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Links from GEO DataSets

Items: 20

1.

Aberrant EVI1 splicing contributes to EVI1-rearranged leukemia II

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL16791 GPL19057
10 Samples
Download data: BIGWIG
Series
Accession:
GSE202211
ID:
200202211
2.

Aberrant EVI1 splicing contributes to EVI1-rearranged leukemia (RNA-Seq)

(Submitter supplied) Detailed genomic and epigenomic analyses of MECOM (the MDS1 and EVI1 complex locus) have revealed that inversion or translocation of chromosome 3 at MECOM drive inv(3)/t(3;3) myeloid leukemias and revealed MECOM germline mutations in patients with MECOM-associated bone marrow failure syndromes. Here we identify a novel, previously unannotated oncogenic RNA-splicing derived isoform of EVI1 which is frequently present in inv(3)/t(3;3) AML and directly contributes to leukemic transformation. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
2 Samples
Download data: TXT, XLSX
Series
Accession:
GSE202208
ID:
200202208
3.

Aberrant EVI1 splicing contributes to EVI1-rearranged leukemia (ChIP-Seq)

(Submitter supplied) Detailed genomic and epigenomic analyses of MECOM (the MDS1 and EVI1 complex locus) have revealed that inversion or translocation of chromosome 3 at MECOM drive inv(3)/t(3;3) myeloid leukemias and revealed MECOM germline mutations in patients with MECOM-associated bone marrow failure syndromes. Here we identify a novel, previously unannotated oncogenic RNA-splicing derived isoform of EVI1 which is frequently present in inv(3)/t(3;3) AML and directly contributes to leukemic transformation. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
8 Samples
Download data: BIGWIG
Series
Accession:
GSE202207
ID:
200202207
4.

Aberrant EVI1 splicing contributes to EVI1-rearranged leukemia

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL24676 GPL21103 GPL16791
19 Samples
Download data: RESULTS, TXT
Series
Accession:
GSE190656
ID:
200190656
5.

Aberrant EVI1 splicing contributes to EVI1-rearranged leukemia [mouse_RNA-seq]

(Submitter supplied) Detailed genomic and epigenomic analyses of MECOM (the MDS1 and EVI1 complex locus) have revealed that inversion or translocation of chromosome 3 at MECOM drive inv(3)/t(3;3) myeloid leukemias and revealed MECOM germline mutations in patients with MECOM-associated bone marrow failure syndromes. Here we identify a novel, previously unannotated oncogenic RNA-splicing derived isoform of EVI1 which is frequently present in inv(3)/t(3;3) AML and directly contributes to leukemic transformation. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
12 Samples
Download data: RESULTS
Series
Accession:
GSE190655
ID:
200190655
6.

Aberrant EVI1 splicing contributes to EVI1-rearranged leukemia [K562_RNA-seq]

(Submitter supplied) Detailed genomic and epigenomic analyses of MECOM (the MDS1 and EVI1 complex locus) have revealed that inversion or translocation of chromosome 3 at MECOM drive inv(3)/t(3;3) myeloid leukemias and revealed MECOM germline mutations in patients with MECOM-associated bone marrow failure syndromes. Here we identify a novel, previously unannotated oncogenic RNA-splicing derived isoform of EVI1 which is frequently present in inv(3)/t(3;3) AML and directly contributes to leukemic transformation. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
3 Samples
Download data: RESULTS
7.

Aberrant EVI1 splicing contributes to EVI1-rearranged leukemia [ChIP-seq]

(Submitter supplied) Detailed genomic and epigenomic analyses of MECOM (the MDS1 and EVI1 complex locus) have revealed that inversion or translocation of chromosome 3 at MECOM drive inv(3)/t(3;3) myeloid leukemias and revealed MECOM germline mutations in patients with MECOM-associated bone marrow failure syndromes. Here we identify a novel, previously unannotated oncogenic RNA-splicing derived isoform of EVI1 which is frequently present in inv(3)/t(3;3) AML and directly contributes to leukemic transformation. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
4 Samples
Download data: TXT
Series
Accession:
GSE190652
ID:
200190652
8.

EVI1 drives leukemogenesis through aberrant activation of ERG

(Submitter supplied) Chromosomal rearrangements involving EVI1 (MECOM) define a subtype of acute myeloid leukemia (AML) that is associated with a two-year survival rate of <10%. Gene regulatory functions of EVI1 are largely elusive and no targeted therapeutics exist. We developed experimentally tractable murine and human leukemia models that recapitulate phenotypic and transcriptional features of EVI1-rearranged AML and enable large-scale loss-of-function screens. more...
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
4 related Platforms
38 Samples
Download data: BIGWIG, TXT
Series
Accession:
GSE195497
ID:
200195497
9.

Oncogene EVI1 Drives Acute Myeloid Leukemia Via a Targetable Interaction with CTBP2

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL24676 GPL16791
37 Samples
Download data: BIGWIG, NARROWPEAK, SF
Series
Accession:
GSE243621
ID:
200243621
10.

Oncogene EVI1 Drives Acute Myeloid Leukemia Via a Targetable Interaction with CTBP2 [ChIP-Seq]

(Submitter supplied) Acute myeloid leukemia (AML) driven by the activation of EVI1 due to chromosome 3q26/MECOM rearrangements is incurable with current chemotherapy regimens. Insight into the mechanism by which EVI1 drives myeloid transformation is needed to target EVI1 in those leukemias. Here we demonstrate recurrent interaction of CTBP1/2 with a unique PLDLS motif in EVI1, which is indispensable for leukemic transformation of 3q26/MECOM rearranged AML. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL24676 GPL16791
31 Samples
Download data: BIGWIG, NARROWPEAK
Series
Accession:
GSE236010
ID:
200236010
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.

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
13.

Identification of therapeutic targets of the hijacked super-enhancer complex in EVI1-rearranged leukemia

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Other; Expression profiling by high throughput sequencing
Platforms:
GPL20301 GPL11154
21 Samples
Download data: BW, TSV
Series
Accession:
GSE153307
ID:
200153307
14.

Identification of therapeutic targets of the hijacked super-enhancer complex in EVI1-rearranged leukemia (4C-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 identified PARP1 as an interactor of G2DHE-associated transcription factors. In this dataset, we studied the interaction of genomic loci between the EVI1 promoter and G2DHE by 4C-Seq in the 3q-rearranged AML cell line MUTZ-3 treated with the PARP1 inhibitors olaparib, talazoparib or the DMSO vehicle control for 24 h.
Organism:
Homo sapiens
Type:
Other
Platform:
GPL11154
3 Samples
Download data: BW
Series
Accession:
GSE153306
ID:
200153306
15.

Identification of therapeutic targets of the hijacked super-enhancer complex in EVI1-rearranged leukemia (ChIP-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. In silico and in vitro analyses revealed that binding sites for CEBPA are critical for G2DHE function. Here, we used ChIP-Seq to show association of the CEBPA transcription factor with the G2DHE sequence in the 3q-rearranged cell line MOLM-1
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
2 Samples
Download data: BW
Series
Accession:
GSE153305
ID:
200153305
16.

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
17.

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
18.

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
19.
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
20.

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
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