GEO DataSets

Analysis of T-ALL cell lines treated with γ-secretase inhibitor (GSI) to block Notch signaling. Cell lines include parental cells and cells transduced with ICN (a GSI-independent form of activated Notch1) or with c-Myc (a downstream Notch1 target). Results provide insight into Notch1 role in T-ALL.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 2 agent, 5 cell line, 3 genotype/variation sets

Platform:

GPL570

Series:

GSE29959

30 Samples

Download data: CEL

(Submitter supplied) Analysis of five Notch signaling-dependent human T-ALL cell lines (ALLSIL, DND41, HPBALL, KOPTK1, TALL-1) treated with gamma-secretase inhibitor (GSI) to block Notch signaling. Samples include parental cells, cells rescued by retroviral transduction with ICN (a GSI-independent form of activated Notch1), and cells retrovirally transduced with c-Myc (an important downstream target of Notch1). Results allow segregation of bona fide Notch targets from other genes affected by gamma-secretase inhibition as well as from targets downstream of c-Myc.

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS4291

Platform:

GPL570

30 Samples

Download data: CEL

(Submitter supplied) In an attempt to identify miRNAs regulated by oncogenic Notch signaling, we performed miRNA profiling of human T-cell acute lymphoblastic leukemia (T-ALL) cells with or without the treatment of γ-secretase inhibitor (GSI) to block Notch signaling. We found miR-223 levels to increase after GSI treatment suggesting that active Notch signaling represses miR-223 expression. We confirmed insulin-like growth factor-1 receptor (IGF1R) to be regulated by miR-223, but were unable to demonstrate functional effects on T-ALL cell growth by overexpression or knock-down of miR-223 alone.

Organism:

Rattus norvegicus; Murid gammaherpesvirus 4; Betapolyomavirus hominis; Homo sapiens; Mus musculus; Human alphaherpesvirus 1; Human betaherpesvirus 5; Murid betaherpesvirus 1; Human immunodeficiency virus 1; human gammaherpesvirus 4; JC polyomavirus; Human gammaherpesvirus 8; Betapolyomavirus macacae

Type:

Non-coding RNA profiling by array

Platform:

GPL7723

4 Samples

Download data: TXT

(Submitter supplied) Human T-cell Acute lymphoblastic Leukemia cell line CEM was transfected with either shRNA against ZMIZ1 or scrambled shRNA. Four (non-paired) biological replicates of each condition had mRNA assays performed using Affymetrix HG_U133_plus_2 arrays, with 54675 probe-sets. A supplementary Excel workbook holding the same processed data as the series matrix file is provided, with some probe set annotation, and a simple statistical comparison. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

8 Samples

Download data: CEL, XLS

(Submitter supplied) MicroRNAs (miRNAs) have emerged as novel cancer genes. In particular, the 17~92 cluster of miRNAs is highly expressed in haematopoietic cancers and promotes lymphomagenesis in vivo1,2. Clinical use of these findings hinges on isolating the oncogenic activity within the 17~92 cluster and defining its relevant target genes. Here we show that miR-19 is sufficient to promote leukaemogenesis in Notch1 induced T-cell lymphoblastic leukaemia (T-ALL) in vivo. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL8321

6 Samples

Download data: CEL, CHP

(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) To gain insights how loss of PIK3R1 confers resistance to pharmacological Notch inhibition in T-ALL cells, we performed gene expression analysis. Libraries for mRNA-seq were prepared with the Stranded mRNA Ligation method (Illumina) starting from 1µg RNA, according to manufacturer’s instructions. Libraries, all bearing unique dual indices, were subsequently loaded at 250pM in a HiSeq 4000 instrument (Illumina) and sequenced according to manufacturer’s instructions, yielding paired-end reads of 75 nucleotides. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL20301

18 Samples

Download data: CSV, TXT

(Submitter supplied) The efficacy of targeted therapies for treatment of cancer patients is often limited by development of drug resistance. Potential resistance mechanisms to pharmacological Notch1 inhibition mediated by GSI or CB-103 in T-ALL are currently unclear. Thus, we performed a genome-wide loss-of-function (LoF) CRISPR/Cas9 screen to identify genes responsible for resistance to Notch inhibition and novel combination therapies for efficient treatment of human T-ALL. more...

Organism:

Homo sapiens

Type:

Other

Platform:

GPL18573

10 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) Gain-of-function mutations in NOTCH1 are common in T-cell lymphoblastic leukemias making this receptor a promising target for drugs such as gamma-secretase inhibitors (GSI), which block a proteolytic cleavage required for NOTCH1 activation. However, the enthusiasm for these therapies has been tempered by tumor resistance and the paucity of information on the oncogenic programs regulated by oncogenic NOTCH1. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

40 Samples

Download data: CEL

(Submitter supplied) Gain-of-function mutations in NOTCH1 are common in T-cell lymphoblastic leukemias making this receptor a promising target for drugs such as gamma-secretase inhibitors, which block a proteolytic cleavage required for NOTCH1 activation. However, the enthusiasm for these therapies has been tempered by tumor resistance and the paucity of information on the oncogenic programs regulated by oncogenic NOTCH1. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

20 Samples

Download data: CEL

(Submitter supplied) The clinical and cytogenetic features associated with T-cell acute lymphoblastic leukemia (T-ALL) are not predictive of early treatment failure. Based on the hypothesis that microarrays might identify patients who fail therapy, we used the Affymetrix U133 Plus 2.0 chip and prediction analysis of microarrays (PAM) to profile 50 newly diagnosed patients who were treated in the Children's Oncology Group (COG) T-ALL Study 9404. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platforms:

GPL570 GPL96

92 Samples

Download data: CEL