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Links from GEO DataSets

Items: 20

1.

Expression profile of small nucleolar RNA (snoRNA) in human acute myeloid leukemia with different leukemia stem cell frequency

(Submitter supplied) Leukemogenesis requires enhanced self-renewal activity, which is induced by specific oncogenes. The underlying molecular mechanisms remain incompletely understood. We measured snoRNA expression in human primary AML samples that contained determined leukemia stem cells frequency. We identified that expression of C/D box snoRNAs was closely associated with leukemia stem cell frequency.
Organism:
Homo sapiens
Type:
Non-coding RNA profiling by high throughput sequencing
Platform:
GPL15456
20 Samples
Download data: TXT
Series
Accession:
GSE95721
ID:
200095721
2.

AML1-ETO induces leukemia via C/D box snoRNA/RNPs.

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by array; Non-coding RNA profiling by high throughput sequencing; Expression profiling by high throughput sequencing
4 related Platforms
94 Samples
Download data: CEL, TXT
Series
Accession:
GSE80602
ID:
200080602
3.

Nascent RNA-seq in Kasumi-1 cells

(Submitter supplied) Amino Enhancer of Split (AES) is essential for AML1-ETO induced self-renewal and leukemogenesis. To study the effect of AES on transcription regulation in AML1-ETO expressing Kasumi-1 cells, nascent transcripts in control (shctr) and AES knockdown (shAES) Kasumi-1 cells were labelled with uridine analogue 4-thioduridine with subsequent nascent RNA purification and next generation sequencing (Nascent RNA-seq).
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
4 Samples
Download data: TXT
Series
Accession:
GSE80582
ID:
200080582
4.

Identification of Amino Enhancer of Split (AES) and DDX21 binding snoRNAs by RIP-Seq.

(Submitter supplied) We studied AES and DDX21 binding RNAs in Kasumi-1 cells stably expressing V5-tagged AES. RNA immunoprecipitation was performed with V5 antibody (for AES), DDX21 antibody and control IgG. We found that AES as well as DDX21 RIP samples showed enrichment for small nucleolar RNAs (snoRNAs) compared to control IgG. We also showed that AES and DDX21 binding snoRNAs showed significant overlap. Our studies provide mechanisms how AES regulates snoRNAs and rRNA modification.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL15456
6 Samples
Download data: TXT
Series
Accession:
GSE80581
ID:
200080581
5.

Expression data from AML1-ETO9a mouse primary leukemia blast

(Submitter supplied) Microarray gene profilling indentified snoRNAs are downstream target of Amino Enhancer of Split (AES) and are essential for AML1-ETO9a induced leukemia. Amino Enhancer of Split (Aes) is strongly induced by leukemia oncogenes AML1-ETO, PML-RARα and PLZF-RARα. With a conditional AES knockout mouse model we showed that AES is essential for AML1-ETO9a indeced leukemia. We performed gene expression microarray using mouse primary AML1-ETO9a transformed AES wildtype and knockout and showed that snoRNAs were downregulated in AES knockout cells. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
6 Samples
Download data: CEL
Series
Accession:
GSE80579
ID:
200080579
6.

Expression profile of small nucleolar RNA (snoRNA) in acute myeloid leukemia.

(Submitter supplied) Leukemogenesis requires enhanced self-renewal activity, which is induced by specific oncogenes. The underlying molecular mechanisms remain incompletely understood. We transduced mouse lineage negative bone marrow cells (enriched for hematopoietic stem and progenitor cells) with retrovirus expressing leukemic oncogene AML1-ETO9a, MYC and MLL-AF9 as well as empty vector (MIG). We found that all three oncogenes enhanced snoRNA formation. more...
Organism:
Homo sapiens; Mus musculus
Type:
Non-coding RNA profiling by high throughput sequencing
Platforms:
GPL16173 GPL15456
78 Samples
Download data: TXT
Series
Accession:
GSE80523
ID:
200080523
7.

A Stable Transcription Factor Complex Nucleated by Dimeric AML1-ETO Controls Leukaemogenesis

(Submitter supplied) AML1-ETO, a fusion protein generated by the t(8;21) translocation in acute myeloid leukemia, is a transcription factor implicated in both gene repression and activation. We now show that, in leukemic cells, AML1-ETO resides in and functions through a stable protein complex (AETFC) that contains several hematopoietic transcription factors and cofactors. In conjunction with biochemical and leukemia pathological studies, the ChIP-seq and RNA-seq analyses of the AETFC components in leukemic cells reveal that these components stabilize the complex through multivalent interactions, provide multiple DNA-binding domains for diverse target genes, colocalize genome-wide, cooperatively regulate gene expression, and contribute to leukemogenesis.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL10999 GPL11154
17 Samples
Download data: TXT, WIG
8.

Definition of a Small Core Transcriptional Circuit Regulated by AML1-ETO [ChIP-seq and CUT&RUN]

(Submitter supplied) Transcription factors regulate gene networks controlling normal hematopoiesis and are frequently deregulated in acute myeloid leukemia (AML). Critical to our understanding of the mechanism of cellular transformation by oncogenic transcription factors is the ability to define their direct gene targets. However, gene network cascades can change within minutes to hours, making it difficult to distinguish direct from secondary or compensatory transcriptional changes by traditional methodologies. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
31 Samples
Download data: BW, CSV, XLS
Series
Accession:
GSE160242
ID:
200160242
9.

Definition of a Small Core Transcriptional Circuit Regulated by AML1-ETO

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL24676 GPL18573
74 Samples
Download data: BEDGRAPH, BW, CSV, XLS
Series
Accession:
GSE153281
ID:
200153281
10.

Definition of a Small Core Transcriptional Circuit Regulated by AML1-ETO [ChIP-seq, Cut&Run]

(Submitter supplied) Transcription factors regulate gene networks controlling normal hematopoiesis and are frequently deregulated in acute myeloid leukemia (AML). Critical to our understanding of the mechanism of cellular transformation by oncogenic transcription factors is the ability to define their direct gene targets. However, gene network cascades can change within minutes to hours, making it difficult to distinguish direct from secondary or compensatory transcriptional changes by traditional methodologies. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
9 Samples
Download data: BEDGRAPH, BW, CSV, TXT
Series
Accession:
GSE153279
ID:
200153279
11.

Definition of a Small Core Transcriptional Circuit Regulated by AML1-ETO [PRO-seq]

(Submitter supplied) Transcription factors regulate gene networks controlling normal hematopoiesis and are frequently deregulated in acute myeloid leukemia (AML). Critical to our understanding of the mechanism of cellular transformation by oncogenic transcription factors is the ability to define their direct gene targets. However, gene network cascades can change within minutes to hours, making it difficult to distinguish direct from secondary or compensatory transcriptional changes by traditional methodologies. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
18 Samples
Download data: BEDGRAPH, TXT
Series
Accession:
GSE153267
ID:
200153267
12.

Definition of a Small Core Transcriptional Circuit Regulated by AML1-ETO [RNA-seq]

(Submitter supplied) Transcription factors regulate gene networks controlling normal hematopoiesis and are frequently deregulated in acute myeloid leukemia (AML). Critical to our understanding of the mechanism of cellular transformation by oncogenic transcription factors is the ability to define their direct gene targets. However, gene network cascades can change within minutes to hours, making it difficult to distinguish direct from secondary or compensatory transcriptional changes by traditional methodologies. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL18573 GPL24676
16 Samples
Download data: DIFF
13.

PRMT1 interacts with leukemia fusion protein AML1-ETO for activation of transcription and transformation

(Submitter supplied) Fusion protein AML1-ETO resulted from t(8;21) translocation is highly related to leukemia development. We have previously shown that the expression of AE9a, a spliced form of AML1-ETO, can rapidly cause leukemia in mouse. To understand how AML1-ETO is involved in leukemia development, we used AE9a leukemia model to identify a novel AE9a interacting proteins PRMT1 (protein arginine methyltransferase 1) from primary leukemic cells expressing AE9a. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
12 Samples
Download data: TXT
Series
Accession:
GSE28135
ID:
200028135
14.

Interaction of c-Myb with p300 is required for the induction of acute myeloid leukemia (AML) by human AML oncogenes

(Submitter supplied) The MYB oncogene is widely expressed in acute leukemias and is important for the continued proliferation of leukemia cells, raising the possibility that MYB may be a therapeutic target. However realization of this potential requires (i) a significant therapeutic window for MYB inhibition, given its essential role in normal hematopoiesis; and (ii) an approach for developing an effective therapeutic. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6885
16 Samples
Download data: TXT
Series
Accession:
GSE34224
ID:
200034224
15.

Targeting of SMARCA4 bromodomain selectively inhibits leukemic cell proliferation

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platforms:
GPL570 GPL16699
24 Samples
Download data: CEL, TXT
Series
Accession:
GSE67924
ID:
200067924
16.

Comparison of gene expression changes in AML cells after SMARCA4, SMARCD2 or DPF2 knock-down

(Submitter supplied) We explored the role of SMARCA4 and the two Brahma associated factors SMARCD2 and DPF2 in leukaemia. We observed the selective requirement for these factors for leukemic cell expansion, as well as extended survival of mice transplanted with leukaemic cells with reduced expression of these genes. Gene expression profiling revealed largely similar alterations with the down-regulation of each of these three factors, suggesting a concerted function in transformed blood cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL16699
12 Samples
Download data: TXT
Series
Accession:
GSE67923
ID:
200067923
17.

Gene expression changes in MV4-11 cells upon SMARCA4 knock-down and PFI-3 treatment

(Submitter supplied) Pharmacological inhibition of the SMARCA4 bromodomain inhibited human leukemic cell proliferation, phenocopying SMARCA4 knockdown in these cells. We performed microarray analysis of global gene expression changes in MV4-11 cells after 6 days of PFI-3 treatment and after SMARCA4 knock-down. With this analysis we identified several genes whose expression was similarly up- or down-regulated upon inhibitor treatment and SMARCA4 depletion.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
12 Samples
Download data: CEL
Series
Accession:
GSE67920
ID:
200067920
18.

AML1-ETO-induced FOXO1 activates a self-renewal program in pre-leukemia stem cells

(Submitter supplied) Blocking the self-renewal of pre-leukemia stem cells could prevent AML relapse. In this study we show that FOXO1 is an essential self-renewal factor in leukemic and pre-leukemic cells expressing the t(8;21)-associated oncogene AML1-ETO (AE). FOXO1 is consistently upregulated in t(8;21) AML and functions as a critical oncogenic mediator rather than a tumor suppressor. Expression of FOXO1 in human CD34+ cells promotes a pre-leukemic state, partially phenocopying the cellular and transcriptional effects of AE expression. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
2 Samples
Download data: BEDGRAPH
Series
Accession:
GSE80773
ID:
200080773
19.

TAF1 is critical for AE driven leukemogenesis [ATAC-seq]

(Submitter supplied) TAF1 is essential for AE driven leukemogenesis. Depletion of TAF1 impairs the recruitment of AE to its target genes, interfereing with its control of gene expression. The bromodomains of TAF1 associate with K43 acetylated AE and this association plays a role in the proliferationof AE expressing AML cells.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
6 Samples
Download data: BIGWIG
Series
Accession:
GSE134018
ID:
200134018
20.

TAF1 is critical for AE driven leukemogenesis [RNA-seq]

(Submitter supplied) TAF1 is essential for AE driven leukemogenesis. Depletion of TAF1 impairs the recruitment of AE to its target genes, interfering with its control of gene expression. The bromodomains of TAF1 associate with K43 acetylated AE and this association plays a role in the proliferation of AE expressing AML cells.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
19 Samples
Download data: TXT
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