Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

BCR::ABL1-induced enhancer reprogramming uncovers hypersensitivity of Ph+B-ALL cells to enhancer-targeting drugs [PCHiC]

ABSTRACT: To better understand how BCR::ABL1 establishes the Ph+B-ALL-defining transcriptional program, we adopted an integrative multi-omics approach to study the transcriptome, enhancer activities, and 3-dimensional interactions of enhancers with target genes in Ph+B-ALL cells. We performed an in-depth analysis of cells from human Ph+B-ALL patients and a murine Ph+B-ALL model using ChIP-Seq, RNA-Seq, and Hi-C-based methods to link enhancers to the promoters they regulate.

ORGANISM(S): Homo sapiens

PROVIDER: GSE279643 | GEO | 2026/02/27

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

BCR::ABL1-induced enhancer reprogramming uncovers hypersensitivity of Ph+B-ALL cells to enhancer-targeting drugs

2026-02-27 | GSE279589 | GEO

BCR::ABL1-induced enhancer reprogramming uncovers hypersensitivity of Ph+B-ALL cells to enhancer-targeting drugs [ChIP-Seq]

Project description:To better understand how BCR::ABL1 establishes the Ph+B-ALL-defining transcriptional program, we adopted an integrative multi-omics approach to study the transcriptome, enhancer activities, and 3-dimensional interactions of enhancers with target genes in Ph+B-ALL cells. We performed an in-depth analysis of cells from human Ph+B-ALL patients and a murine Ph+B-ALL model using ChIP-Seq, RNA-Seq, and Hi-C-based methods to link enhancers to the promoters they regulate. We further interfered with enhancer function to explore their role in Ph+B-ALL and investigated BCR::ABL1-regulated TFs that are recruited to them using targeted proteasomal degradation and RNA interference (RNAi).

2026-02-27 | GSE279644 | GEO

BCR::ABL1-induced enhancer reprogramming uncovers hypersensitivity of Ph+B-ALL cells to enhancer-targeting drugs [RNA-Seq]

2026-02-27 | GSE279594 | GEO

BCR::ABL1-induced enhancer reprogramming uncovers hypersensitivity of Ph+B-ALL cells to enhancer-targeting drugs [PCHiC]

Project description:BCR::ABL1-induced enhancer reprogramming uncovers hypersensitivity of Ph+B-ALL cells to enhancer-targeting drugs [PCHiC]

| PRJNA1173754 | ENA

BCR::ABL1-induced enhancer reprogramming uncovers hypersensitivity of Ph+B-ALL cells to enhancer-targeting drugs

Project description:BCR::ABL1-induced enhancer reprogramming uncovers hypersensitivity of Ph+B-ALL cells to enhancer-targeting drugs

| PRJNA1173556 | ENA

BCR::ABL1-induced enhancer reprogramming uncovers hypersensitivity of Ph+B-ALL cells to enhancer-targeting drugs [RNA-Seq]

Project description:BCR::ABL1-induced enhancer reprogramming uncovers hypersensitivity of Ph+B-ALL cells to enhancer-targeting drugs [RNA-Seq]

| PRJNA1173554 | ENA

BCR::ABL1-induced enhancer reprogramming uncovers hypersensitivity of Ph+B-ALL cells to enhancer-targeting drugs [ChIP-Seq]

Project description:BCR::ABL1-induced enhancer reprogramming uncovers hypersensitivity of Ph+B-ALL cells to enhancer-targeting drugs [ChIP-Seq]

| PRJNA1173753 | ENA

Genome wide mapping of IKAROS binding (ChIP-Seq) in human patient-derived BCR-ABL1+ (Ph+) pre-B ALL xenograft cells

Project description:IKAROS is an important tumor suppressor in human pre-B ALL and is mutated or deleted in a high percentage of human BCR-ABL1+ (Ph+) pre-B ALL. We here report the genome-wide binding of IKAROS in two independent patient-derived BCR-ABL1+ (Ph+) pre-B ALL xenograft cells that express wild type full-length IKAROS.

2017-02-06 | GSE58825 | 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

SHP2 Is Required for BCR-ABL1-Induced Hematologic Neoplasms

Project description:BCR-ABL1-targeting tyrosine kinase inhibitors (TKIs) have revolutionized treatment of Philadelphia chromosome-positive (Ph+) hematologic neoplasms. Nevertheless, acquired TKI resistance remains a major problem in chronic myeloid leukemia (CML), and TKIs are less effective against Ph+ B-cell acute lymphoblastic leukemia (B-ALL). GAB2, a scaffolding adaptor that binds and activates SHP2, is essential for leukemogenesis by BCR-ABL1, and a GAB2 mutant lacking SHP2 binding cannot mediate leukemogenesis. Using a genetic loss-of-function approach and bone marrow transplantation (BMT) models for CML and BCR-ABL1+ B-ALL, we show that SHP2 is required for BCR-ABL1-evoked myeloid and lymphoid neoplasia. Ptpn11 deletion impairs initiation and maintenance of CML-like myeloproliferative neoplasm, and compromises induction of BCR-ABL1+ B-ALL. SHP2, and specifically, its SH2 domains, PTP activity and C-terminal tyrosines, is essential for BCR-ABL1+, but not WT, pre-B cell proliferation. The MEK/ERK pathway is regulated by SHP2 in WT and BCR-ABL1+ pre-B cells, but is only required for the proliferation of BCR-ABL1+ cells. SHP2 is required for SRC family kinase (SFK) activation only in BCR-ABL1+ pre-B cells. RNAseq reveals distinct SHP2-dependent transcriptional programs in BCR-ABL1+ and WT pre-B cells. Our results suggest that SHP2, via SFKs and ERK, represses MXD3/4 to facilitate a MYC-dependent proliferation program in BCR-ABL1-transformed pre-B cells.

2017-06-06 | GSE99656 | 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