Articles

The rate of thrombus formation in patients with myelofibrosis is not well-defined. The intersection of IPSS score and JAK mutation may reliably indicate risk of vascular events in these patients. Read More ›

Patients with advanced myelofibrosis and heavy mutation burden have limited safe and effective therapeutic options. Preliminary clinical trial evidence indicates bomedemstat provides clinical benefit to patients in this population. Read More ›

Evidence suggests fedratinib, a selective JAK2 inhibitor, demonstrates safety and efficacy in patients with myelofibrosis previously treated with ruxolitinib with appropriate mitigation strategies. Read More ›

Myelofibrosis is associated with poor overall survival and clinical outcomes. Treatment with ruxolitinib earlier in disease course shows promise for improving symptoms and overall survival. Read More ›

Criteria to assess presenting patterns of organ damage have not been extensively evaluated. Preliminary evidence suggests identifying these patterns could be useful in profiling organ dysfunction in avapritinib clinical trials. Read More ›

Gilteritinib plus azacitidine led to significantly higher composite complete remission rates but did not provide a survival advantage compared with azacitidine alone in patients with newly diagnosed FLT3^mut+ AML ineligible for intensive induction chemotherapy. Read More ›

MRD status at the time of allogeneic stem-cell transplantation and the number of remissions prior to transplant were shown to be important independent prognostic factors in patients with AML. Read More ›

Cladribine has long been established as an efficient therapy in systemic mastocytosis and remains a valuable treatment option even as new therapies emerge. Read More ›

In the first-in-human phase 1/2 AUGMENT 101 study, SNDX-5613 demonstrated an acceptable safety profile and promising antileukemic activity in patients with heavily pretreated relapsed/refractory MLL-rearranged and NPM1-mutated acute leukemias. Read More ›

Hereditary alpha-tryptasemia may promote development of systemic mastocytosis. Screening for variations in copy number of the alpha tryptase gene may provide early evidence for diagnosis of mastocytosis. Read More ›