All-oral decitabine-cedazuridine and venetoclax regimens show promise for AML treatment, with potential improvements in patient convenience and care.
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Acute Myeloid Leukemia Research
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FGF18 from stromal fibroblasts promotes AML progression by activating FGFR3 signaling and suppressing immune responses, with elevated levels linked to poor prognosis.
- Open access
Menin-MLL inhibitors increase JUND activity in MLL-rearranged leukemic cells, contributing to tumor growth and therapy resistance.
- Open access
Ziftomenib combined with venetoclax and azacitidine achieves a 46% composite complete remission rate in relapsed/refractory NPM1-mutated AML patients at the 600 mg dose.
Fibro-inflammatory remodeling in bone marrow is a defining feature of clonal hematopoiesis of indeterminate potential, with a significant expansion of fibroblasts and extracellular matrix changes.
- Open access
- 1 cites
Greatwall kinase controls cytokinesis and cell cycle in AML cells via a novel pathway independent of ENSA-PP2A-B55, revealing a unique regulatory mechanism.
- Open access
The transactivation domain (TAD) is essential for nuclear import of phosphorylated STAT5, with two key residues D754 and D758 critical for this process.
- Open access
Degrading NSD2 with a targeted ligand degrader reverses oncogenic chromatin changes and improves survival in t(4;14) multiple myeloma models.
RAS-pathway activation, through diverse genetic and nongenetic mechanisms, drives resistance to FLT3 and BCL2 inhibitors in AML, with resistance linked to monocytic differentiation.
- Open access
PKMYT1 inhibition induces DNA damage and cell death specifically in del(17p) multiple myeloma cells, offering a targeted therapeutic approach.
IDH3A-driven citrate accumulation controls metabolic fitness and venetoclax resistance in AML stem cells, with knockdown impairing leukemia maintenance.
Inhibiting TET2 reprograms myeloid cells to enhance radiotherapy and suppress metastasis, improving outcomes in lung cancer models.
Epigenetic plasticity driven by genomic and cytogenetic changes enables therapy resistance and disease progression in multiple myeloma, with nearly 900 patient samples revealing key transitions.
- Open access
Inhibiting WNK1, an atypical kinase overexpressed in T-ALL, induces cell cycle arrest and disrupts mitosis, offering a promising therapeutic target with significant effects.
- Open access
Translational regulation of Sf1 via a conserved 5' UTR modulates hematopoietic stem cell fate by controlling spliceosome activity and gene splicing.
- Open access
Genomic and epigenomic profiling reveal over 40 molecular subtypes of acute lymphoblastic leukemia, enhancing classification and informing treatment strategies.
Genomic evolution in myeloproliferative neoplasms reveals distinct pathways to disease progression and therapy-related mutagenesis.
- Open access
Polyclonal competition drives clonal hematopoiesis, with about 3 fit clones entering the HSC pool annually and rarely exceeding 5% frequency, mainly emerging later in life.
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