Myelofibrosis

Using Janus kinase inhibitors, having experienced a previous thrombosis episode, and higher age were associated with a heightened risk of a new thromboembolic event.

Allogeneic stem cell transplant (allo-SCT) conditioning with busulfan/fludarabine with thiotepa and posttransplant cyclophosphamide induced improved 2-year progression-free survival and overall survival in patients with myelofibrosis, especially older adults.

Treatment with ruxolitinib in patients with myelofibrosis and anemia was associated with more inpatient medical center and emergency department visits while increasing health care-related financial burdens compared with nonanemic patients.

Measures including disease-free survival and overall survival were improved in patients with MF who underwent hematopoietic stem cell transplantation (HSCT) and a 3D volumetric splenomegaly analysis.

At 1- and 2-year follow-up points, ruxolitinib led to considerable improvements in survival in patients with myelofibrosis who develop graft-versus-host disease (GVHD).

Even for patients with myelofibrosis who could otherwise proceed directly to hematopoietic cell transplantation, pre-transplant treatment with ruxolitinib led to improved survival benefits.

Using chromosome genomic array testing in combination with existing risk stratification models can better determine patients with myelofibrosis who can benefit from transplant.

Cytopenic myelofibrosis is characterized by poorer prognosis and more severe anemia and thrombocytopenia compared with proliferative myelofibrosis.

Circulating lactate is increased in patients with myelofibrosis and corresponds with the remodeling of lactate export channel monocarboxylate transporter 4, suggesting a link with fibrosis establishment.

More accurate prognostic risk assessment could aid pharmacists in the management and counseling of patients with primary myelofibrosis.

Myelofibrosis patients with CALR mutations have lower responses to symptoms and higher rates of anemia after 6 months of therapy with ruxolitinib.

Diagnosing anemia, a serious and common complication of patients with myelofibrosis, could be made easier with the use of red cell distribution width assessment.

Data indicates fedratinib’s role as an effective second-line treatment in patients with myelofibrosis who have been previously treated with a JAK inhibitor, such as ruxolitinib, though more research is necessary.

Patients with myelofibrosis have a higher likelihood of having a cardiovascular risk factor when compared with essential thrombocythemia or polycythemia vera.

Stem cell transplantation rates increased the longer patients remained on therapy for myelofibrosis.

Treatment options may include treating the anemia with blood transfusions, androgen therapy, thalidomide, and other medications.

Gecacitinib is a novel inhibitor targeting both JAK and ACVR1.

Measuring end points such as molecular response, cytokines, and histomorphometry may show a greater range of benefits.

Improvements were observed regardless of whether patients initiated ruxolitinib in the second or third line of treatment.

Navtemadlin has demonstrated meaningful efficacy and safety as a monotherapy or combination treatment in various preclinical and clinical trials.

Pelabresib is an investigational, oral, small molecule that inhibits bromodomain and extraterminal (BET) proteins.

The data support the use of supportive anemia care agents in combination with ruxolitinib (Jakafi; Incyte Corp).

Anemia is a very common adverse effect associated with the use of ruxolitinib.

Anemia is a common adverse effect of ruxolitinib, calling for new approaches to mitigate risks.

The addition of navitoclax was associated with durable response and potential disease modification.

Rusfertide may sustain hematocrit levels in patients with polycythemia vera.

According to the study, 20% of patients with myeloproliferative neoplasms progress to blast phase.

The nomogram model demonstrated good predictive capabilities to assess progression risk to overt primary myelofibrosis.

Approximately 15% of patients with polycythemia vera will progress to myelofibrosis.

The study was conducted on a small subgroup of Japanese patients with myelofibrosis.