GEO DataSets

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus; Homo sapiens

Type:

Methylation profiling by array

Platforms:

GPL9886 GPL17019

25 Samples

Download data: TXT

(Submitter supplied) Genomic DNA is isolated from spleen (RUNX1 model and normal control) and bone marrow (NHD13 model and normal control). We used MCAM to identify genes that have methylation changes.

Organism:

Mus musculus

Type:

Methylation profiling by array

Platform:

GPL17019

6 Samples

Download data: TXT

(Submitter supplied) Genomic DNA is isolated from bone marrow (MDS patient) and whole blood (normal control). We used MCAM to identify genes that have methylation changes.

Organism:

Homo sapiens

Type:

Methylation profiling by array

Platform:

GPL9886

19 Samples

Download data: TXT

(Submitter supplied) Setd2, the histone H3 lysine 36 methyltransferase, plays an important role in the pathogenesis of hematologic malignancies. The research on the role of Setd2 in leukemogenesis has made great progress, but its role in MDS is still unknown. Here, we knock out Setd2 in the NUP98-HOXD13 transgenic (NHD13 Tg) mouse, and demonstrate that loss of Setd2 accelerates the transformation of MDS into AML. The conditional deletion of Setd2 also interferes the differentiation of hematopoietic stem and progenitor cells (HSPCs), and results in the decrease of granulocyte monocyte progenitor (GMP) cells, increase of megakaryocyte erythroid progenitor (MEP) cells and common myeloid progenitor (CMP) cells. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing

Platforms:

GPL21273 GPL17021

18 Samples

Download data: BED, BROADPEAK, BW, COV, TXT, XLSX

(Submitter supplied) Recent studies have showed that loss-of-function mutations of EZH2, a catalytic component of polycomb repressive complex 2, are often associated with RUNX1 mutations in myelodysplastic syndrome (MDS) patients. We established a novel MDS model mouse by transducing a RUNX1S291fs mutant in hematopoietic stem cells followed by deletion of Ezh2 and found that Ezh2 loss significantly promoted RUNX1S291fs-induced MDS.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL10787

8 Samples

Download data: TXT

(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

(Submitter supplied) Methylation profiling by high throughput sequencing

Organism:

Homo sapiens

Type:

Methylation profiling by high throughput sequencing

Platform:

GPL20301

233 Samples

Download data: XLSX

(Submitter supplied) Mutations of RUNX1 are detected in patients with myelodysplastic syndrome (MDS). In particular, C-terminal truncation mutations lack a transcription regulatory domain and have increased DNA binding through the runt homology domain (RHD). The expression of the RHD, RUNX1(41-214), in mouse hematopoietic cells induced progression to MDS and acute myeloid leukemia (AML). Analysis of pre-myelodysplastic animals revealed expansion of c-Kit+Sca-1+Lin- (KSL) cells and skewed differentiation to myeloid at the expense of the lymphoid lineage. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS4441

Platform:

GPL8321

9 Samples

Download data: CEL

Analysis of c-Kit+Sca-1+Lin- hematopoietic stem cells (HSCs) lacking Runx1 or expressing the runt homology domain, RUNX1 (41-214). RUNX1(41-214) expression induces myelodysplastic syndrome (MDS) in mice. Results provide insight into molecular basis of MDS progression induced by RUNX1 (41-214).

Organism:

Mus musculus

Type:

Expression profiling by array, count, 3 genotype/variation sets

Platform:

GPL8321

Series:

GSE40155

9 Samples

Download data: CEL

(Submitter supplied) An increasing body of work reveals aberrant hypermethylation of genes occurring in and potentially contributing to the pathogenesis of myeloid malignancies. Several of these diseases, such as myelodysplastic syndromes (MDS), are responsive to DNA methyltransferase inhibitors. In order to determine the extent of promoter hypermethylation in such tumors we compared the distribution of DNA methylation of 14,000 promoters in MDS and secondary AML patients enrolled in a phase I trial of 5-azacytidine and the histone deacetylase inhibitor entinostat against de novo AML patients and normal CD34+ bone marrow cells. more...

Organism:

Homo sapiens

Type:

Methylation profiling by genome tiling array

Platform:

GPL6604

64 Samples

Download data: PAIR

(Submitter supplied) GFI1 is a transcription factor and was implicated in the development of MDS. Reduced expression of GFI1 or presence of the GFI1-36N variant leads to epigenetic changes. Using GFI1-36S, -36N -KD, NUP98-HOXD13-tg mice and curcumin (a natural histone acetyltransferase inhibitor (HATi)), we now demonstrate that expansion of GFI1-36N or –KD, NUP98-HODXD13 leukemic cells can be delayed. Curcumin treatment significantly reduced AML progression in GFI1-36N or -KD mice and prolonged AML-free survival. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL17021

8 Samples

Download data: BW, TXT

(Submitter supplied) Gene expression profile of AML generated via 3 related transgenes is compared.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

12 Samples

Download data: TXT

(Submitter supplied) Analysis of Lin-c-Kit+Sca-1- haematopoietic stem cells (HSCs) expressing the Nup98-HoxD13 (NHD13) fusion gene. NHD13 induces myelodysplastic syndrome (MDS) in mice. Results provide insight into the molecular basis of the myelodysplastic phenotype

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

6 Samples

Download data: TSV

(Submitter supplied) Here we used Illumina NGS for high-throughput profiling of the DNA methylome in two human colon cancer derived cell lines, two human normal bone marrow CD34+ controls and in five human Acutre Myeloid Leukeima patient samples. These data can be used to determine the CpG cytosine methylation pattern at base pair resolution in each sample and to determine differentially methylated cytosines and regions between samples

Organism:

Homo sapiens

Type:

Methylation profiling by high throughput sequencing

Platforms:

GPL10999 GPL11154

19 Samples

Download data: TXT

(Submitter supplied) Transcriptomic comparison of stages of clonal evolution of Fanconi anemia modeled using induced pluripotent stem cells.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL16791

12 Samples

Download data: TXT

(Submitter supplied) Myelodysplastic syndromes (MDS) are a heterogeneous group of clonal disorders characterized variably by the presence of peripheral cytopenias, bone marrow hypercellularity and dysplastic changes in the bone marrow. While MDS patients have an increased risk of progression to acute myeloid leukemia (AML), most MDS patients actually succumb to progressive bone marrow failure. Amongst patients classified as low-risk MDS, different clinical evolutions have been observed, with some patients remaining relatively stable for long periods of time (herein, stable MDS), while others show more progressive disease, with worsening cytopenias, and often increased transfusion requirements (herein, progressive MDS). more...

Organism:

Homo sapiens

Type:

Methylation profiling by high throughput sequencing

Platform:

GPL11154

44 Samples

Download data: TXT

(Submitter supplied) mDia1-miR146a double knockout (DKO) mice develop aging related MDS and eventually progress to AML at moribund stage. To investigate the rescue effect from IL6 deficiency, we created mDia1-miR146a-IL6 triple knockout (TKO) mice. Singel cell RNA seq was used to investigate the bone marrow cellularity change and pathway involved during the disease progression.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL28457

4 Samples

Download data: MTX, TSV

(Submitter supplied) The MLL-PTD mutation is found in patients with MDS and AML, and not in other hematological malignancies. Previously, we showed that Mll-PTD knock-in heterozygous mice (MllPTD/WT mice) present with several MDS-associated features. However, these phenotypes are insufficient to constitute bona fide MDS. MllPTD/WT mice do not generate MDS or AML in primary or transplant recipient mice. This suggests that additional genetic and/or epigenetic defects are necessary for transformation to MDS or AML. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL15103

4 Samples

Download data: TXT

(Submitter supplied) Hypoxia inducible factor-1α (HIF-1α) is a critical transcription factor for the hypoxic response, angiogenesis, normal hematopoietic stem cell regulation, and cancer development. Importantly, HIF-1α is also a key regulator for immune cell activation. In order to determine whether HIF-1α is sufficient for developing MDS phenotypes, we generated blood specific inducible HIF-1α transgenic mice. Using Vav1-Cre/Rosa26-loxP-Stop-loxP (LSL) rtTA driver, stable HIF-1α can be induced in a doxycycline administration dependent manner. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL15103

4 Samples

Download data: XLS

(Submitter supplied) The MLL-PTD mutation is found in patients with MDS and AML, and not in other haematological malignancies. Previously, we showed that Mll-PTD knock-in heterozygous mice present with several MDS-associated features, such as increased self-renewal and apoptosis in HSPCs, expansion of the myeloid progenitor population, ineffective haematopoiesis, and skewed myeloid differentiation. MLL is an epigenetic regulator: its C-terminal Su[var]3–9, enhancer of zeste, trithorax (SET) domain has methyltransferase activity on lysine 4 on histone 3 (H3K4), which is retained in the MLL-PTD mutant. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL13112

2 Samples

Download data: BEDGRAPH, TXT