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Links from GEO DataSets

Items: 20

1.

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
2.

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
3.

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
4.

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:
Mus musculus; Homo sapiens
Type:
Methylation profiling by high throughput sequencing
Platforms:
GPL13112 GPL11154
44 Samples
Download data: TXT
Series
Accession:
GSE77026
ID:
200077026
5.

Hepatic leukemia factor is a novel leukemic stem cell regulator in DNMT3A, NPM1, and FLT3-ITD triple mutated AML

(Submitter supplied) RNA-Seq of primary human AML samples sorted based on GPR56 and CD34 expression.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
20 Samples
Download data: TXT
Series
Accession:
GSE129094
ID:
200129094
6.

RNA-Seq of GPR56+/- populations

(Submitter supplied) Insights into the complex clonal architecture of acute myeloid leukemia (AML) unravelled by deep sequencing technologies have challenged the concept of AML as a hierarchically organised disease initiated and driven by rare self-renewing leukemic stem cells (LSCs). The lack of clone-specific surface markers, however, precludes prospective isolation and functional characterisation of distinct clones. Here, we performed RNA-Sequencing and assessed LSC frequencies for 56 primary AML samples in xenograft assays. We found that G-protein coupled receptor 56 (GPR56) identified the engrafting fraction in CD34positive samples and was associated with most high-risk mutations and poor outcome. Furthermore, variant allele frequency analysis revealed different clonal composition of engrafting GPR56+ versus non-engrafting GPR56- fractions identifying GPR56 as a discriminator of leukemic sub-clones with high and low leukemia initiating capacity. Our data suggest that the NSG-model rather than reproducing the full clonal diversity of the human disease selects for leukemic sub-clones based on their distinct functional properties.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
22 Samples
Download data: TXT
Series
Accession:
GSE68623
ID:
200068623
7.

WGBS assessment of global methylation alterations in Dnmt3aKO/FLT3-ITD lymphoid leukemia

(Submitter supplied) We generated global DNA methylation maps of FLT3-ITD and Dnmt3aKO/FLT3-ITD lymphoid leukemias, as well as normal control thymocytes.
Organism:
Mus musculus
Type:
Methylation profiling by high throughput sequencing
Platforms:
GPL17021 GPL13112
6 Samples
Download data: TXT
Series
Accession:
GSE80725
ID:
200080725
8.

Trancription factor Fli1 occupancy in Dnmt3aKO/FLT3-ITD lymphoid leukemia

(Submitter supplied) We mapped binding of FLI1 in Dnmt3aKO/FLT3-ITD leukemias over-expressing Dnmt3a or GFP.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
8 Samples
Download data: BED, BW
Series
Accession:
GSE80724
ID:
200080724
9.

Enhancer chromatin marks in Dnmt3aKO/FLT3-ITD lymphoid leukemia

(Submitter supplied) We mapped H3K4me1 and H3K27ac chromatin marks in Dnmt3aKO/FLT3-ITD and FLT3-ITD lymphoid leukemias
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
7 Samples
Download data: BW, NARROWPEAK
Series
Accession:
GSE80723
ID:
200080723
10.

Molecular profiling of mouse Dnmt3a/FLT3-ITD leukemia models

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL17021 GPL13112
56 Samples
Download data: BED, BW, NARROWPEAK, TXT
Series
Accession:
GSE61971
ID:
200061971
11.

RRBS assessment of global methylation alterations alterations in Dnmt3aKO/FLT3-ITD leukemia

(Submitter supplied) Using RRBS we assessed global DNA methylation changes in two mouse models of oncogenic FLT3-driven leukemia in the presence and absence of Dnmt3a.
Organism:
Mus musculus
Type:
Methylation profiling by high throughput sequencing
Platforms:
GPL13112 GPL17021
16 Samples
Download data: TXT
Series
Accession:
GSE61970
ID:
200061970
12.

Gene expression alterations in Dnmt3aKO/FLT3-ITD leukemia

(Submitter supplied) We assessed global gene expression profiles in two mouse models of oncogenic FLT3-driven leukemia in the presence and absence of Dnmt3a.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL13112 GPL17021
19 Samples
Download data: DIFF, GTF, TXT
Series
Accession:
GSE61969
ID:
200061969
13.

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
14.

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
15.

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
16.

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
17.

Tet2-/-Flt3ITD and WT stem and progenitor cells

(Submitter supplied) The study was a comparison of gene expression using RNA-seq. We analyzed the stem and progenitor cells from WT and Vav-cre+ Tet2fl/fl Flt3-ITD (T2F3) mice. We isolated stem cells LSK (lin- sca+ kit+) and granulocyte-macrophage progenitors GMP (lin- sca- kit+ fcgr+ cd34+) cells from bone marrow. Comparisons were made across genotypes WT vs. T2F3 and cell types LSK vs. GMP.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18635
12 Samples
Download data: TXT
Series
Accession:
GSE57244
ID:
200057244
18.

FLT3-ITD mutations and TET2 loss synergistically alter global DNA methylation in AML

(Submitter supplied) Studies of AML patient samples have shown that specific combinations of AML disease alleles confer an adverse outcome, however, in vivo models do not exist for the majority of common, poor-prognosis genotypes. Here we show that TET2/FLT3 mutations can cooperate to induce AML in vivo using a genetically engineered mouse model, and that this model has a defined stem-cell population with a characteristic transcriptional and epigenetic profile. more...
Organism:
Homo sapiens; Mus musculus
Type:
Methylation profiling by high throughput sequencing
Platforms:
GPL13112 GPL11154
15 Samples
Download data: TXT
Series
Accession:
GSE57114
ID:
200057114
19.

Whole-exome sequencing identifies mutations of BCOR in acute myeloid leukemia with normal karyotype

(Submitter supplied) Among acute myeloid leukemias (AML) with normal karyotype (CN-AML), NPM1 and CEBPA mutations define WHO provisional entities accounting for ~60% of cases, but the remaining ~40% remains poorly characterized. By whole exome-sequencing (WES) of one CN-AML patient lacking mutations in NPM1, CEBPA, FLT3, MLL-PTD and IDH1, we newly identified a clonal somatic mutation in BCOR (BCL6 co-repressor), a gene located in chromosome X. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS4280
Platform:
GPL570
24 Samples
Download data: CEL
Series
Accession:
GSE30442
ID:
200030442
20.
Full record GDS4280

BCL6 corepressor somatic mutation in acute myeloid leukemia with normal karyotype: Ficoll-enriched mononuclear cells

Analysis of mononuclear cells from normal karyotype, acute myeloid leukemia (CN-AML) patients with BCL6 corepressor (BCOR) mutation. CN-AML BCOR mutations are associated with oculo-facio-cardiodental genetic syndrome and poor outcome. Results provide insight into role of BCOR in CN-AML pathogenesis.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 2 genotype/variation sets
Platform:
GPL570
Series:
GSE30442
24 Samples
Download data: CEL
DataSet
Accession:
GDS4280
ID:
4280
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