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Links from GEO DataSets

Items: 20

1.

Expression profile of hematopoietic stem and progenitor cell (HSPC) compartment of FLT3-ITD and FLT3-ITD miR-155-/- mice

(Submitter supplied) The miR-155-dependent differences in gene expression in the HSPC compartment of FLT3-ITD mice is unknown. In this experiment, we performed RNA sequencing on FLT3-ITD and FLT3-ITD miR-155-/- mouse LKS cells.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
6 Samples
Download data: TXT
Series
Accession:
GSE86526
ID:
200086526
2.

Gene expression profile of Sca-1+ versus Sca-1- endothelial cells selected from the bone marrow of normal B6 mice

(Submitter supplied) Different gene expression profile was observed in bone marrow Sca-1+ versus Sca-1- endothelial cells
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
9 Samples
Download data: TXT
Series
Accession:
GSE180104
ID:
200180104
3.

CircMYBL2 Regulates FLT3-ITD FLT3AML Translation in AML

(Submitter supplied) CircMYBL2 is more highly expressed in AML patients with FLT3-ITD mutations than in those without the FLT3-ITD mutation. We found that circMYBL2 knockdown specifically inhibits proliferation and promotes the differentiation of FLT3-ITD AML cells in vitro and in vivo. We used the ribosome profiling and RNA-seq libraries sequenced with Illumina HiSeq 2500 to identify the mRNA that circMYBL2 targeted. Interestingly, we found that circMYBL2 significantly influences the protein level of mutant FLT3 kinase, which contributes to the activation of FLT3-ITD-dependent signaling pathways. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Other
Platform:
GPL24676
8 Samples
Download data: CSV, TXT
4.

Dnmt3a haploinsufficiency transforms Flt3-ITD myeloproliferative disease into a rapid, spontaneous, and fully-penetrant acute myeloid leukemia

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
102 Samples
Download data
Series
Accession:
GSE77849
ID:
200077849
5.

Dnmt3a haploinsufficiency transforms Flt3-ITD myeloproliferative disease into a rapid, spontaneous, and fully-penetrant acute myeloid leukemia (Single Cell RNA-Seq)

(Submitter supplied) Cytogenetically normal acute myeloid leukemia (CN-AML) represents nearly 50% of human acute myeloid leukemia (AML) cases with a 5-year overall survival of approximately 30%. In CN-AML with poorer prognosis, mutations in the de novo DNA methyltransferase (DNMT3A) and the FMS-like tyrosine kinase 3 (Flt3) commonly co-occur (1-3). We demonstrate that mice with Flt3-internal-tandem duplication (Flt3ITD) and inducible deletion of Dnmt3a spontaneously develop a rapidly-lethal, completely-penetrant, and transplantable AML of normal karyotype. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
96 Samples
Download data: TXT
Series
Accession:
GSE77847
ID:
200077847
6.

Dnmt3a haploinsufficiency transforms Flt3-ITD myeloproliferative disease into a rapid, spontaneous, and fully-penetrant acute myeloid leukemia (Bulk RNA-Seq)

(Submitter supplied) Cytogenetically normal acute myeloid leukemia (CN-AML) represents nearly 50% of human acute myeloid leukemia (AML) cases with a 5-year overall survival of approximately 30%. In CN-AML with poorer prognosis, mutations in the de novo DNA methyltransferase (DNMT3A) and the FMS-like tyrosine kinase 3 (Flt3) commonly co-occur (1-3). We demonstrate that mice with Flt3-internal-tandem duplication (Flt3ITD) and inducible deletion of Dnmt3a spontaneously develop a rapidly-lethal, completely-penetrant, and transplantable AML of normal karyotype. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
6 Samples
Download data: TXT
Series
Accession:
GSE77846
ID:
200077846
7.

Dnmt3a haploinsufficiency transforms Flt3-ITD myeloproliferative disease into a rapid, spontaneous, and fully-penetrant acute myeloid leukemia

(Submitter supplied) Cytogenetically normal acute myeloid leukemia (CN-AML) represents nearly 50% of human acute myeloid leukemia (AML) cases with a 5-year overall survival of approximately 30%. In CN-AML with poorer prognosis, mutations in the de novo DNA methyltransferase (DNMT3A) and the FMS-like tyrosine kinase 3 (Flt3) commonly co-occur (1-3). We demonstrate that mice with Flt3-internal-tandem duplication (Flt3ITD) and inducible deletion of Dnmt3a spontaneously develop a rapidly-lethal, completely-penetrant, and transplantable AML of normal karyotype. more...
Organism:
Homo sapiens; Mus musculus
Type:
Methylation profiling by high throughput sequencing
Platforms:
GPL13112 GPL11154
44 Samples
Download data: TXT
Series
Accession:
GSE77026
ID:
200077026
8.

FLT3 inhibition upregulates HDAC8 via FOXO to inactivate p53 and promote maintenance of FLT3-ITD+ acute myeloid leukemia

(Submitter supplied) Internal tandem duplication (ITD) mutations within the FMS-like receptor tyrosine kinase-3 (FLT3) can be found in up to 25~30% of acute myeloid leukemia (AML) patients and confer a poor prognosis. Although FLT3 tyrosine kinase inhibitors (TKIs) have shown clinical responses, the overall outcome of FLT3-ITD+ AML patients remains poor, and most of them would relapse very shortly. TKIs can not eliminate primitive FLT3-ITD+ AML cells, which are potential sources of relapse. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
6 Samples
Download data: TXT
Series
Accession:
GSE138057
ID:
200138057
9.

FLT3-ITD mutation expands dendritic cells and alters CD4+ T cells in acute myeloid leukemia

(Submitter supplied) Fms-like tyrosine kinase 3 (FLT3) is a critical receptor for functional dendritic cell (DC) development. Mutations associated with FLT3 are commonly observed in acute myeloid leukemia (AML) patients. Internal tandem duplication (FLT3-ITD) results in ligand-independent constitutive signaling and promotes tumor survival. Basic characterization of dendritic cells in the context of AML is lacking, therefore we investigated how FLT3-ITD impacts DC homeostasis and what downstream affects on the immune system may be. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
16 Samples
Download data: MTX, TSV
Series
Accession:
GSE238156
ID:
200238156
10.

Fetal and neonatal hematopoietic progenitors are functionally and transcriptionally resistant to Flt3-ITD mutations.

(Submitter supplied) Gene expression in control and Flt3-ITD, Stat5 and Runx1 mutant HSCs and HPCs from different developmental stages.
Organism:
Mus musculus
Type:
Expression profiling by array
Platforms:
GPL10787 GPL21163
117 Samples
Download data: TXT
Series
Accession:
GSE81153
ID:
200081153
11.

Role of NFATc1 in patients with FLT3-ITD AML

(Submitter supplied) Diagnostic samples of peripheral blood form acute myeloid leukemia were analysed for gene expression differences MLL Munich Leukemia Laboratory
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
325 Samples
Download data: CEL, PDF
Series
Accession:
GSE61804
ID:
200061804
12.

Expression data from KSL and GMP cells of FLT3/ITD and FLT3/ITD-SmoM2 mice

(Submitter supplied) FLT3/ITD-SmoM2 mice developed rapidly fatal myeloid leukemia compared to FLT3/ITD only mice, suggesting that overactivation of the Hedgehog signaling pathway via SmoM2 can drive myeloid disease progression We used the Affymetrix Mouse 430_2.0 microarray to detail global gene expression responsible for disease progression in sorted bone marrow cells and found that the Hedgehog signaling pathway contributes to disease progression by enhancing FLT3 signaling
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS5806
Platform:
GPL1261
6 Samples
Download data: CEL, CHP
Series
Accession:
GSE67134
ID:
200067134
13.
Full record GDS5806

FLT3/ITD-SmoM2 acute myeloid leukemia model: sorted bone marrow cells

Analysis of KSL and GMP cells isolated from bone marrow of Flt3/ITD-SmoM2 transgenics at around 3 months of age when they developed leukemia. Wild-type and FLT3/ITD littermates of the FLT3/ITD-SmoM2 animals were also examined. Results provide insight into the role of SmoM2 in leukemic progression.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 2 cell type, 3 genotype/variation sets
Platform:
GPL1261
Series:
GSE67134
6 Samples
Download data: CEL, CHP
14.

GATM-Mediated Creatine Biosynthesis Enables Maintenance of FLT3-ITD-Mutant Acute Myeloid Leukemia

(Submitter supplied) RNA-seq was used to demonstrate the differential expression genes in MOLM14 and MV4-11 cells after FLT3 inhibition.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL18573 GPL24676
24 Samples
Download data: CSV
Series
Accession:
GSE181586
ID:
200181586
15.

Autophagy inhibition impairs leukemia stem cell function in FLT3-ITD AML but has antagonistic interactions with tyrosine kinase inhibition

(Submitter supplied) The FLT3-ITD mutation is associated with poor prognosis in acute myeloid leukemia (AML). FLT3 tyrosine kinase inhibitors (TKIs) demonstrate clinical efficacy but fail to target leukemia stem cells (LSC) and do not generate sustained responses. Autophagy is an important cellular stress response contributing to hematopoietic stem cells (HSC) maintenance and promoting leukemia development. Here we investigated the role of autophagy in regulating FLT3-ITD AML stem cell function and response to TKI treatment. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
32 Samples
Download data: XLSX
Series
Accession:
GSE169750
ID:
200169750
16.

Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus; Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL18573 GPL19057
37 Samples
Download data: BW, NARROWPEAK
Series
Accession:
GSE163932
ID:
200163932
17.

Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [MV411_OCI-AML3_DMSO_AC220_24hr]

(Submitter supplied) We performed 3'-RNA-Sequencing on RNA isolated from human MV4-11 and OCI-AML3 cells which had been treated with DMSO or the FLT3 inhibitor Quizartinib (AC220) to perform differential gene expression analysis.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
12 Samples
Download data: CSV
Series
Accession:
GSE163930
ID:
200163930
18.

Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [iFLT3-ITD-Depletion_In VIVO]

(Submitter supplied) We performed 3'-RNA-Sequencing on RNA isolated from murine MLL-AF9/iFLT3-ITD cells where the inducible iFLT3-ITD transgene had been depleted for 48 hours compared to non-depleted conditions in vivo to perform differential gene expression analysis.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
6 Samples
Download data: CSV
Series
Accession:
GSE163927
ID:
200163927
19.

Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [iFLT3-ITD-Depletion_In VITRO]

(Submitter supplied) We performed 3'-RNA-Sequencing on RNA isolated from murine MLL-AF9/iFLT3-ITD cells where the inducible iFLT3-ITD transgene had been depleted for 24 or 48 hours compared to non-depleted conditions in vitro to perform differential gene expression analysis.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
9 Samples
Download data: CSV
Series
Accession:
GSE163926
ID:
200163926
20.

Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [MV411_OCI-AML3_ATF4_RNAP2_CHIP]

(Submitter supplied) We performed ChIP-seq on MV4-11 or OCI-AML3 cells which had been treated with DMSO or 5 nM of the FLT3 inhibitor Quizartinib (AC220) to determine the location of ATF4 or RNAPII across the genome.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
10 Samples
Download data: BW, NARROWPEAK
Series
Accession:
GSE163922
ID:
200163922
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