GEO DataSets

Analysis of peripheral blood from Cbfb+/MYH11 and Cbfb-/- E12.5 embryos with that of their wildtype littermates. Cbfb+/MYH11 embryos had defects in both primitive and definitive hematopoiesis. Results provide insight into the mechanisms by which CBFB-MYH11 may contribute to leukemogenesis.

Organism:

Mus musculus

Type:

Expression profiling by array, transformed count, 3 genotype/variation, 2 specimen sets

Platform:

GPL1261

Series:

GSE19194

14 Samples

Download data: CEL, CHP

(Submitter supplied) It is known that CBFB-MYH11, the fusion gene generated by inversion of chromosome 16 in human acute myeloid leukemia, is causative for oncogenic transformation. However, the mechanism by which CBFB-MYH11 initiates leukemogenesis is not clear. Previously published reports showed that CBFB-MYH11 dominantly inhibits RUNX1 and CBFB, and such inhibition has been suggested as the mechanism for leukemogenesis. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS4040

Platform:

GPL1261

14 Samples

Download data: CEL, CHP

(Submitter supplied) To clarify the role of Gata2 in the development of Cbfb-MYH11 induced leukemia, we generated conditional Cbfb-MYH11 knockin mice with Gata2 heterozygous knockout. Leukemic cells with Gata2 heterozygous knockout gained higher number of genetic mutations and showed more aggressive phenotype in both primary and transplanted recipient mice. We compared gene expression profilings between Gata2+/+ and Gata2+/f leukemic cells with Cbfb-MYH11.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

6 Samples

Download data: TXT

(Submitter supplied) Inversion of chromosome 16 is a consistent finding in patients with acute myeloid leukemia subtype M4 with eosinophilia (AML M4Eo), which generates a CBFB-MYH11 fusion gene. It is generally considered that CBFβ-SMMHC, the fusion protein encoded by CBFB-MYH11, is a dominant negative repressor of RUNX1. However, recent findings challenge the RUNX1-repression model for CBFβ-SMMHC mediated leukemogenesis. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing; Other

Platforms:

GPL21626 GPL24247 GPL21493

33 Samples

Download data: BEDPE, DIFF, H5, TXT

(Submitter supplied) Results showed that Chd7 deficiency delay Cbfb-MYH11 induced leukemia, to explore the mechanism, We also performed microarray analysis on c-Kit+ leukemic cells to determine gene expression differences between Mx1-Cre, Cbfb+/56M and Chd7f/f, Mx1-Cre, Cbfb+/56M leukemic cells.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL16570

6 Samples

Download data: CEL

(Submitter supplied) CHD7 interacts with CBFb-SMMHC through RUNX1 and modulates their gene expression regulation and is important for CBFB-MYH11 leukemogenesis in the mouse model.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

9 Samples

Download data: TXT

(Submitter supplied) Different mechanisms for CBF-MYH11 function in acute myeloid Leukemia (AML) with inv(16) have been proposed such as tethering of RUNX1 outside the nucleus, interference with transcription factor complex assembly and recruitment of histone deacetylases, all resulting in transcriptional repression of RUNX1 target genes. Here, through genome-wide CBF-MYH11 binding site analysis and quantitative interaction proteomics we found that CBF-MYH11 localizes to RUNX1 occupied promoters where it interacts with TAL1, FLI1 and TBP associated factors (TAFs) in the context of the hematopoietic transcription factors ERG, GATA2 and PU.1/SPI1 and the co regulators EP300 and HDAC1. more...

Organism:

Homo sapiens

Type:

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

Platforms:

GPL10999 GPL11154

27 Samples

Download data: BEDGRAPH, WIG

(Submitter supplied) Chromosomal translocations are one of the hallmarks of acute myeloid leukemia (AML), often leading to gene fusions and expression of an oncofusion protein. Over recent years it has become clear that most of the AML associated oncofusion proteins molecularly adopt distinct mechanisms for inducing leukemogenesis. Still these unique molecular properties of the chimeric proteins converge and give rise to a common pathogenic molecular mechanism. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

1 Sample

Download data: WIG

(Submitter supplied) ZBTB7A is frequently mutated in acute myeloid leukemia (AML) with t(8;21) translocation. However, the oncogenic collaboration between mutated ZBTB7A and the RUNX1-RUNX1T1 fusion gene in AML t(8;21) remains unclear. Here, we investigate the role of ZBTB7A and its mutations in the context of normal and malignant hematopoiesis.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18460

37 Samples

Download data: TXT

(Submitter supplied) The CBFβ-MYH11 fusion generated by inv(16) aberration is proposed to block normal myeloid differentiation, but whether this subtype of leukemia cells is poised for an unique cell lineage remains unclear. Here, we surveyed the functional consequences of CBFβ-MYH11 in inv(16) patient blasts and two inducible systems by multi-omics profiling. The primary inv(16) cells stay closer with megakaryocyte and erythrocyte lineages along the cell differentiation trajectory, and share common transcriptomic signatures and epigenetic determiners. more...

Organism:

Homo sapiens

Type:

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

Platforms:

GPL11154 GPL18573

17 Samples

Download data: BW

(Submitter supplied) We searched for genes which are mutated in a manner that is linked with gene mutations involved in DNA de/methylation in AML. We found that recurrent CBFB-MYH11 fusions, which result in the expression of fusion protein comprising core-binding factor β (CBFB) and myosin heavy chain 11 (MYH11), occur mutually exclusively with DNMT3A mutations. The CBFB-MYH11 fusion tumors show DNA hypomethylation patterns similar to cancers with loss-of-function mutation of DNMT3A. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL16791

15 Samples

Download data: TXT

(Submitter supplied) Runx/Cbfb heterodimers play important roles in the development of hematopoietic cells in mouse embryos and adults. In order to identify genes that are regulated by Runx/Cbfb, we purified Lin– c-kit+ Sca1+ (LSK) cells and Lin– c-kit+ Sca1– CD16/32+ (GMP) cells from Vav1-iCre x Cbfb(F/F) and Vav1-iCre x Cbfb(F/+) mice and profiled gene expression using microarray.

Organism:

Mus musculus

Type:

Expression profiling by array

Datasets:

GDS5413 GDS5414

Platform:

GPL6246

8 Samples

Download data: CEL

Analysis of purified Lin-c-kit+Sca1-CD16/32+ GMP cells from Cbfβ-conditional knockout mice. Runx/Cbfb heterodimers play important roles in hematopoietic cell development. Results provide insight into molecular mechanisms by which Cbfβ regulates cell fate decisions in bone marrow progenitors.

Organism:

Mus musculus

Type:

Expression profiling by array, transformed count, 2 genotype/variation sets

Platform:

GPL6246

Series:

GSE55227

4 Samples

Download data: CEL

Analysis of purified Lin-c-kit+Sca1+ LSK cells from Cbfβ- conditional knockout mice. Runx/Cbfb heterodimers play important roles in hematopoietic cell development. Results provide insight into molecular mechanisms by which Cbfβ regulates cell fate decisions in bone marrow progenitors.

Organism:

Mus musculus

Type:

Expression profiling by array, transformed count, 2 genotype/variation sets

Platform:

GPL6246

Series:

GSE55227

4 Samples

Download data: CEL

(Submitter supplied) RUNX1 is among the most frequently mutated genes in human leukemia, and the loss or dominant-negative suppression of RUNX1 function is found in myelodysplastic syndrome and acute myeloid leukemia (AML). However, how post-translational modifications (PTMs) of RUNX1 affect its in vivo function and whether PTM dysregulation of RUNX1 can cause leukemia are largely unknown. We performed targeted deep sequencing on a family with 3 occurrences of AML and identified a novel RUNX1 mutation R237K. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL21103

4 Samples

Download data: BEDGRAPH

(Submitter supplied) RUNX1 is among the most frequently mutated genes in human leukemia, and the loss or dominant-negative suppression of RUNX1 function is found in myelodysplastic syndrome and acute myeloid leukemia (AML). However, how post-translational modifications (PTMs) of RUNX1 affect its in vivo function and whether PTM dysregulation of RUNX1 can cause leukemia are largely unknown. We performed targeted deep sequencing on a family with 3 occurrences of AML and identified a novel RUNX1 mutation R237K. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

6 Samples

Download data: DIFF, FPKM_TRACKING

(Submitter supplied) Acute myeloid leukemia (AML) harboring inv(16)(p13q22) expresses high levels of miR-126. Here we show that the CBFB-MYH11 (CM) fusion gene upregulates miR-126 expression through aberrant miR-126 transcription and perturbed miR-126 biogenesis via the HDAC8/RAN-XPO5-RCC1 axis. Aberrant miR-126 upregulation promotes survival of leukemia-initiating progenitors and is critical for initiating and maintaining CM-driven AML. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17021

10 Samples

Download data: TXT

(Submitter supplied) We show that the microRNA transcriptome undergoes a global state transition during the initiation and progression of acute myeloid leukemia, and accurately predicts time to disease development.

Organism:

Mus musculus

Type:

Non-coding RNA profiling by high throughput sequencing

Platform:

GPL17021

231 Samples

Download data: TSV

(Submitter supplied) Temporal dynamics of gene expression are informative of changes associated with disease development and evolution. Given the complexity of high-dimensionaltemporal datasets, an analytical framework guided by a robust theory is needed to interpret time-sequential changes and to predict system dynamics. Herein, we use acute myeloid leukemia as a proof-of-principle to model gene expression dynamics in a transcriptome state-space constructed based on time-sequential RNA-sequencing data. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17021

248 Samples

Download data: TSV, TXT

(Submitter supplied) In order to identify genes that are activated in differentiating WT ESCs, but are missing in Tal-1-/- and Runx1-/- ESCs, and which might be involved in the generation of definitive hematopoietic progenitors and their specification thereafter, we performed microarray analyses on purified Flk-1+ cells, differentiated from these ESCs for 4, 5, and 6 days “in vitro”.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

15 Samples

Download data: CEL, CHP