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Links from GEO DataSets

Items: 20

1.

Genome-wide analysis of gene expression in MLL translocation transformed mouse leukemia cell lines

(Submitter supplied) The purpose of this study is to investigate the transcriptional programs as it relates to disease latency initiated by different MLL fusion proteins, including: MLL-AF1p, MLL-AF6, MLL-Gas7, MLL-AF9 and MLL-ENL. Leukemia cell lines were established by transforming kit+ mouse bone marrow cells with retroviruses coding MLL-AF1p, MLL-AF6, MLL-Gas7, MLL-AF9 or MLL-ENL. At early phase after the cell lines were established, cells growing at exponential phase (cell density at 0.5~1x106/ml) were harvested for RNA extraction and sequencing purpose.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
12 Samples
Download data: TXT
Series
Accession:
GSE73457
ID:
200073457
2.

Gene expression induced by DOT1L and Menin inhibition in cell line models of leukemia

(Submitter supplied) Gene expression upon DOT1L inhibition, or Menin inhibition, or a combination of DOT1L and Menin inhibiting agents, was assessed in several MLL-rearranged human cell lines and a mouse model of MLL-AF9 leukemia. The goal of the study was to explore the mechanisms by which the EPZ0004777 and MI-2-2 chemicals collaborate to induce differentiation and cell death in MLL-AF4 and MLL-AF9 leukemias.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by array
Platforms:
GPL1261 GPL570
56 Samples
Download data: CEL
Series
Accession:
GSE63664
ID:
200063664
3.

Genetic deletion or small molecule inhibition of the arginine methyltransferase PRMT5 exhibit anti-tumoral activity in mouse models of MLL-rearranged AML

(Submitter supplied) The hematological malignancies classified as Mixed Lineage leukemias (MLL) harbor fusions of the MLL1 gene to partners that are members of transcriptional elongation complexes. MLL-rearranged leukemias are associated with extremely poor prognosis and response to conventional therapies and efforts to identify molecular targets are urgently needed. Using mouse models of MLL-rearranged acute myeloid leukemia (AML), here we show that genetic inactivation or small molecule inhibition of the protein arginine methyltransferase PRMT5 exhibit anti-tumoral activity in MLL-fusion protein driven transformation. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
6 Samples
Download data: TXT
Series
Accession:
GSE100820
ID:
200100820
4.

miR-196b targets both oncogenic and tumor suppressor genes in MLL-associated leukemia

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by array
Platforms:
GPL5175 GPL6246
48 Samples
Download data: CEL
Series
Accession:
GSE34186
ID:
200034186
5.

Affymetrix gene arrays of leukemic BM samples from 24 mice including 9 primary

(Submitter supplied) To identify such targets of leukemia-related miRNAs such as miR-196b, we conducted Affymetrix gene arrays of leukemic BM samples from 24 mice including 9 primary (including 3 each of negative control, MLL-AF9, and miR-196b+MLL-AF9) and 15 secondary (including 3 negative control, 6 MLL-AF9, and 6 miR-196b+MLL-AF9) recipient mice
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
24 Samples
Download data: CEL
Series
Accession:
GSE34185
ID:
200034185
6.

Identification of miR-181 target genes and a common prognostic gene signature in AML

(Submitter supplied) Increased expression levels of miR-181 family members have been shown to be associated with favorable outcome in patients with cytogenetically normal acute myeloid leukemia. Here we show that increased expression of miR-181a and miR-181b is also significantly (P < .05; Cox regression) associated with favorable overall survival in cytogenetically abnormal AML (CA-AML) patients. We further show that up-regulation of a gene signature composed of 4 potential miR-181 targets (including HOXA7, HOXA9, HOXA11, and PBX3), associated with down-regulation of miR-181 family members, is an independent predictor of adverse overall survival on multivariable testing in analysis of 183 CA-AML patients. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL13781
65 Samples
Download data: TXT
Series
Accession:
GSE30258
ID:
200030258
7.

Functional diversity of inhibitors tackling the differentiation arrest of MLL-rearranged leukemia

(Submitter supplied) Purpose: The chromosomal rearrangements of the mixed-lineage leukemia (MLL) gene have been extensively characterized as a potent oncogenic driver on the molecular and mechanistic level in acute lymphoblastic (ALL) and acute myeloid (AML) leukemia. For its oncogenic function the MLL fusion protein is hijacking the the multi enzyme super elongation complex (SEC) leading to elevated expression of MLL target genes (e.g. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
305 Samples
Download data: TSV
8.

Zinc finger protein 521 overexpression is a feature of MLL-rearranged acute myeloid leukemia and contributes to the maintenance of myeloid differentiation block

(Submitter supplied) ZNF521 is a multiple zinc finger transcription factor previously identified because abundantly and selectively expressed in normal CD34+ hematopoietic stem and progenitor cells. From microarray datasets, aberrant expression of ZNF521 has been reported in both pediatric and adult acute myeloid leukemia (AML) patients with MLL gene rearrangements. However, a proper validation of microarray data is lacking, likewise ZNF521 contribution in MLL-rearranged AML is still uncertain. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
6 Samples
Download data: CEL
Series
Accession:
GSE79110
ID:
200079110
9.

PBX3 cooperates with MEISI in causing rapid acute myeloid leukemia and recapitulates the core transcriptome of MLL-rearranged leukemia

(Submitter supplied) To investigate whether co-expression of PBX3/MEIS1 can mimic that of MLL-AF9, HOXA9/MEIS1 or HOXA9/PBX3 in inducing leukemogenesis, we conducted in vivo mouse bone marrow transplantation (BMT) assays. Briefly, normal mouse bone marrow (BM) progenitor (i.e., lineage negative; Lin-) cells collected from B6.SJL (CD45.1) donor mice (CD45.1) were retrovirally co-transduced with MSCVneo-MLL-AF9+MSCV-PIG (MLL-AF9), MSCVneo-HOXA9+MSCV-PIG (HOXA9), MSCVneo-HOXA9+MSCV-PIG-MEIS1 (HOXA9+MEIS1), MSCVneo-HOXA9+MSCV-PIG-PBX3 (HOXA9+PBX3), MSCV-PIG-PBX3+MSCVneo-MEIS1 (PBX3+MEIS1), MSCVneo+MSCV-PIG-PBX3 (PBX3) , MSCVneo+MSCV-PIG-MEIS1 (MEIS1), or MSCVneo+MSCV-PIG (normal control; NC). more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL16570
20 Samples
Download data: CEL
Series
Accession:
GSE68643
ID:
200068643
10.

Leucegene: AML sequencing (part 5)

(Submitter supplied) RNA sequencing of human leukemia
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
263 Samples
Download data: TXT
Series
Accession:
GSE67039
ID:
200067039
11.

Leucegene: AML sequencing (part 4)

(Submitter supplied) RNA sequencing of human leukemia
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
22 Samples
Download data: TXT
Series
Accession:
GSE66917
ID:
200066917
12.

Leucegene: AML sequencing (part 3)

(Submitter supplied) RNA sequencing of human leukemia
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
82 Samples
Download data: TXT
Series
Accession:
GSE62190
ID:
200062190
13.

Effect of Menin cKO on MLL-AF9 transformed cells

(Submitter supplied) We determined the effect of conditional deletion of Menin in MLL-AF9 transformed leukemia cells
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
4 Samples
Download data: XLSX
Series
Accession:
GSE117933
ID:
200117933
14.

MLL-AF6 leukemia

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing
4 related Platforms
10 Samples
Download data: CEL, WIG
Series
Accession:
GSE43069
ID:
200043069
15.

Expression data from a human MLL-AF6 positive AML cell line

(Submitter supplied) The MLL gene on chromosome 11 fuses to the AF6 gene on chromosome 6 in a balanced chromosomal translocation that is characetristic of certain adult and pediatric human leukemias. We established a murine leukemia model of MLL-AF6 using the retroviral MLL-AF6 contruct in a bone marrow transplantation system. The ML2 human MLL-AF6 positive leukemia cell line was used for gene expression profiling to assess the transctiptional profile in MLL-AF6 leukemias.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
1 Sample
Download data: CEL
Series
Accession:
GSE43068
ID:
200043068
16.

Expression data from MLL-AF6 positive leukemia cells

(Submitter supplied) The MLL gene on chromosome 11 fuses to the AF6 gene on chromosome 6 in a balanced chromosomal translocation that is characetristic of certain adult and pediatric human leukemias. We established a murine leukemia model of MLL-AF6 using the retroviral MLL-AF6 contruct in a bone marrow transplantation system.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
3 Samples
Download data: CEL
Series
Accession:
GSE43067
ID:
200043067
17.

Genome wide mapping of histone 3 lysine 79 dimethylation in MLL rearranged and control human leukemia cell lines

(Submitter supplied) We report the genome wide distribution of H3K79 dimethylation in the human MLL-AF6 rearranged cell line ML2 as well as the human MOLM13 and HL60 cell lines
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
3 Samples
Download data: WIG
Series
Accession:
GSE43063
ID:
200043063
18.

Genome wide mapping of histone 3 lysine 79 dimethylation in MLL-AF6 murine leukemias

(Submitter supplied) We report the genome wide distribution of H3K79 dimethylation in mouse MLL-AF6 positive leukemias to assess whether this epigenetic mark drives MLL-target gene expression.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
3 Samples
Download data: WIG
Series
Accession:
GSE43062
ID:
200043062
19.

The MLL-Menin interaction is a molecular dependency in NUP98-rearranged AML

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18573 GPL19057
84 Samples
Download data: NARROWPEAK, TXT
Series
Accession:
GSE175597
ID:
200175597
20.

The MLL-Menin interaction is a molecular dependency in NUP98-rearranged AML [RNA-Seq]

(Submitter supplied) Using mouse and human models of NUP98-rearrranged leukemia, we demonstrate that inhibition of MLL-Menin impairs leukemogenic gene expression and disrupts chromatin binding of MLL1 and NUP98 fusion proteins at a critical subset of genes that is essential for sustaining the undifferentiated leukemia phenotype.
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL19057 GPL18573
57 Samples
Download data: TXT
Series
Accession:
GSE175596
ID:
200175596
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