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Links from GEO DataSets

Items: 19

1.

Proteasome Inhibition Targets the KMT2A Transcriptional Complex

(Submitter supplied) We quantitatively evaluated H2Bub and H3K79me2 epigenetic marks genome wide in a KMT2A rearranged B lineage acute lymphoblastic leukemia cell line after treatment with bortezomib over a 6 hour time course by ChIP-Rx. We identified rapid and concordant depletion of these epigenetic marks within two hours. To look at gene expression changes, RNA sequencing was performed on KMT2A rearranged B lineage acute lymphoblastic leukemia patient samples in the presence and absence of bortezomib exposure.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL24676 GPL11154
26 Samples
Download data: BW, TXT
2.

DNA methylation profiling of pediatric B lymphoblastic leukemia with KMT2A rearrangement identifies hypomethylation at enhancer sites

(Submitter supplied) Genome wide DNA methylation profiling of 26 pediatric KMT2Ar rearranged ALLs in comparison to 22 previously profiled samples of different non-neoplastic human B-cell precursor populations (GSE45459). The Illumina Infinium 450k Human DNA methylation Beadchip was used.
Organism:
Homo sapiens
Type:
Methylation profiling by array; Third-party reanalysis
Platform:
GPL13534
26 Samples
Download data: TXT
Series
Accession:
GSE76585
ID:
200076585
3.

Gene expression data from infants (<1 year of age) diagnosed with Acute Lymphoblastic Leukemia (ALL)

(Submitter supplied) Acute Lymphoblastic Leukemia (ALL) in infants (<1 year) is characterized by a poor prognosis and a high incidence of MLL translocations. Several studies demonstrated the unique gene expression profile associated with MLL-rearranged ALL, but generally small cohorts were analyzed as uniform patient groups regardless of the type of MLL translocation, while the analysis of translocation-negative infant ALL remained unacknowledged.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
73 Samples
Download data: CEL
Series
Accession:
GSE19475
ID:
200019475
4.

Transcriptional effect of EGR3 overexpression in the cell line SEM

(Submitter supplied) FLAG-tagged EGR3 was overexpressed in the cell line SEM to study transcriptional consequences in the t(4;11) cellular context.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
6 Samples
Download data: TXT
Series
Accession:
GSE225710
ID:
200225710
5.

Gene expression data from children diagnosed with ALL in vitro sensitive or resistant to prednisolone

(Submitter supplied) Although the prognosis for childhood Acute Lymphoblastic Leukemia (ALL) in general has improved tremendously over the last decades, the survival chances for infants (<1 year of age) with ALL remains poor. A major obstacle hampering successful treatment results in infant ALL is cellular resistance to several drugs currently used in the treatment of ALL, especially to prednisolone (or prednisone). Therefore we set out to search for genes differentially expressed between from infant (children <1 year of age) and non-infant (children >1 year of age) ALL samples either resistant or sensitive to prednisolone.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL96
52 Samples
Download data: CEL, CHP
Series
Accession:
GSE19143
ID:
200019143
6.

Molecular fingerprints for bone marrow cells, pediatric acute lymphoblastic leukemia

(Submitter supplied) The overall goal of this study was to characterize bone marrow cells based on their transcriptome, surface protein expression and BCR- and TCR VDJ-profile for accurate identification of clinically relevant cell states. This submission includes pediatric B-cell acute lymphoblastic leukemia samples. This project has received funding from the European Union Horizon 2020 research and innovation programme under grant agreement No 824110 (EASI-Genomics)
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Other
Platform:
GPL24676
12 Samples
Download data: CSV, MTX, TSV
Series
Accession:
GSE230295
ID:
200230295
7.

Mechanistic study of Wee1 kinase inhibition with AZD1775 exposes drug targetable vulnerabilities in acute B-lymphoblastic leukemia [scRNA-seq PDX MLL-7]

(Submitter supplied) This study characterized the effect of WEE1 kinase inhibition using AZD1775 treatment on single-cell gene expression profile using the 10x Genomics protocol in the acute lymphoblastic leukemia cells
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
8 Samples
Download data: MTX, TSV
Series
Accession:
GSE220476
ID:
200220476
8.

Mechanistic study of Wee1 kinase inhibition with AZD1775 exposes drug targetable vulnerabilities in acute B-lymphoblastic leukemia

(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; Other
Platforms:
GPL24676 GPL18573 GPL11154
57 Samples
Download data: BED, BIGWIG, MTX, TSV
Series
Accession:
GSE220114
ID:
200220114
9.

Mechanistic study of Wee1 kinase inhibition with AZD1775 exposes drug targetable vulnerabilities in acute B-lymphoblastic leukemia [scMultiome]

(Submitter supplied) This study characterized the effect of WEE1 kinase inhibition using AZD1775 treatment on single-cell accessible chromatin and gene expression profile using the 10x Genomics multiome protocol (ATAC + Gene Expression Assay) in the acute lymphoblastic leukemia cell line RS4;11 that represents the KMT2A-rearranged subtype.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
4 Samples
Download data: BED, H5, TSV
Series
Accession:
GSE220112
ID:
200220112
10.

Mechanistic study of Wee1 kinase inhibition with AZD1775 exposes drug targetable vulnerabilities in acute B-lymphoblastic leukemia [GROseq]

(Submitter supplied) Nascent transcription and enhancer activity was studied using GRO-seq in the acute lymphoblastic leukemia cell line RS4;11 upon inhibition of the WEE1 kinase.
Organism:
Homo sapiens
Type:
Other
Platform:
GPL11154
12 Samples
Download data: BIGWIG
Series
Accession:
GSE220099
ID:
200220099
11.

Mechanistic study of Wee1 kinase inhibition with AZD1775 exposes drug targetable vulnerabilities in acute B-lymphoblastic leukemia [scATAC-seq]

(Submitter supplied) This study characterized the effect of WEE1 kinase inhibition using AZD1775 treatment on single-cell accessible chromatin and gene expression profile in the acute lymphoblastic leukemia cell line RS4;11 that represents the KMT2A-rearranged subtype.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
2 Samples
Download data: BED, TSV
Series
Accession:
GSE218805
ID:
200218805
12.

Mechanistic study of Wee1 kinase inhibition with AZD1775 exposes drug targetable vulnerabilities in acute B-lymphoblastic leukemia [scRNA-seq]

(Submitter supplied) This study characterized the effect of WEE1 kinase inhibition using AZD1775 treatment on single-cell gene expression profile using the 10x Genomics protocol in the acute lymphoblastic leukemia cell lines RS4;11 (KMT2A-rearranged subtype) and Nalm6 (other subtype).
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
3 Samples
Download data: MTX, TSV
Series
Accession:
GSE218621
ID:
200218621
13.

Wee1 inhibition in acute lymphoblastic leukemia with MLL rearrangement.

(Submitter supplied) Enhancer activity and RUNX1 binding was studied using ChIP-seq in mixed lineage leukemia t(4;11) rearranged acute lymphoblastic leukemia upon inhibition of the WEE1 kinase.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
16 Samples
Download data: BIGWIG
Series
Accession:
GSE148195
ID:
200148195
14.

RUNX1 overexpression in precursor B acute leukemia cells

(Submitter supplied) Overexpression of the transcription factor RUNX1 was studied in Nalm-6 precursor B acute lymphoblastic leukemia cells. The active enhancer histone marker H3K27ac and RUNX1 were measured using ChIP-seq. The effect on gene expression was analyzed using single cell RNA-sequencing.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL24676 GPL18573
12 Samples
Download data: BIGWIG, MTX, TSV
Series
Accession:
GSE148192
ID:
200148192
15.

RUNX2 is a dependency factor in immature and KMT2A-rearranged T-cell acute lymphoblastic leukemia

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL18573 GPL19057
54 Samples
Download data: BED, NARROWPEAK
Series
Accession:
GSE151823
ID:
200151823
16.

RUNX2 is a dependency factor in immature and KMT2A-rearranged T-cell acute lymphoblastic leukemia [KMT2A-MLLT1_ Runx2 ko RNA-seq]

(Submitter supplied) T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignancy with a high incidence of relapse. Here we show that Runt-related transcription factor 2, RUNX2 is upregulated in high-risk T-ALL with KMT2A rearrangements (KMT2A-R) or immature phenotype. In KMT2A-R cells, we identified RUNX2 as a direct target of the KMT2A chimeras, while it reciprocally binds the KMT2A promoter, establishing a regulatory feed-forward mechanism. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
9 Samples
Download data: TXT
Series
Accession:
GSE151822
ID:
200151822
17.

RUNX2 is a dependency factor in immature and KMT2A-rearranged T-cell acute lymphoblastic leukemia [KARPAS-45 AI-10-104 RNA-seq]

(Submitter supplied) T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignancy with a high incidence of relapse. Here we show that Runt-related transcription factor 2, RUNX2 is upregulated in high-risk T-ALL with KMT2A rearrangements (KMT2A-R) or immature phenotype. In KMT2A-R cells, we identified RUNX2 as a direct target of the KMT2A chimeras, while it reciprocally binds the KMT2A promoter, establishing a regulatory feed-forward mechanism. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
8 Samples
Download data: TXT
18.

RUNX2 is a dependency factor in immature and KMT2A-rearranged T-cell acute lymphoblastic leukemia [KARPAS-45 RUNX2 shRNA knockdown RNA-seq]

(Submitter supplied) T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignancy with a high incidence of relapse. Here we show that Runt-related transcription factor 2, RUNX2 is upregulated in high-risk T-ALL with KMT2A rearrangements (KMT2A-R) or immature phenotype. In KMT2A-R cells, we identified RUNX2 as a direct target of the KMT2A chimeras, while it reciprocally binds the KMT2A promoter, establishing a regulatory feed-forward mechanism. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
30 Samples
Download data: TXT
19.

RUNX2 is a dependency factor in immature and KMT2A-rearranged T-cell acute lymphoblastic leukemia [RUNX2 ChIP-seq]

(Submitter supplied) T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignancy with a high incidence of relapse. Here we show that Runt-related transcription factor 2, RUNX2 is upregulated in high-risk T-ALL with KMT2A rearrangements (KMT2A-R) or immature phenotype. In KMT2A-R cells, we identified RUNX2 as a direct target of the KMT2A chimeras, while it reciprocally binds the KMT2A promoter, establishing a regulatory feed-forward mechanism. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
7 Samples
Download data: BED, NARROWPEAK
Series
Accession:
GSE151819
ID:
200151819
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