GEO DataSets

(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:

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

Type:

Non-coding RNA profiling by array

Platform:

GPL7723

4 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) 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

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) 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) In T-cell acute lymphoblastic leukemia (T-ALL) NOTCH 1 receptors are frequently mutated. This leads to aberrantly high Notch signaling, but how this translates into deregulated cell cycle control and the transformed cell type is poorly understood. In this report, we analyze downstream responses resulting from the high level of NOTCH 1 signaling in T-ALL. Notch activity, measured immediately downstream of the NOTCH 1 receptor, is high, but expression of the canonical downstream Notch response genes HES 1 and HEY 2 is low both in primary cells from T-ALL patients and in T-ALL cell lines. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS2794

Platform:

GPL570

6 Samples

Download data: CEL

Analysis of T-cell acute lymphoblast leukemia (T-ALL) MOLT4 cells following gamma-secretase inhibitor (GSI) DAPT treatment. Gamma-secretase activity is required for Notch 1 receptor signaling. Results provide insight into the role of Notch signaling in T-ALL development.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 2 protocol sets

Platform:

GPL570

Series:

GSE6495

6 Samples

Download data: CEL

(Submitter supplied) We recently identified a subset of down-regulated miRNAs such as miR-145 and miR-133a in squamous cell carcinoma. Cell growth inhibitions occurred in miR-145 and miR-133a transfectants compared with the controls, suggesting that both miRNAs function as tumor suppressors. The aims of our expression studies were identification of these miRNAs target genes.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL4133

4 Samples

Download data: TXT

(Submitter supplied) We recently identified a subset of down-regulated miRNAs such as miR-145 and miR-133a in bladder cancer. Cell growth inhibitions occurred in miR-145 and miR-133a transfectants compared with the controls, suggesting that both miRNAs function as tumor suppressors. The aims of our expression studies were identification of these miRNAs target genes.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL4133

4 Samples

Download data: TXT

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

Organism:

Homo sapiens; Mus musculus

Type:

Non-coding RNA profiling by array

Platforms:

GPL19324 GPL20161

19 Samples

Download data: TXT

(Submitter supplied) Primary mouse cells (CD4-CD8- (DN) and CD4+CD8+ (DP) thymus and T-ALL (early-stage - ES and late-stage - LS) and mouse T-ALL cell line M295 were assessed for microRNA expression

Organism:

Mus musculus

Type:

Non-coding RNA profiling by array

Platform:

GPL19324

13 Samples

Download data: TXT

(Submitter supplied) T-ALL cell line CUTLL1 was assessed for microRNA expression. Cells were treated with DMSO (ctr) or DAPT (10uM) to inhibit Notch1 cleavage for 3d and then harvested.

Organism:

Homo sapiens

Type:

Non-coding RNA profiling by array

Platform:

GPL20161

6 Samples

Download data: TXT

(Submitter supplied) T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive T-cell malignancy characterized by genotypically-defined and phenotypically divergent cell populations, governed by adaptive landscapes. Clonal expansions are associated to genetic and epigenetic events, and modulation of external stimuli that affect the hierarchical structure of subclones and support the dynamics of leukemic subsets. Recently, extracellular vesicles (EVs) such exosomes were also shown to play a role in leukemia. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL23159

8 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

(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) The NOTCH signaling cascade, which is deregulated in T-cell acute lymphoblastic leukemia (T-ALL) and many other human cancers, offers an attractive target for molecular therapy. One approach employs gamma-secretase inhibitors (GSIs) to suppress production of the intracellular form of NOTCH (NICD), leading to cell growth arrest and apoptosis. Here we show that missense mutations or homozygous deletion of FBW7, which encodes a ubiquitin ligase that targets the NICD for destruction, mediate constitutive NICD expression. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL4372

36 Samples

Download data: TXT

(Submitter supplied) The NOTCH1 signaling pathway is a critical determinant of cell fate decisions and drives oncogenesis through mechanisms that are incompletely understood. To elucidate tumorigenic pathways that cooperate with activated Notch1 in leukemogenesis,we performed miRNA expression profiling of normal CD4+CD8+ thymocytes, non-malignant ICN1 over-expressing CD4+CD8+ cells and ICN1-induced tumor CD4+CD8+ cells.

Organism:

Rattus norvegicus; Homo sapiens; Mus musculus

Type:

Non-coding RNA profiling by array

Platform:

GPL6350

3 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) miRNA profiling has been performed on primary tumor samples collected at diagnosis from pediatric patients affected by T-cell lymphoblastic lymphoma.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL8227

12 Samples

Download data: TXT

(Submitter supplied) This two-color miRNA chip was perfored to identify the downstream miRNAs regulated by Notch signaling in macrophage polarization.

Organism:

Mus musculus

Type:

Non-coding RNA profiling by array

Platform:

GPL13493

6 Samples

Download data: TXT