SOHO 2024: Focus on MPN
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Pacritinib demonstrated superiority to best available therapy for spleen volume reduction, total symptom score, and more.
Patients with splenomegaly are more likely to be referred for HSCT.
Selinexor plus ruxolitinib was well tolerated, reduced symptom burden, and led to spleen volume reduction.
One year of pacritinib treatment stabilized or improved thrombocytopenia and anemia in patients with myelofibrosis.
The phase III PERSIST-2 study compared symptom results from pacritinib with those of best available therapy and ruxolitinib.
Patients' genomic profiles and baseline laboratory values have implications for their treatment outcomes with these agents.
The International Prognostic Scoring System, Dynamic International Prognostic Scoring System, and other models were applied.
A retrospective study found momelotinib plus pacritinib led to reduced need for red blood cell transfusion in patients.
A real-world retrospective study evaluated transfusion dependent or nondependent patients at ruxolitinib initiation.
Management of asymptomatic, clinically stable disease is not necessarily improved by implementing routine hemostasis tests.
Investigational agent DISC-0974 produced anemia response independent of patient transfusion dependency or JAK inhibitor use.
A study observed that addition of pelabresib to ruxolitinib led to bone marrow microenvironment improvement.
History of thrombotic events, hematocrit ≤0.45 L/L, and JAK2 p.V617F were identified as risk factors for progression.
LOXL2 upregulation is associated with key inflammatory signaling pathways in primary myelofibrosis.
Treatment with selinexor reduced hepcidin and pro-inflammatory cytokines in patients with myelofibrosis.
The rates of baseline comorbidities and constitutional symptoms were higher in patients with anemia versus those without.
New or worsening anemia following initiation of ruxolitinib does not appear to diminish clinical benefit.
Hemoglobin improvement at week 24 after transfusion is associated with improved HRQOL in myelofibrosis and anemia.
Prospective analysis suggest that 4.3% of patients with ET progressed to myelofibrosis over five years of follow up.
Patients with MF or ET with CALR or JAK2 mutations carried similar symptom burdens according to prospective data.
The phase III MANIFEST-2 trial compared pelabresib plus ruxolitinib with placebo plus ruxolitinib in JAKi-naive patients.
The findings were from a retrospective study of patient data from the US Flatiron Health electronic health record database.
A retrospective analysis covered two phase III trials of the JAK2 inhibitor in patients with and without monocytosis.
A study evaluated progression according to hemoglobin levels, platelet counts, constitutional symptoms, and other markers.
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