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.
Chronic Myeloid Leukemia Treatments
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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
Combining genetics and MRD assessment identifies adult Ph- ALL patients who benefit from allo-HSCT, with a 3-year OS of up to 81% in low-risk groups.
- 1 cites
IGH::FENDRR and KRAS mutations define a novel B-ALL subtype with 85% poor chemotherapy response.
- Open access
ELN-DAVID issues key laboratory and clinical guidelines for FLT3-ITD MRD testing in AML patients in remission, supporting its role in current care standards.
Menin inhibition reduces megakaryocyte proliferation and fibrosis, showing promise as a therapy for myeloproliferative neoplasms with potent anti-tumor activity.
- Open access
The miR-15b/16-2 cluster acts as a tumor suppressor in T-cell acute lymphoblastic leukemia, impairing leukemic growth and progression by downregulating key oncogenes.
- Open access
Ziftomenib, a potent menin-KMT2A inhibitor, induces leukemia regression and reduces tumor burden in models of KMT2A-rearranged leukemia, with strong gene downregulation.
- 6 cites
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