In this activity, three myelofibrosis experts discuss how new advances and research should be applied in clinical practice using updated data presented at the ASH annual meeting. Determining the optimal course of action following JAK inhibitor treatment failure/intolerance/disease progression is extremely difficult because there is no standard course of action. Fortunately, research is identifying new agents that appear to be effective either alone or when combined with ruxolitinib in newly diagnosed and/or progressing patients.

JAK inhibitors are considered standard therapy for the treatment of symptomatic MF. While ruxolitinib has been the only available JAK inhibitor for this indication for nearly a decade, the more recent approval of fedratinib and pacritinib for front-line MF has broadened treatment options for these patients. 

In this activity, a panel of myelofibrosis experts provide an overview of key data presented at ASH. Led by Dr. Verstovsek, our faculty will offer insights on new agents, new mechanisms of action for the treatment of myelofibrosis associated anemia, and provide perspectives on the future role of “add-on” therapies.

Join Dr. Spivak as he discusses risk stratification and management strategies for polycythemia vera (PV). Topics include the pathophysiology and mutational foundation of PV, predicting risk and PV prognosis, current treatment strategies and controversies, and the role of targeted therapies in managing PV.

Join Dr. Mascarenhas as he discusses new and emerging treatment approaches for relapsed/refractory myelofibrosis (MF). Topics include a review of the COMFORT-1 and -2 and the JAKARTA2 trials of ruxolitinib and fedratinib, and recently released outcomes of trials evaluating investigational agents such as momelotinib, pacritinib, navitoclax, pelabresib, and imetelstat.

Join Dr. Mesa as he discusses new opportunities for JAK inhibitors in myelofibrosis (MF). Topics will include the ruxolitinib phase 3 COMFORT I and II trials, management of early-onset treatment-associated cytopenia, and outcomes associated with fedratinib in the JAKARTA and JAKARTA-2 trials

In this activity, Dr. Srdan Verstovsek will discuss management of myelofibrosis-associated anemia. He will provide guidance on thresholds for red blood cell transfusion, criteria for selecting anemia therapy, and current and emerging treatment options for managing anemia, including erythropoiesis-stimulating agents (ESAs), anabolic steroids, corticosteroids, immunomodulatory agents, Janus kinase (JAK) inhibitors, anti-hemojuvelin antibodies, ALK2 receptor inhibitors, and luspatercept.

Explore new data on MPN presented at the 2020 ASH Annual meeting. In this activity, experts will discuss long-term outcomes of the CONTINUATION-PV trial comparing ropegylated interferon versus hydroxyurea; phase 2 study results of idasanutlin as second-line therapy; the efficacy of PTG-300 for anemia; results from the SIMPLIFY-2 study of momelotinib; data on CPI-0610; outcomes of imetelstat in high-risk patients; navitoclax in relapsed/refractory myelofibrosis; and the potential utility of the LSD1 inhibitor bomedemstat (IMG-7289).

This activity was previously presented as a live webinar with Q&A on March 08, 2021. Please note: If you participated in the live webinar, you are ineligible to receive an additional 1.0 contact hour of credit and may not re-submit for credit previously awarded.

Mutational testing is an integral part of the management of myeloproliferative neoplasms (MPNs), as results from this assessment can both guide treatment selection and provide prognostic information. In this article, Dr. Aaron Gerds discusses best practice regarding the utility of mutational testing in clinical practice when treating patients with MPNs.

Approaching management and diagnosis of a patient with polycythemia vera (PV) can be challenging. In this activity, Dr. Rampal explains the goals of therapy, prognostication of thrombosis, and therapies in first-line treatment. He also discusses the patient-related features to consider when developing a treatment plan.

Management of myeloproliferative neoplasms has evolved considerably since the identification of JAK2 and targeted therapy that has improved disease-related symptoms and quality of life. Our renowned faculty will provide updates in the latest data related to diagnosis, treatment options, guidelines, and standards of care through a highly interactive educational experience. Three real-life case scenarios will be presented, and the faculty will discuss treatment options and the journey of each patient.

This activity was previously presented as a webinar with live Q&A in September of 2020. Please note: If you participated in the live webinar, you are ineligible to receive an additional 1.25 contact hours of credit and may not re-submit for credit previously awarded.

The approval of ruxolitinib established JAK inhibitor therapy as the standard of care for intermediate- and high-risk myelofibrosis (MF), and the recent approval of fedratinib further supports the important role of JAK inhibitors in this setting. There is an urgent need for novel targeted therapies and new approaches. This article summarizes some of the most compelling data from key clinical trials investigating novel treatment approaches for MF and concludes with strategies to improve physician-patient communication.

It is well known that JAK/STAT signaling plays a central role in the pathogenesis of myelofibrosis (MF), and the demonstrated efficacy of the JAK inhibitor ruxolitinib in myelofibrosis has established it as standard of care in intermediate- and high-risk disease. Based on the success of ruxolitinib in this setting, other JAK inhibitors have been under investigation to further improve clinical outcomes in MF. The recent approval of fedratinib in both the frontline and second-line setting has expanded treatment options for MF, and pacritinib and momelotinib are also showing great promise in clinical trials. In this article, Dr. Elizabeth Hexner will review recent data supporting the role of JAK inhibitors for the treatment of MF.