Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA sequence of acute lymphoblastic leukemia cells with NRIP1::PDGFRB fusion

ABSTRACT: Philadelphia chromosome (Ph)-like acute lymphoblastic leukemia (ALL) is a subset of ALL with a high rate of treatment failure. PDGFRB gene fusion is one of the hallmarks of Ph-like ALL. We identified a novel oncogenic PDGFRB fusion gene, NRIP1::PDGFRB, from a pediatric patient with ALL

ORGANISM(S): Homo sapiens

PROVIDER: GSE242858 | GEO | 2023/12/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA sequence of acute lymphoblastic leukemia cells with NRIP1::PDGFRB fusion

Project description:RNA sequence of acute lymphoblastic leukemia cells with NRIP1::PDGFRB fusion

| PRJNA1015177 | ENA

Affymetrix SNP6.0 array data for EBF1-PDGFRB rearranged acute lymphoblastic leukemia

2016-04-05 | GSE77557 | GEO

Affymetrix SNP6.0 array data for EBF1-PDGFRB rearranged acute lymphoblastic leukemia

Project description:The EBF1-PDGFRB gene fusion accounts for <1% B-cell precursor acute lymphoblastic leukaemia and occurs within the Philadelphia-like ALL subtype. We performed Affymetrix SNP 6.0 array was undertaken patients who tested positive for EBF1-PDGFRB rearrangement by FISH and/or RT-PCR. We performed Affymetrix SNP 6.0 array on genomic DNA extracted from bone marrow samples taken at diagnosis in 9 patients, at relapse in one patient and at remission in one patient.

2016-04-05 | E-GEOD-77557 | biostudies-arrayexpress

PdgfrB signaling impairs skeletal muscle regeneration

Project description:Genetically deleting PdgfrB in mature myocytes enhances skeletal muscle regeneration and fusion capability whereas activating PdgfrB inhibits it.

2024-10-15 | GSE279532 | GEO

ERG and c-MYC Co-regulate a Critical Gene Network in BCR-ABL1 B-cell Acute Lymphoblastic Leukemia

Project description:Philadelphia chromosome-positive B-cell acute lymphoblastic leukaemia (Ph+B-ALL), characterised by the BCR-ABL1 fusion gene, remains a poor prognosis cancer that needs new therapeutic approaches. Transcriptomic profiling and pathway analysis identified up-regulation of the oncogenic transcription factors ERG and c-MYC, with enrichment of genes involved in metabolic processes including ribosome biogenesis.

2024-01-25 | GSE213791 | GEO

Genome-wide maps of chromatin state in Ba/F3 cell with PAX5-KIDINS220 fusion protein

Project description:PAX5-KIDINS220 (PAX5-K220) is a novel chimeric fusion gene identified in a pediatric Philadelphia chromosome (Ph)-like acute lymphoblastic leukemia (ALL) patient, but the function of the encoded fusion protein has not yet been analyzed. Here, using in vitro murine assays and ChIP-sequencing, we demonstrate that PAX5-K220 is a nuclear protein that inhibits PAX5 transcriptional activity in a dominant-negative fashion, resulting in a B-cell differentiation block. Gene expression analysis and ChIP-sequencing revealed that PAX5-K220 is associated with multiple pathways related to chemotaxis and migration.

2019-03-30 | GSE129021 | GEO

SFPQ-ABL1 and BCR-ABL1 utilise different signalling networks to drive B-cell acute lymphoblastic leukaemia

Project description:Philadelphia-like (Ph-like) acute lymphoblastic leukaemia (ALL) is a high-risk subtype of B-cell ALL characterised by a gene expression profile resembling Philadelphia Chromosome positive ALL (Ph+ ALL) in the absence of BCR-ABL1. Tyrosine kinase activating fusions, some involving ABL1, are recurrent drivers of Ph-like ALL and are targetable with tyrosine kinase inhibitors (TKIs). We identified a rare instance of SFPQ-ABL1 in a child with Ph-like ALL. SFPQ-ABL1 expressed in cytokine-dependent cell lines was sufficient to transform cells which were sensitive to ABL1-targeting TKIs. In contrast to BCR-ABL1, SFPQ-ABL1 localised to the nuclear compartment and was a weaker driver of cellular proliferation. Phosphoproteomics analysis showed upregulation of cell cycle, DNA replication and spliceosome pathways, and downregulation of signal transduction pathways, including ErbB, NF-kappa B, VEGF, and MAPK signalling in SFPQ-ABL1-, compared to BCR-ABL1-expressing cells. SFPQ-ABL1 expression did not activate PI3K/AKT signalling and was associated with phosphorylation of G2/M cell cycle proteins. SFPQ-ABL1 was sensitive to navitoclax and S-63845 and promotes cell survival through upregulation of Mcl-1 and Bcl-xL. SFPQ-ABL1 has functionally distinct mechanisms by which it drives ALL, including subcellular localisation, proliferative capacity, and activation of cellular pathways, highlighting the role that fusion partners have in mediating the function of ABL1 fusions.

2022-05-20 | PXD028925 | Pride

PdgfrB signaling alters the beige adipogenic niche

Project description:Ageing beige adipose progenitor cells overexpress platelet derived growth factor receptor beta (PdgfrB) to prevent beige adipogenesis. Genetically deleting PdgfrB in restores beige adipocyte generation whereas activating PdgfrB in juvenile mice blocks beige fat formation.

2023-03-06 | GSE226695 | 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.

2010-09-10 | GSE23743 | GEO

Philadelphia chromosome (Ph)-positive acute lymphoblastic leukemia (ALL)

Project description:Philadelphia chromosome (Ph)-positive acute lymphoblastic leukemia (ALL)

| PRJNA786930 | ENA