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Links from GEO DataSets

Items: 19

1.

Analyses of T-ALL (COG study)

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array; Expression profiling by high throughput sequencing
Platforms:
GPL570 GPL11154 GPL17303
117 Samples
Download data: CEL
Series
Accession:
GSE77741
ID:
200077741
2.

RNA sequencing of T-ALL (COG study)

(Submitter supplied) The clinical and cytogenetic features associated with T-cell acute lymphoblastic leukemia (T-ALL) are not predictive of early treatment failure or relapse. We investigated 213 newly diagnosed patients who were treated in the Children's Oncology Group (COG) T-ALL Studies 9404 and 0434 and identified a cluster cases characterized by increased expression of HOX9/10. In samples with >8-fold HOXA9/10 deregulation, the presence of specific molecular lesions were confirmed through a systematic review of cytogenetic databases, FISH and PCR testing. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL11154 GPL17303
17 Samples
Download data: TXT
3.

Microarray analyses of T-ALL (COG study)

(Submitter supplied) The clinical and cytogenetic features associated with T-cell acute lymphoblastic leukemia (T-ALL) are not predictive of early treatment failure or relapse. We used the Affymetrix U133 Plus 2.0 chip to profile 100 newly diagnosed patients who were treated in the Children's Oncology Group (COG) T-ALL AALL0434. We performed unsupervised hierarchical clustering of 25 HOXA probe sets within the cohort of 100 T-ALL cases. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
100 Samples
Download data: CEL
Series
Accession:
GSE70536
ID:
200070536
4.

PBX3 cooperates with MEISI in causing rapid acute myeloid leukemia and recapitulates the core transcriptome of MLL-rearranged leukemia

(Submitter supplied) To investigate whether co-expression of PBX3/MEIS1 can mimic that of MLL-AF9, HOXA9/MEIS1 or HOXA9/PBX3 in inducing leukemogenesis, we conducted in vivo mouse bone marrow transplantation (BMT) assays. Briefly, normal mouse bone marrow (BM) progenitor (i.e., lineage negative; Lin-) cells collected from B6.SJL (CD45.1) donor mice (CD45.1) were retrovirally co-transduced with MSCVneo-MLL-AF9+MSCV-PIG (MLL-AF9), MSCVneo-HOXA9+MSCV-PIG (HOXA9), MSCVneo-HOXA9+MSCV-PIG-MEIS1 (HOXA9+MEIS1), MSCVneo-HOXA9+MSCV-PIG-PBX3 (HOXA9+PBX3), MSCV-PIG-PBX3+MSCVneo-MEIS1 (PBX3+MEIS1), MSCVneo+MSCV-PIG-PBX3 (PBX3) , MSCVneo+MSCV-PIG-MEIS1 (MEIS1), or MSCVneo+MSCV-PIG (normal control; NC). more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL16570
20 Samples
Download data: CEL
Series
Accession:
GSE68643
ID:
200068643
5.

Gene expression induced by DOT1L and Menin inhibition in cell line models of leukemia

(Submitter supplied) Gene expression upon DOT1L inhibition, or Menin inhibition, or a combination of DOT1L and Menin inhibiting agents, was assessed in several MLL-rearranged human cell lines and a mouse model of MLL-AF9 leukemia. The goal of the study was to explore the mechanisms by which the EPZ0004777 and MI-2-2 chemicals collaborate to induce differentiation and cell death in MLL-AF4 and MLL-AF9 leukemias.
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by array
Platforms:
GPL1261 GPL570
56 Samples
Download data: CEL
Series
Accession:
GSE63664
ID:
200063664
6.

Genome-wide analysis of gene expression in MLL translocation transformed mouse leukemia cell lines

(Submitter supplied) The purpose of this study is to investigate the transcriptional programs as it relates to disease latency initiated by different MLL fusion proteins, including: MLL-AF1p, MLL-AF6, MLL-Gas7, MLL-AF9 and MLL-ENL. Leukemia cell lines were established by transforming kit+ mouse bone marrow cells with retroviruses coding MLL-AF1p, MLL-AF6, MLL-Gas7, MLL-AF9 or MLL-ENL. At early phase after the cell lines were established, cells growing at exponential phase (cell density at 0.5~1x106/ml) were harvested for RNA extraction and sequencing purpose.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
12 Samples
Download data: TXT
Series
Accession:
GSE73457
ID:
200073457
7.

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
8.

DNA methylation in infant ALL

(Submitter supplied) The aggressive MLL-rearranged leukemias are well-known for their unique gene-expression profiles. The goal of this study was to characterize the MLL-specific DNA methylation profiles in infant acute lymphoblastic leukemia (ALL). Genome-wide DNA methylation profiling was performed on primary infant ALL samples. The majority of infant ALL samples demonstrated severe DNA hypermethylation compared with normal pediatric bone marrows, which implies that targeting of DNA methylation may be an interesting option for future therapeutic strategies in MLL-rearranged infant ALL. more...
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL4126
60 Samples
Download data: TXT
Series
Accession:
GSE18400
ID:
200018400
9.

In vitro prednisolone resistance signature in MLL-rearranged infant ALL

(Submitter supplied) Acute Lymphoblastic Leukemia (ALL) in infants (<1 year of age) is characterized by a high incidence of MLL translocations which is associated with a poor prognosis. Contributing to this poor prognosis is cellular drug resistance, especially to glucocorticoids like prednisolone. Although in vitro prednisolone resistance mechanisms have been proposed in pediatric ALL, it has never been studied in MLL-rearranged infant ALL, which are highly resistant to glucocorticoids in vitro and in vivo.
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS4297
Platform:
GPL570
43 Samples
Download data: CEL
Series
Accession:
GSE32962
ID:
200032962
10.
Full record GDS4297

MLL-rearranged infant acute lymphoblastic leukemia in vitro resistant to prednisolone

Analysis of primary MLL-rearranged ALL samples (>90% leukemic blasts) from untreated infants. In vitro prednisolone sensitivity was assessed by a 4day cytotoxicity (MTT) assay. Results provide insight into the molecular basis of glucocorticoid resistance in MLL-rearranged infant ALL patients.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 2 disease state sets
Platform:
GPL570
Series:
GSE32962
43 Samples
Download data: CEL
DataSet
Accession:
GDS4297
ID:
4297
11.

MLL is essential for NUP98-HOXA9-induced leukemia

(Submitter supplied) Rearrangements involving the NUP98 gene resulting in fusions to several partner genes occur in acute myeloid leukemia and myelodysplastic syndromes. This study demonstrates that the second FG repeat domain of the NUP98 moiety of the NUP98-HOXA9 fusion protein is important for its cell immortalization and leukemogenesis activities. We demonstrate that NUP98-HOXA9 interacts with MLL via this FG repeat domain and that, in the absence of MLL, NUP98-HOXA9-induced cell immortalization and leukemogenesis are severely inhibited. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
8 Samples
Download data: CEL
Series
Accession:
GSE93923
ID:
200093923
12.

Genes regulated by Meis1 in murine Mll-AF9 leukemia cells

(Submitter supplied) Leukemias with MLL-rearrangements are characterized by high expression of the homeo box gene MEIS1. In these studies, we knocked down Meis1 expression by shRNA lentivirus transduction in murine Mll-AF9 leukemia cells. Meis1 knockdown resulted in decreased proliferation and survival of murine Mll-AF9 leukemia cells. We also observed reduced clonogenic capacity and increased monocytic differentiation. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
10 Samples
Download data: CEL
Series
Accession:
GSE14101
ID:
200014101
13.

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
14.

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
15.

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
16.

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
17.

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
18.

3D Genome Analysis Identifies Enhancer Hijacking Mechanism for High-Risk Factors in Human T-Lineage Acute Lymphoblastic Leukemial (T-ALL)

(Submitter supplied) The goals of this study are to determine whether alterations in the 3D genome organization are associated with the malignant transformation of T-ALL. We report integrated analyses of 3D genome alterations and differentially expressed genes (DEGs) in 18 newly diagnosed T-ALL patients and 4 healthy T cell controls. We found that 3D genome reorganization at the compartment, topologically associated domains (TAD), and loop levels in different subtypes of T-ALL. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Other
Platform:
GPL20795
52 Samples
Download data: BEDPE, BW, H5, HIC, TXT, XLS
19.

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
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