Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Human SUP-B15 cells: CNV compared to reference genome.

ABSTRACT: Copy Number Variaton (CNV) detection of human BCR-ABL positive acute lymphoblastic leukemia (ALL) cell line, SUP-B15.

ORGANISM(S): Homo sapiens

PROVIDER: GSE239416 | GEO | 2023/07/29

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Human SUP-B15 cells: CNV compared to reference genome.

Project description:Human SUP-B15 cells: CNV compared to reference genome.

| PRJNA999241 | ENA

ChIP-seq assay for BRG1 in human SUP-B15 and Nalm-6 cell lines

Project description:Abstract: BRG1 is highly expressed in adult B-cells acute lymphoblastic leukemia and is associated with poor prognosis. High expression of BRG1 promotes the proliferation and resistance to apoptosis of B-ALL cells. BRG1 exerts these functions mainly through activation of the PI3K/AKT signaling pathway. In order to understand the specific regulatory mechanism, we used ChIP-seq to detect the DNA fragments bound by BRG1 in SUP-B15 and Nalm-6 cell lines.

2024-09-13 | GSE249559 | GEO

Effect of imatinib on philadelphia chromosome positive acute lymphoblastic leukemia

Project description:The Philadelphia chromosome (Ph) encodes the oncogenic BCR-ABL1 tyrosine kinase, which defines a subset of acute lymphoblastic leukemia (ALL) with a particularly unfavorable prognosis. In this study, the tyrosine kinase inhibitor imatinib was used for pharmacological inhibition of BCR-ABL1. Gene expression profiles of Ph+ ALL cell lines were analyzed in response to imatinib treatment. Four Ph+ ALL cell lines (BV-173, NALM-1, SUP-B15, and TOM1) were either treated with 10µM STI571 (Imatinib) for 16 hours or cultured in absence of STI571.

2010-09-10 | E-GEOD-23743 | biostudies-arrayexpress

Analysis of extracellular matrix and adhesion molecules expression in ALL cell line

2010-05-01 | GSE18516 | GEO

Analysis of extracellular matrix and adhesion molecules expression in ALL cell line

Project description:The acute lymphoblastic leukemia cells lines JM-1, REH, Nalm-27, and SUP-B15 were analyzed for baseline expression of extacellular matrix and adhesion molecules using a pathway focused cDNA microarray (SABiosciences). RNA isolated from the ALL cell lines JM-1, REH, Nalm-27, and SUP-B15 was analyzed using the Extracellular Matrix and Adhesion Molecules Oligo GEArray (SABIosciences).

2010-05-01 | E-GEOD-18516 | biostudies-arrayexpress

Inhibition of BCL6-dependent gene expression in Philadelphia chromosome positive acute lymphoblastic leukemia

Project description:The Philadelphia chromosome (Ph) encodes the oncogenic BCR-ABL1 tyrosine kinase, which defines a subset of acute lymphoblastic leukemia (ALL) with a particularly unfavorable prognosis. Tyrosine kinase inhibitors (TKI) are widely used to treat patients with leukemia driven by BCR-ABL1 and other oncogenic tyrosine kinases. In response to TKI-treatment, BCR-ABL1 ALL cells upregulate BCL6 protein levels by ~90-fold, i.e. to similar levels as in diffuse large B cell lymphoma (DLBCL) with BCL6 translocations. In this study, we analyzed the gene expression changes after treatment with Imatinib or Imatinib + RI-BPI. Three Ph+ ALL cell lines (BV-173, SUP-B15 and TOM-1) were treated in the presence or absence of 10 μM STI571 (Imatinib) or in the presence of both 10 μM STI571 and 20 μM RI-BPI for 24 hours.

2011-03-01 | E-GEOD-24381 | biostudies-arrayexpress

Glucocorticoids induced transcriptional regulation in acute lymphoblastic leukemia

Project description:Four acute lymphoblastic leukemia cell lines SUP-B15, JURKAT, MOLT-3, and CCRF-CEM cells were treated with glucocorticoids such as dexamethasone and prednisolone for six hours before RNA extraction.

2020-12-18 | E-MTAB-9250 | biostudies-arrayexpress

Wnt/Ca2+/NFAT signaling maintains survival of Ph+ leukemia cells upon inhibition of Bcr-Abl

Project description:Although Bcr-Abl kinase inhibitors have proven effective in the treatment of chronic myeloid leukemia (CML), they generally fail to completely eradicate Bcr-Abl+ leukemia cells. To identify genes whose inhibition sensitizes Bcr-Abl+ leukemias to killing by Bcr-Abl inhibitors, we performed an RNAi-based synthetic lethal screen with imatinib in CML cells. This screen identified numerous components of a Wnt/Ca2+/NFAT signaling pathway. Antagonism of this pathway led to impaired NFAT activity, decreased cytokine production and enhanced sensitivity to Bcr-Abl inhibition. Furthermore, NFAT inhibition with cyclosporin A facilitated leukemia cell elimination by the Bcr-Abl inhibitor dasatinib and markedly improved survival in a mouse model of Bcr-Abl+ acute lymphoblastic leukemia (ALL). Targeting this pathway in combination with Bcr-Abl inhibition could improve treatment of Bcr-Abl+ leukemias.

2010-07-15 | GSE21499 | GEO

Wnt/Ca2+/NFAT signaling maintains survival of Ph+ leukemia cells upon inhibition of Bcr-Abl

2010-07-15 | E-GEOD-21499 | biostudies-arrayexpress

pre-B cells from normal control, preleukemic, fully leukemic and fully leukemic, nilotinib-treated P190 BCR/ABL transgenic mice

Project description:Precursor B-lineage acute lymphoblastic leukemia (pre-B ALL) can be subdivided into different categories based on genetic abnormalities. One type of pre-B ALL is characterized by the presence of the Philadelphia (Ph) chromosome, the derivative chromosome 22 that is one product of a reciprocal translocation between chromosomes 22 and 9. The 22/9 translocation fuses the 5’ part of the BCR gene to the 3’ end of the c-ABL gene. The resulting BCR/ABL fusion encodes a Bcr/Abl protein with deregulated Abl kinase activity. Two major fusion proteins are found in Ph-positive leukemias which differ in molecular weight and the size of the Bcr moiety. The P190 Bcr/Abl protein is common in Ph-positive ALL. Targeted tyrosine kinase inhibitors such as nilotinib are used therapeutically to treat this type of leukemia. The 22/9 translocation fuses the 5’ part of the BCR gene to the 3’ end of the c-ABL gene. The resulting BCR/ABL fusion encodes a Bcr/Abl protein with deregulated Abl kinase activity. Two major fusion proteins are found in Ph-positive leukemias which differ in molecular weight and the size of the Bcr moiety. The P190 Bcr/Abl protein is common in Ph-positive ALL. Targeted tyrosine kinase inhibitors such as nilotinib are used therapeutically to treat this type of leukemia.

2018-02-05 | GSE110104 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data