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GenomicsSuper-enhancers-driven SOX4/SMAD3 enhances AXL signaling via membrane phospholipid remodeling to accelerate leukemia progression [ChIP-seq]
Cancer often involves aberrant epigenetic activation. In CML-BP, super - enhancer - driven SOX4 and SMAD3 form an auto - regulatory axis. They co - regulate epigenome, activate AXL - related pathways, and mediate membrane phospholipid remodeling. Bemcentinib, an AXL inhibitor, can inhibit CML - BP p...
ORGANISM(S): Homo sapiens 
2026-05-15 | GSE292716 | GEO
GenomicsSuper-enhancers-driven SOX4/SMAD3 enhances AXL signaling via membrane phospholipid remodeling to accelerate leukemia progression [CUT&Tag]
Cancer often involves aberrant epigenetic activation. In CML-BP, super - enhancer - driven SOX4 and SMAD3 form an auto - regulatory axis. They co - regulate epigenome, activate AXL - related pathways, and mediate membrane phospholipid remodeling. Bemcentinib, an AXL inhibitor, can inhibit CML - BP p...
ORGANISM(S): Homo sapiens 
2026-05-15 | GSE292718 | GEO
TranscriptomicsSuper-enhancers-driven SOX4/SMAD3 enhances AXL signaling via membrane phospholipid remodeling to accelerate leukemia progression [RNA-Seq]
Cancer often involves aberrant epigenetic activation. In CML-BP, super - enhancer - driven SOX4 and SMAD3 form an auto - regulatory axis. They co - regulate epigenome, activate AXL - related pathways, and mediate membrane phospholipid remodeling. Bemcentinib, an AXL inhibitor, can inhibit CML - BP p...
ORGANISM(S): Homo sapiens 
2026-05-15 | GSE292717 | GEO
TranscriptomicsThe distinct expression features between chronic phase and B-lymphoblastic crisis samples from patients with CML
Chronic myeloid leukemia (CML) is a biphasic clonal hematopoietic stem cell disorder driven by the Philadelphia chromosome (Ph)-encoded BCR::ABL1 oncogene. The blast phase (BP) in CML progressed from indolent chronic phase (CP), usually has a dismal outcome. Single-cell RNA sequencing (scRNA-seq) ha...
ORGANISM(S): Homo sapiens 
2026-06-30 | GSE337046 | GEO
TranscriptomicsSingle-cell mapping portrays the distinct expression features between chronic phase and B-lymphoblastic crisis samples from patients with CML
Background: Chronic myeloid leukemia (CML) is a biphasic clonal hematopoietic stem cell disorder driven by the Philadelphia chromosome (Ph)-encoded BCR::ABL1 oncogene. The blast phase (BP) in CML progressed from indolent chronic phase (CP), usually has a dismal outcome. Single-cell RNA sequencing (s...
ORGANISM(S): Homo sapiens 
2026-06-02 | GSE333588 | GEO
Transcriptomicsgamma-catenin (junction plakoglobin, Jup) dependent signals mediate the progression of BCR-ABL1+ B-ALL
The BCR-ABL1 translocation product is the cause of Chronic Myeloid Leukemia (CML) and of a significant fraction of adult-onset B-Acute Lymphoblastic Leukemia (B-ALL) cases. Here we identify an essential role for gamma-catenin (junction plakoglobin) in B lineage restricted cells for the progression o...
ORGANISM(S): Mus musculus 
2014-02-08 | E-GEOD-54793 | biostudies-arrayexpress
UnknownTargeting FLT3-TAZ signaling to suppress drug resistance in blast phase chronic myeloid leukemia.
Not available
S-EPMC10626670 | biostudies-literature
UnknownHeterogeneous leukemia stem cells in myeloid blast phase chronic myeloid leukemia.
Not available
S-EPMC5737170 | biostudies-literature
UnknownPrognostic factors and survival outcomes in patients with chronic myeloid leukemia in blast phase in the tyrosine kinase inhibitor era: Cohort study of 477 patients.
Not available
S-EPMC5673547 | biostudies-literature
UnknownTreatment of blast phase chronic myeloid leukaemia: A rare and challenging entity.
Not available
S-EPMC9796596 | biostudies-literature
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