GEO DataSets

Analysis of thymic tumors from Ikaros-deficient (IkL/L) mice with a Notch promoter/exon1 deletion. The deletion of Notch1 promoter results in oncogenic activation of Notch1 and significantly accelerates leukemogenesis. Results provide insight into role of Notch activation in pathogenesis of T-ALL.

Organism:

Mus musculus

Type:

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

Platform:

GPL1261

Series:

GSE23972

6 Samples

Download data: CEL

(Submitter supplied) This dataset comprises expression profiles from 3 thymic lymphomas from Ikaros deficient mice (IkL/L model, see Dumortier et al, Mol. Cell. Biol. 26, 209-220, 2006 for a description of the tumor model) and 3 thymic lymphomas from IkL/L mice that harbor a mutation of the Notch1 gene (deletion of floxed sequences comprising the promoter and exon 1 with the CD4-Cre transgene). The results from this experimpent is that the expression of Notch target genes was unexpectedly not altered in the tumors with the Notch1 deletion. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS4174

Platform:

GPL1261

6 Samples

Download data: CEL

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

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

16 Samples

Download data: TXT

(Submitter supplied) To examine Ikaros tumor suppressor mechanisms, we have utilized inducible RNAi to dynamically restore endogenous Ikaros expression in T-ALL driven by its knockdown. This causes rapid transcriptional repression of Notch1 and associated targets including Myc, even in leukemias harboring spontaneous activating Notch1 mutations (producing aberrant ICN1) similar to those found in 60% of human T-ALL. Ikaros restoration results in sustained regression of Notch1-wild type leukemias while endogenous or engineered ICN1 expression promotes rapid disease relapse, indicating that ICN1 functionally antagonizes Ikaros in T-ALL.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

2 Samples

Download data: TXT

(Submitter supplied) To examine Ikaros tumor suppressor mechanisms, we have utilized inducible RNAi to dynamically restore endogenous Ikaros expression in T-ALL driven by its knockdown. This causes rapid transcriptional repression of Notch1 and associated targets including Myc, even in leukemias harboring spontaneous activating Notch1 mutations (producing aberrant ICN1) similar to those found in 60% of human T-ALL. Ikaros restoration results in sustained regression of Notch1-wild type leukemias while endogenous or engineered ICN1 expression promotes rapid disease relapse, indicating that ICN1 functionally antagonizes Ikaros in T-ALL.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

2 Samples

Download data: TXT

(Submitter supplied) To examine Ikaros tumor suppressor mechanisms, we have utilized inducible RNAi to dynamically restore endogenous Ikaros expression in T-ALL driven by its knockdown. This causes rapid transcriptional repression of Notch1 and associated targets including Myc, even in leukemias harboring spontaneous activating Notch1 mutations (producing aberrant ICN1) similar to those found in 60% of human T-ALL. Ikaros restoration results in sustained regression of Notch1-wild type leukemias while endogenous or engineered ICN1 expression promotes rapid disease relapse, indicating that ICN1 functionally antagonizes Ikaros in T-ALL.

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:

Homo sapiens

Type:

Expression profiling by array; Expression profiling by high throughput sequencing

Platforms:

GPL11154 GPL19197

144 Samples

Download data: TXT

(Submitter supplied) Genetic studies in T-cell acute lymphoblastic leukemia have uncovered a remarkable complexity of oncogenic and loss-of-function mutations. Amongst this plethora of genetic changes, NOTCH1 activating mutations stand out as the most frequently occurring genetic defect, identified in more than 50% of T-cell acute lymphoblastic leukemias, supporting an essential driver role for this gene in T-cell acute lymphoblastic leukemia oncogenesis. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

4 Samples

Download data: TSV

(Submitter supplied) Genetic studies in T-cell acute lymphoblastic leukemia have uncovered a remarkable complexity of oncogenic and loss-of-function mutations. Amongst this plethora of genetic changes, NOTCH1 activating mutations stand out as the most frequently occurring genetic defect, identified in more than 50% of T-cell acute lymphoblastic leukemias, supporting an essential driver role for this gene in T-cell acute lymphoblastic leukemia oncogenesis. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

12 Samples

Download data: TSV

(Submitter supplied) Genetic studies in T-cell acute lymphoblastic leukemia have uncovered a remarkable complexity of oncogenic and loss-of-function mutations. Amongst this plethora of genetic changes, NOTCH1 activating mutations stand out as the most frequently occurring genetic defect, identified in more than 50% of T-cell acute lymphoblastic leukemias, supporting an essential driver role for this gene in T-cell acute lymphoblastic leukemia oncogenesis. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL19197

13 Samples

Download data: TXT

(Submitter supplied) Genetic studies in T-cell acute lymphoblastic leukemia have uncovered a remarkable complexity of oncogenic and loss-of-function mutations. Amongst this plethora of genetic changes, NOTCH1 activating mutations stand out as the most frequently occurring genetic defect, identified in more than 50% of T-cell acute lymphoblastic leukemias, supporting an essential driver role for this gene in T-cell acute lymphoblastic leukemia oncogenesis. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL19197

8 Samples

Download data: TXT

(Submitter supplied) Genetic studies in T-cell acute lymphoblastic leukemia have uncovered a remarkable complexity of oncogenic and loss-of-function mutations. Amongst this plethora of genetic changes, NOTCH1 activating mutations stand out as the most frequently occurring genetic defect, identified in more than 50% of T-cell acute lymphoblastic leukemias, supporting an essential driver role for this gene in T-cell acute lymphoblastic leukemia oncogenesis. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL19197

16 Samples

Download data: TXT

(Submitter supplied) Genetic studies in T-cell acute lymphoblastic leukemia have uncovered a remarkable complexity of oncogenic and loss-of-function mutations. Amongst this plethora of genetic changes, NOTCH1 activating mutations stand out as the most frequently occurring genetic defect, identified in more than 50% of T-cell acute lymphoblastic leukemias, supporting an essential driver role for this gene in T-cell acute lymphoblastic leukemia oncogenesis. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL19197

12 Samples

Download data: TXT

(Submitter supplied) Genetic studies in T-cell acute lymphoblastic leukemia have uncovered a remarkable complexity of oncogenic and loss-of-function mutations. Amongst this plethora of genetic changes, NOTCH1 activating mutations stand out as the most frequently occurring genetic defect, identified in more than 50% of T-cell acute lymphoblastic leukemias, supporting an essential driver role for this gene in T-cell acute lymphoblastic leukemia oncogenesis. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL19197

64 Samples

Download data: TXT

(Submitter supplied) Genetic studies in T-cell acute lymphoblastic leukemia have uncovered a remarkable complexity of oncogenic and loss-of-function mutations. Amongst this plethora of genetic changes, NOTCH1 activating mutations stand out as the most frequently occurring genetic defect, identified in more than 50% of T-cell acute lymphoblastic leukemias, supporting an essential driver role for this gene in T-cell acute lymphoblastic leukemia oncogenesis. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL19197

15 Samples

Download data: TXT

(Submitter supplied) The transcription factor Ikaros represses Notch signaling. Since Ikaros and Notch treanscriptional mediator RBPJ both recognize sequences that contain the same core TGGGAA motif, it was hypothesized that Ikaros represses Notch signaling by targeting Notch response elements and competing with RBPJ for their binding. Here we used the mouse T-cell leukemia cell line T29 to compare the genomic binding profiles of Ikaros and RBPJ by ChIP-seq.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11002

6 Samples

Download data: WIG

(Submitter supplied) We used an immature mouse T cell line engineered to express a biotinylated form of the cleaved form of Notch1 (ICN1). ICN1-bound sites were precipitated with streptavidin-coated beads and subjected to ChIP-sequencing.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11002

2 Samples

Download data: WIG

(Submitter supplied) The mouse Ikaros-deficient thymic lymphoma cell line T29 was treated with a gamma-secretase inhibitor or vehicle (DMSO) for 36h and subjected to transcriptome analysis.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

4 Samples

Download data: CEL

(Submitter supplied) The aim of the experiment was to visualize genes under the control of Ikaros during early T cell development. We used mice carrying floxed Ikaros alleles that were crossed with the Rosa26-CreERT2 mice, and which were injected with tamoxifen for 4 days. DN4 thymocytes were sorted from 4 mice (5-6 week-old) which are positive or not for the Rosa26-CreERT2 transgene.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

4 Samples

Download data: CEL

(Submitter supplied) Double positive thymocytes (CD4+CD8+CD3lo) were sorted from 3-4-week old mice from Ikf/f CD4-Cre+ or Ikf/f CD4-Cre- mice (2 mice per genotype) and their transcriptome analyzed.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

4 Samples

Download data: CEL