relapse are leukemic stem cells (LSCs), whose properties were hardly reflected in these experimental setups. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21493
10 Samples
Download data: TXT
Series
Accession:
GSE123255
ID:
200123255
8.

Gene expression changes in U937 cells in response to ectopic expression of EVI1 and/or etoposide treatment

(Submitter supplied) Overexpression of ecotropic viral integration site 1 (EVI1) is associated with aggressive disease in acute myeloid leukemia (AML). Despite of its clinical importance, little is known about the mechanism through which EVI1 confers resistance to antileukemic drugs. Here, we show that a human myeloid cell line constitutively overexpressing EVI1 after infection with a retroviral vector (U937_EVI1) was partially resistant to etoposide and daunorubicin as compared to empty vector infected control cells (U937_vec). more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS5809
Platform:
GPL11532
8 Samples
Download data: CEL
Series
Accession:
GSE66660
ID:
200066660
9.
Full record GDS5809

Anti-leukemia drug etoposide effect on ecotropic viral integration site 1-overexpressing myeloid cells

Analysis of myeloid cell line U937 overexpressing ecotropic viral integration site 1 (EVI1) and cultured in the presence of antileukemic drug etoposide. Results provide insight into molecular mechanisms through which EVI1 confers resistance to drugs used in myeloid leukemia therapy.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 2 agent, 2 protocol sets
Platform:
GPL11532
Series:
GSE66660
8 Samples
Download data: CEL
10.

Effects of EVI1 and EVI1Δ324 mild expression in HeLa cells

(Submitter supplied) We studied the variations of mRNA amounts after Flag-EVI1, Flag-EVI1Δ324, or Flag expression in HeLa cells. Despites EVI1 discovery in 1988, its recognized role as a dominant oncogene in myeloid leukemia and more recently in epithelial cancers, only a few target genes were known and it was not clear why EVI1 was involved in cancer progression. Here we obtained the genomic binding occupancy and expression data for EVI1 in human cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
12 Samples
Download data: CEL
Series
Accession:
GSE42251
ID:
200042251
11.

Genome-wide DNA methylation profiling of Acute Myeloid Leukemia

(Submitter supplied) We hypothesized that DNA methylation distributes into specific patterns in cancer cells, which reflect critical biological differences. We therefore examined the methylation profiles of 344 patients with acute myeloid leukemia (AML). Clustering of these patients by methylation data segregated patients into 16 groups. Five of these groups defined new AML subtypes that shared no other known feature. In addition, DNA methylation profiles segregated patients with CEBPA aberrations from other subtypes of leukemia, defined four epigenetically distinct forms of AML with NPM1 mutations, and showed that established AML1-ETO, CBFb-MYH11 and PML-RARA leukemia entities are associated with specific methylation profiles. more...
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL6604
352 Samples
Download data: PAIR
Series
Accession:
GSE18700
ID:
200018700
12.

Targeting the Creatine Kinase Pathway in EVI1-Positive Acute Myeloid Leukemia

(Submitter supplied) Purpose: Identify new targets in EVI1-Positive Acute Myeloid Leukemia Methods: Treatment with cyclocreatine of EVI1-driven AML cell lines TF-1, UT-7 and UCSD-AML1. Cyclocreatine was purchased from Sigma-Aldrich (Sigma). TF-1, UT-7 and UCSD-AML1 cells were treated in quadruplicate with either vehicle or 3 mM cyclocreatine for 24 hours. Total RNA was extracted and profiled by RNA sequencing (HiSeq, Illumina) at BioMicroCenter from Massachusetts Institute of Technology (Cambridge, MA, USA). more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
24 Samples
Download data: TXT
Series
Accession:
GSE86151
ID:
200086151
13.

Expression data from Evi1-transduced primary bone marrow cells

(Submitter supplied) Evi1 is essential for proliferation of hematopoietic stem cells and implicated in the development of myeloid disorders. Particularly, high Evi1 expression defines one of the largest clusters in acute myeloid leukemia and is significantly associated with extremely poor prognosis. Improvement of the therapeutic outcome of leukemia with activated Evi1 is one of the most challenging issues. However, mechanistic basis of Evi1-mediated leukemogenesis has not been fully elucidated. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS3714
Platform:
GPL1261
8 Samples
Download data: CEL
Series
Accession:
GSE22434
ID:
200022434
14.
Full record GDS3714

Ecotropic viral integration site-1 expression effect on primary bone marrow cells

Analysis of C57BL/6 mononuclear bone marrow cells transduced with ecotropic viral integration site-1 (EVI-1). EVI-1 is one of the dominant oncogenes associated with murine and human myeloid leukemia. Results provide insight into the mechanistic basis of Evi1-mediated leukemogenesis.
Organism:
Mus musculus
Type:
Expression profiling by array, transformed count, 2 protocol sets
Platform:
GPL1261
Series:
GSE22434
8 Samples
Download data: CEL
DataSet
Accession:
GDS3714
ID:
3714
15.

Changes in gene expression resulting from expression of MN1 in human CD34+ cells

(Submitter supplied) Reintroduction of CEBPA in MN1-overexpressing hematopoietic cells prevents their hyper-proliferation and restores myeloid differentiation. Forced expression of MN1 in primitive mouse hematopoietic cells causes acute myeloid leukemia and impairs all-trans retinoic acid (ATRA) induced granulocytic differentiation. Here, we studied the effects of MN1 on myeloid differentiation and proliferation using primary human CD34+ hematopoietic cells, lineage depleted mouse bone marrow cells, and bipotential (granulocytic/monocytic) human AML-cell lines. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
2 Samples
Download data: CEL
Series
Accession:
GSE16745
ID:
200016745
16.

EVI1 carboxy-terminal phosphorylation is ATM-mediated and sustains transcriptional modulation and self-renewal via enhanced CtBP1 association

(Submitter supplied) The transcriptional regulator EVI1 has an essential role in early hematopoiesis and development. However, aberrantly high expression of EVI1 has potent oncogenic properties and confers poor prognosis and chemo-resistance in leukemia and solid tumors. To investigate to what extent EVI1 function might be regulated by posttranslational modifications, we carried out mass spectrometry- and antibody-based analyses and uncovered an ATM-mediated double phosphorylation of EVI1 at the carboxy-terminal S858/S860 SQS motif. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
24 Samples
Download data: CSV
Series
Accession:
GSE115643
ID:
200115643
17.

Phase I Dose Escalation Study of ATRA Combined with the LSD1 inhibitor Tranylcypromine in AML and MDS

(Submitter supplied) Preclinical studies have shown that combining the LSD1 inhibitor tranylcypromine (TCP) with all-trans retinoic acid (ATRA) induces differentiation and impairs survival in non-APL acute myeloid leukemia (AML). We conducted a Phase 1 clinical trial (NCT02273102) to evaluate the safety and preliminary activity of ATRA in combination with TCP in patients with relapsed/refractory AML and myelodysplasia (MDS). more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
30 Samples
Download data: TXT
Series
Accession:
GSE151594
ID:
200151594
18.

mRNA expression quantitative Analysis of MOLM-13 and THP-1 treated with JOA compared with control

(Submitter supplied) The goals of this study are toevaluate the mRNA expressions of genes in MOLM-13 and THP-1 cell lines treated with JOA
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
12 Samples
Download data: TXT
Series
Accession:
GSE167083
ID:
200167083
19.

Disease-stabilizing treatment based on all-trans retinoic acid and valproic acid in acute myeloid leukemia

(Submitter supplied) Acute myeloid leukemia (AML) is an aggressive malignancy that can only be cured by intensive therapy. However, many elderly and unfit patients cannot receive such treatment due to an unacceptable risk of treatment-related morbidity and mortality. Disease-stabilizing therapy is then the only possible strategy, one alternative being treatment based on all-trans retinoic acid (ATRA) combined with the histone deacetylase inhibitor valproic acid and possibly low-toxicity conventional chemotherapy.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
47 Samples
Download data: TXT
Series
Accession:
GSE106096
ID:
200106096
20.

Identification of therapeutic targets of the hijacked super-enhancer complex in EVI1-rearranged leukemia (RNA-Seq)

(Submitter supplied) Chromosomal aberrations in acute myeloid leukemia (AML), such as inv(3) and t(3;3), lead to deregulation of the EVI1 oncogene by the GATA2 distal hematopoietic enhancer (G2DHE). In this project, we aimed to study the transcription factor complexes involved in the regulation of the G2DHE sequence. We have identified PARPi as a member of the G2DHE complex. Here, we used RNA-Seq to analyze transcriptomic changes after PARP inhibition with olaparib and talazoparib and to compare those to EVI1 knockdown.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
16 Samples
Download data: TSV
Series
Accession:
GSE167005
ID:
200167005
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