GEO DataSets

(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) 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

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) Genome-wide mapping and characterization of novel Notch-regulated long non-coding RNAs in acute leukemia

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

31 Samples

Download data: TXT

(Submitter supplied) Acute lymphoblastic leukemia (ALL) is an heterogeneous disease comprising several subentities that differ for both immunophenotypic and molecular characteristics. Over the years, the biologic understanding of this neoplasm has largely increased. Gene expression profiling has recently allowed to identify specific signatures for the different ALL subsets and permitted identification of pathways deregulated by a given lesion. more...

Organism:

Homo sapiens

Type:

Expression profiling by array; Non-coding RNA profiling by array

Platforms:

GPL570 GPL8191

39 Samples

Download data: CEL, XLS

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

Organism:

Homo sapiens

Type:

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

Platforms:

GPL570 GPL11154

36 Samples

Download data: BW, CEL

(Submitter supplied) Here we modeled T-ALL resistance to Notch inhibition, identifying ‘persister’ cells that readily expand in the presence of gamma secretase inhibitor (GSI) and the absence of Notch signaling. Rare persister cells are already present in naïve T-ALL populations, and the reversibility of the phenotype is suggestive of an epigenetic mechanism. Relative to GSI-sensitive cells, persisters activate distinct signaling and gene expression programs, and exhibit global chromatin compaction. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

28 Samples

Download data: BW

(Submitter supplied) Here we modeled T-ALL resistance to Notch inhibition, identifying ‘persister’ cells that readily expand in the presence of gamma secretase inhibitor (GSI) and the absence of Notch signaling. Rare persister cells are already present in naïve T-ALL populations, and the reversibility of the phenotype is suggestive of an epigenetic mechanism. Relative to GSI-sensitive cells, persisters activate distinct signaling and gene expression programs, and exhibit global chromatin compaction. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

8 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

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) The SCL and LMO1 oncogenic transcription factors reprogram thymocytes into self-renewing pre-leukemic stem cells (pre-LSCs). Here we report that SCL directly interacts with LMO1 to activate the transcription of a self-renewal program coordinated by LYL1.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL339

6 Samples

Download data: CEL

(Submitter supplied) We have determined the consequences of ICN1 overexpression from retroviral vectors introduced into bone marrow cells. Even though the tumors consist of phenotypically heterogeneous cells, no evidence for tumor stem cells was found.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

9 Samples

Download data: CEL, CHP

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

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

66 Samples

Download data

(Submitter supplied) The clinical development of targeted therapies has been hampered by their limited intrinsic antitumor activity and the rapid emergence of resistance, highlighting the need to identify highly active and synergistic drug combinations. However, empirical synergistic drug screening approaches are challenging and elucidating the mechanisms that underlie such drug interactions is typically complex. Here we performed an expression based screen and network analyses to identify drugs amplyfiying the antitumor effects of NOTCH inhibition in T-ALL. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

54 Samples

Download data: TXT