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Links from GEO DataSets

Items: 20

1.

Expression data from cultured human acute megokaryblastic myeloid leukemia and acute myeloid leukemia cell lines

(Submitter supplied) The genetic lesions that drive acute megakaryoblastic leukemia (AMKL) have not been fully elucidated. To search for AMKL gene, we subjected 9 AMKL cell lines and 39 non-AMKL acute myeloid leukemia cell lines to microarray gene expression analysis.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
48 Samples
Download data: CEL
Series
Accession:
GSE98578
ID:
200098578
2.

Human models of NUP98-KDM5A megakaryocytic leukemia contribute to uncover new biomarkers and therapeutic vulnerabilities

(Submitter supplied) We generated human synthetic models of NUP98-KDM5A leukemia and compared gene expression profiles to primary pediatric samples.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL18573 GPL11154
24 Samples
Download data: TXT
3.

caArray_orkin-0038: Identification of distinct molecular phenotypes in acute megakaryoblastic leukemia by gene expression profiling

(Submitter supplied) Individuals with Down syndrome (DS) are predisposed to develop acute megakaryoblastic leukemia (AMKL), characterized by expression of truncated GATA1 transcription factor protein (GATA1s) due to somatic mutation. The treatment outcome for DS-AMKL is more favorable than for AMKL in non-DS patients. To gain insight into gene expression differences in AMKL, we compared 24 DS and 39 non-DS AMKL samples. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL96
80 Samples
Download data: CEL
Series
Accession:
GSE83449
ID:
200083449
4.

Expression profiling of acute megakaryoblastic leukemia

(Submitter supplied) mononuclear cells were isolated on a density gradient and RNA extracted using Trizol and the Promega SV column RNA purification. Affymetrix U133A chips were hybridised using standard procedures at the core facility of Dana Farber Cancer Institute. Keywords: disease state analysis
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL96
80 Samples
Download data
Series
Accession:
GSE4119
ID:
200004119
5.

CBFA2T3::GLIS2 pediatric acute megakaryoblastic leukemia is sensitive to BCL-XL inhibition by navitoclax and DT2216

(Submitter supplied) We engineered human models of CBFA2T3::GLIS2 acute megakaryoblastic leukemia and compared gene expression profiles to primary pediatric samples.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
19 Samples
Download data: TXT
Series
Accession:
GSE209628
ID:
200209628
6.

Mouse Models of Pediatric Acute Megakaryoblastic Leukemia Reveal Novel Therapeutic Vulnerabilities

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
54 Samples
Download data
Series
Accession:
GSE208187
ID:
200208187
7.

Mouse Models of Pediatric Acute Megakaryoblastic Leukemia Reveal Novel Therapeutic Vulnerabilities [DSP750]

(Submitter supplied) Pediatric acute megakaryoblastic leukemia (AMKL) is an aggressive blood cancer associated with poor therapeutic response and high mortality. We developed CBFA2T3-GLIS2-driven mouse models of AMKL that recapitulate the phenotypic and transcriptional signatures of the human disease. We show that CBFA2T3-GLIS2 and GLIS2 modulate similar transcriptional networks. Oncogenic RAS cooperates with GLIS2 to trigger AMKL, enhancing the penetrance and decreasing the latency of CBFA2T3-GLIS2-dependent AMKL. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
22 Samples
Download data: TXT
Series
Accession:
GSE208186
ID:
200208186
8.

Mouse Models of Pediatric Acute Megakaryoblastic Leukemia Reveal Novel Therapeutic Vulnerabilities [DSP601-649-749]

(Submitter supplied) Pediatric acute megakaryoblastic leukemia (AMKL) is an aggressive blood cancer associated with poor therapeutic response and high mortality. We developed CBFA2T3-GLIS2-driven mouse models of AMKL that recapitulate the phenotypic and transcriptional signatures of the human disease. We show that CBFA2T3-GLIS2 and GLIS2 modulate similar transcriptional networks. Oncogenic RAS cooperates with GLIS2 to trigger AMKL, enhancing the penetrance and decreasing the latency of CBFA2T3-GLIS2-dependent AMKL. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
24 Samples
Download data: TXT
Series
Accession:
GSE208158
ID:
200208158
9.

Mouse Models of Pediatric Acute Megakaryoblastic Leukemia Reveal Novel Therapeutic Vulnerabilities [DSP798]

(Submitter supplied) Pediatric acute megakaryoblastic leukemia (AMKL) is an aggressive blood cancer associated with poor therapeutic response and high mortality. We developed CBFA2T3-GLIS2-driven mouse models of AMKL that recapitulate the phenotypic and transcriptional signatures of the human disease. We show that CBFA2T3-GLIS2 and GLIS2 modulate similar transcriptional networks. Oncogenic RAS cooperates with GLIS2 to trigger AMKL, enhancing the penetrance and decreasing the latency of CBFA2T3-GLIS2-dependent AMKL. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
8 Samples
Download data: TXT
Series
Accession:
GSE208157
ID:
200208157
10.

RNA-SEQ Quantitative Analysis of the regulation of c-Mpl-del on survival related gene transcriptome in AMKL cells

(Submitter supplied) In the previous studies, we reported that c-Mpl alternative splicing form c-Mpl-del overexpressed in acute megakaryoblasttic leukemia (AMKL) patients and mediated thrombopoietin signaling to promote AMKL cells malignant proliferation and chemotherapy resisitance. To investigate the detailed mechanism of c-Mpl-del mediated AMKL cells survival and chemotherapy resisitance, the AMKL cell Dami stably expressing GFP, c-Mpl-del-GFP or c-Mpl-p-GFP were established by transduction with GFP, c-Mpl-del-GFP or c-Mpl-p-GFP lentiviruses and treated with or without Ara-c (10μM) in the presence of 20ng/mL TPO for RNA-SEQ analysis to exame the expression of survival-related genes. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
5 Samples
Download data: TXT
11.

RNA-SEQ Quantitative Analysis of WT and Mpl-del-overexpressing AMKL cell Transcriptomes

(Submitter supplied) In the previous studies, we reported that Mpl alternative splicing form Mpl-del overexpressed in acute megakaryoblasttic leukemia (AMKL) patients and mediated thrombopoietin signaling to promote AMKL cells malignant proliferation and chemotherapy resisitance. To investigate the detailed mechanism of Mpl-del mediated AMKL cells proliferation and survival, the AMKL cell Dami stably expressing GFP or Mpl-del-GFP were established by transduction with GFP or Mpl-del-GFP lentiviruses and treated with 20ng/ml TPO for RNA-SEQ analysis to examine the expression of proliferation and survival-related genes. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
2 Samples
Download data: TXT
12.

Epigenetic changes in Down syndrome leukemogenesis

(Submitter supplied) Acute megakaryoblastic leukemia (AMKL) is more frequently seen in Down syndrome patients, where it is often preceded by a transient myeloproliferative disorder (DS-TMD). The development of DS-TMD and DS-AMKL require not only the presence of the trisomy 21 but also that of GATA1 mutations. However, despite extensive studies into the genetics of DS-AMKL, not much is known about the epigenetic deregulation associated with this disease. more...
Organism:
Mus musculus; Homo sapiens
Type:
Methylation profiling by genome tiling array
Platforms:
GPL17032 GPL17031
43 Samples
Download data: PAIR
Series
Accession:
GSE46167
ID:
200046167
13.

Global gene expression profile of primary human leukemic blasts

(Submitter supplied) The goal of this study is to define the global gene expression profile of primary leukemic blasts from patients with different forms of myeloid leukemia and different FAB subtypes. Here we report the global gene expression profile of 2 patients with AML FAB M5, 2 patients with AML FAB M7, 3 patients with Down syndrome AML FAB M7 and 3 patients with Down syndrome transient leukemia.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
10 Samples
Download data: CEL
Series
Accession:
GSE19681
ID:
200019681
14.

Identification of miR-125b-2 target genes

(Submitter supplied) The goal of this study is to define miR-125b-2 target genes in the hematopoietic system by genetic alteration of miR-125b expression levels. Here we report the identification of miR-125b-2 targets in the hematopoietic system by repressing miR125b in megakaryoblastic leukemia (AMKL) cell lines and overexpressing miR-125b-2 in hematopoietic stem and progenitor cells (CD34+-HSPCs)
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
10 Samples
Download data: CEL
Series
Accession:
GSE19680
ID:
200019680
15.

The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis.

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Other; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24247
12 Samples
Download data: BW
Series
Accession:
GSE181570
ID:
200181570
16.

The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis [ATAC-seq]

(Submitter supplied) The purpose of this study was to decipher the molecular function of ARID3A. We leveraged gene expression (RNA-Seq) and chromatin profiling (ATAC-Seq and CUT&RUN) to evaluate gene expression changes upon restoring Arid3a expression in the context of the Gata1s mutation and miR-125b overexpression
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24247
1 Sample
Download data: BW
Series
Accession:
GSE181569
ID:
200181569
17.

The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis [CUT&RUN]

(Submitter supplied) The purpose of this study was to decipher the molecular function of ARID3A. We leveraged gene expression (RNA-Seq) and chromatin profiling (ATAC-Seq and CUT&RUN) to evaluate gene expression changes upon restoring Arid3a expression in the context of the Gata1s mutation and miR-125b overexpression
Organism:
Mus musculus
Type:
Other
Platform:
GPL24247
5 Samples
Download data: BW
Series
Accession:
GSE181568
ID:
200181568
18.

The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis [RNA-seq]

(Submitter supplied) The purpose of this study was to decipher the molecular function of ARID3A. We leveraged gene expression (RNA-Seq) and chromatin profiling (ATAC-Seq and CUT&RUN) to evaluate gene expression changes upon restoring Arid3a expression in the context of the Gata1s mutation and miR-125b overexpression
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
6 Samples
Download data: TXT
Series
Accession:
GSE181567
ID:
200181567
19.

Chromosome 21-encoded miR-125b cooperates with GATA1s in trisomy 21-associated megakaryoblastic leukemia by targeting the megakaryocytic transcription factor ARID3A III

(Submitter supplied) The purpose of this study was to decipher the gene expression changes in the ML-DS cell line CMK upon overexpression of ARID3A. For that, we used a doxycycline-inducible gene expression system to overexpress ARID3A
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: XLS
20.

Chromosome 21-encoded miR-125b cooperates with GATA1s in trisomy 21-associated megakaryoblastic leukemia by targeting the megakaryocytic transcription factor ARID3A II

(Submitter supplied) The purpose of this study was to decipher the molecular network underlying the synergy between the GATA1s mutation and miR-125b. We used a doxycycline-regulated inducible system to determine gene expression changes associated with the expression of miR-125b.,
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
24 Samples
Download data: XLS
Series
Accession:
GSE169739
ID:
200169739
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