AJ1-11095, a type II JAK2 inhibitor, produced impressive clinical responses in a phase I study for myelofibrosis, indicating potential advantages over existing inhibitors.
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AJ1-11095, a type II JAK2 inhibitor, produced impressive clinical responses in a phase I study for myelofibrosis, indicating potential advantages over existing inhibitors.
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Navitoclax plus ruxolitinib significantly increases the proportion of patients with ≥35% spleen volume reduction at week 24 in untreated myelofibrosis, reaching 63.2% versus 31.5%.
CALR-mutated myeloproliferative neoplasms originate mainly from expansion of Vwf-positive, platelet-biased hematopoietic stem cells, with CALRdel52 mutations showing greater amplification.
Fibrocytes are the main collagen-producing cells in JAK2V617F-mutated myelofibrosis, accounting for nearly two-thirds of collagen production in the bone marrow.
Genomic evolution in myeloproliferative neoplasms reveals distinct pathways to disease progression and therapy-related mutagenesis.
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.
Aberrant splicing of MBD1 produces the MBD1-L isoform, driving myelodysplastic syndromes (MDS) by reshaping the epigenome and causing hematopoietic defects in humans.
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