GEO DataSets

(Submitter supplied) We have utilized advanced RNAi technology to dynamically restore and subsequently knock down endogenous PU.1 expression in p53-deficient AML cells, which respectively causes differentiation and de-differentiation

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL19057

8 Samples

Download data: BED, BEDGRAPH

(Submitter supplied) We have utilized advanced RNAi technology to dynamically restore endogenous PU.1 expression in p53-deficient AML cells.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

1 Sample

Download data: CSV, TXT

(Submitter supplied) We have utilized advanced RNAi technology to dynamically restore and subsequently knock down endogenous PU.1 expression in p53-deficient AML cells, which respectively causes differentiation and de-differentiation

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

16 Samples

Download data: TXT

(Submitter supplied) We have utilized advanced RNAi technology to dynamically restore and subsequently knock down endogenous PU.1 expression in p53-deficient AML cells, which respectively causes differentiation and de-differentiation

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL19057

8 Samples

Download data: BED, BEDGRAPH

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

Organism:

Mus musculus

Type:

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

Platforms:

GPL13112 GPL19057

53 Samples

Download data: BED, BEDGRAPH, TXT

(Submitter supplied) We have utilized advanced RNAi technology to dynamically restore endogenous PU.1 expression and perform PU.1 ChIP-seq in p53-deficient shPU.1 AML cells in vivo. This causes rapid cell cycle shutdown and myeloid differentiation. PU.1 restoration results in regression and clearance and prolongs survival.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL13112

5 Samples

Download data: BED, BEDGRAPH

(Submitter supplied) We have utilized advanced RNAi technology to dynamically restore endogenous PU.1 expression in p53-deficient shPU.1 AML single cell clones in vitro. This causes rapid cell cycle shutdown and reversible myeloid differentiation.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

9 Samples

Download data: TXT

(Submitter supplied) We have utilized advanced RNAi technology to dynamically restore endogenous PU.1 expression in p53-deficient AML cells. This causes rapid cell cycle shutdown and myeloid differentiation. PU.1 restoration results in regression and clearance and prolongs survival.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

8 Samples

Download data: TXT

(Submitter supplied) We have utilized advanced RNAi technology to dynamically restore endogenous PU.1 expression in p53-deficient AML cells . This causes rapid cell cycle shutdown and myeloid differentiation. PU.1 restoration results in regression and clearance and prolongs survival.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

12 Samples

Download data: TXT

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

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

9 Samples

Download data: CEL

(Submitter supplied) Expression profiling of FACS purified Lin-cKit+ cells from preleukemic compound URE-/+::Msh2-/- mice and control animals (two separate pools of 3 mice each)

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

4 Samples

Download data: CEL

(Submitter supplied) Expression profiling of FACS purified Lin-cKit+ cells from compound URE-/+::Msh2-/- mice with AML and control animals

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

7 Samples

Download data: CEL

(Submitter supplied) Lsd1KO and ATRA treatment in Hoxa9/Meis1- and MN1-transformed myeloid progenitor cells LSD1 has emerged as a promising epigenetic target in the treatment of acute myeloid leukemia (AML). Inhibition of LSD1 has been shown to induce differentiation and facilitate the responsiveness of AML cells to all-trans retinoic acid. We used two murine AML models based on retroviral overexpression of Hoxa9/Meis1 (H9M) or MN1 to study the effect of Lsd1 knockout in AML. more...

Organism:

Mus musculus

Type:

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

Platforms:

GPL17021 GPL21103

26 Samples

Download data: BED, TXT, XLSX

(Submitter supplied) Downregulation of the hematopoietic transcription factor PU.1 in PU.1 low acute myeloid leukemia cells (AML) by novel heterocyclic diamidines or PU.1 inhibitors leads to decrease cell proliferation and apoptosis, representing a new therapeutic strategy for AML treatment. These inhibitors induces decreased PU.1 binding on its target sites, as well as deregulation in PU.1 canonical target genes We used microarray to identify the pathways deregulated after drug treatment.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL16570

6 Samples

Download data: CEL, CHP

(Submitter supplied) A doxycycline-inducible system was used to induce PU.1 expression in cultured myeloid cell lines. The parent cell line used was BN (Kamath et al., Leukemia 22:1214-1225, 2008).

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL16570

6 Samples

Download data: CEL

(Submitter supplied) Fusion proteins involving the ETS factor ERG have been associated with multiple cancers such as Ewing's sarcoma and prostate cancer. In acute myeloid leukemias harboring t(16;21) another ERG fusion protein is expressed, FUS-ERG. Here, we found that this FUS-ERG oncofusion protein acts in the context of a heptad of proteins (ERG, FLI1, GATA2, LYL1, LNMO2, RUNX1 and TAL1) central to proper expression of genes involved in maintaining a stem cell hematopoietic phenotype. more...

Organism:

Homo sapiens

Type:

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

Platforms:

GPL11154 GPL10999

20 Samples

Download data: WIG

(Submitter supplied) CB CD34+ cells were isolated by Miltenyi miniMACS column. Cells were prestimulated in HPGM with 100 ng/ml KITL, FLT3L and TPO for 12 hrs. Cells were transduced with control, CITED2 overexpression lentivectors, shRNA PU.1 lentivectors or both, in two rounds over 48 hrs. Transduced cells were sorted after which RNA was isolated for Illumina beadchip arrays HT12 v4

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

8 Samples

Download data: TXT

(Submitter supplied) Unfavorable patient survival coincides with the lineage plasticity observed in ~20% of human acute leukemias. These cases are assumed to arise from hematopoietic stem cells, which have stable multipotent differentiation potential. However, here we report that plasticity in leukemia can result from instable lineage identity states inherited from differentiating progenitor cells. Using mice with enhanced c-Myc/Bcl2-expression, we show that T-lymphoid progenitors retain broad malignant lineage switching potential with a high capacity to differentiate into myeloid leukemia.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL11180

17 Samples

Download data: CEL

(Submitter supplied) Resistance against chemotherapy remains a major obstacle in treating patients with acute myeloid leukemia (AML). Novel therapeutic concepts are especially desired to target and eliminate resistant AML stem cells. Here we show that AML stem cells harbor the plasticity to switch from a low-cycling, therapy resistant state into an actively proliferating state associated with treatment response. We used patient-derived xenograft (PDX) cells from patients with high risk or relapsed AML, which were lentivirally transduced for marker expression, stained with the proliferation-sensitive dye Carboxyfluorescein succinimidyl ester (CFSE), and re-transplanted into next-recipient mice. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18460

24 Samples

Download data: TXT