All-oral decitabine-cedazuridine and venetoclax regimen shows promise for AML patients, with potential improvements in treatment options.
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All-oral decitabine-cedazuridine and venetoclax regimen shows promise for AML patients, with potential improvements in treatment options.
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LIN28B interacts with β-catenin and regulates Wnt signaling through post-transcriptional modulation in myeloid leukemia cells.
The NG2-ITGA4 axis promotes leukemic aggressiveness in KMT2A-r B-ALL and can be targeted with natalizumab.
Myeloid-specific Tet2 deletion generates myeloid-derived activating cells that enhance radiotherapy and suppress metastasis in lung cancer models.
High NPM1 variant allele frequency (VAF) above 31.44% predicts better survival in NPM1-mutated AML patients.
Menin-MLL inhibitors increase JUND activity in MLL-rearranged leukemic cells, contributing to tumor growth and therapy resistance.
Fibroblast-derived FGF18 promotes AML progression and immune suppression by activating FGFR3 signaling and forming a feed-forward loop in the bone marrow niche.
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.
Greatwall kinase regulates cytokinesis in AML cells through a novel pathway involving MARK3, independent of the ENSA-PP2A-B55 mechanism.
Fibro-inflammatory remodeling is a hallmark of clonal hematopoiesis of indeterminate potential, with fibroblasts expanding and acquiring cancer-associated transcriptional states.
A 12-amino-acid stretch within the STAT5 transactivation domain is essential for its nuclear import, with residues D754 and D758 being critical for this process.
Degrading NSD2 with a targeted ligand degrader reverses oncogenic chromatin changes and improves survival in t(4;14) multiple myeloma models.
IDH3A-driven citrate accumulation controls metabolic fitness and venetoclax resistance in AML stem cells, with knockdown impairing leukemia maintenance.
PKMYT1 inhibition induces DNA damage and cell death specifically in del(17p) multiple myeloma cells, offering a targeted therapeutic approach.
RAS-pathway activation, through diverse genetic and nongenetic mechanisms, drives resistance to FLT3 and BCL2 inhibitors in AML, with resistance linked to monocytic differentiation.
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.
Translational regulation of Sf1 via a conserved 5' UTR modulates hematopoietic stem cell fate by controlling spliceosome activity and gene splicing.
Inhibiting WNK1, an atypical kinase overexpressed in T-ALL, induces cell cycle arrest and disrupts mitosis, offering a promising therapeutic target with significant effects.
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