The NG2-ITGA4 axis promotes leukemic aggressiveness in KMT2A-r B-ALL and can be targeted with natalizumab.
Chronic Myeloid Leukemia Treatments
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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.
CALR-mutated myeloproliferative neoplasms originate mainly from expansion of Vwf-positive, platelet-biased hematopoietic stem cells, with CALRdel52 mutations showing greater amplification.
Venetoclax combined with pediatric-inspired chemotherapy achieves a 91% remission rate and improves survival in adolescents and adults with newly diagnosed Ph-negative ALL.
- Open access
- 1 cites
Bitopic kinase inhibitors designed with optimized parameters can surpass existing drugs like ponatinib in potency and safety, especially against resistant ABL1 mutants.
- Open access
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
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
Chromosome 5q deletion combined with TP53 mutations drives stepwise aneuploidy evolution in myeloid neoplasms with complex karyotypes.
- Open access
- 1 cites
Aberrant splicing of MBD1 produces the MBD1-L isoform, driving myelodysplastic syndromes (MDS) by reshaping the epigenome and causing hematopoietic defects in humans.
- Open access
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