Clinical Pearls for Treating MPN and MF

EP: 1.An Introduction to Myeloproliferative Neoplasms

EP: 2.Understanding Essential Thrombocythemia And Treatment Options

EP: 3.What to Know About Polycythemia Vera and Treatment Options

EP: 4.Monitoring Patients With ET and PV

EP: 5.MPN Outcomes

EP: 6.A Myelofibrosis Diagnosis

EP: 7.MF Prognosis and Common Risks

EP: 8.More About MF Prognosis, Biomarkers, and Treatment

EP: 9.Determining Treatment for MF And Upfront Therapy Options

EP: 10.More Upfront Therapy Options for MF

EP: 11.Selecting a Therapy for Patients With MF

EP: 12.Sequencing MF Therapies and Novel Combinations

EP: 13.Monitoring Patients Being Treated for MF

EP: 14.The Clinical Course for MF and Changing Therapies

EP: 15.Unmet Needs and Potential Advances in MPN and MF

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EP: 16.Clinical Pearls for Treating MPN and MF

Ruben Mesa, MD: This has been a phenomenal discussion. Why don’t we leave on just any key things? People are out there; they’re treating patients with myelofibrosis [MF]. You guys are really some of the foremost experts in the United States in terms of how we care for these patients. Give one clear clinical pearl that you would share with folks. Jamile, why don’t you start us off? What is some helpful pearl that you would share with colleagues or trainees in treating patients with myelofibrosis?

Jamile Shammo, MD, FACP, FASCP: That the disease has to be characterized fully at baseline.

Ruben Mesa, MD: Indeed, you really want to know that baseline, have that information, because the disease can change on you. Angela?

Angela Fleischman, MD, PhD: I would probably say that each patient is unique, and there shouldn’t be a one-size-fits-all treatment for patients. Just as each patient is unique, then their appropriate therapy should also uniquely fit their needs.

Ruben Mesa, MD: Fantastic. Individualized therapy, again begins with a molecular clone, but much more than that. I’m mindful as people say, individualized therapy just means understanding the clone, I always pushed back against that. I’d say you could put the same clone in 2 different people and it’s going to behave differently, let alone their own health, their values, their level of fitness. So individualized treatment starts I think with some of the information we have, but doesn’t end there. Stephen?

Stephen Oh, MD, PhD: My pearl is kind of 2-sided. On the one hand with use of ruxolitinib, what I’ve often seen is that patients are taken off of ruxolitinib because of anemia or worsening anemia, and that is not necessarily completely inappropriate. However, I often find that patients overall feel better, even if their anemia gets worse on ruxolitinib. That is something that needs to be considered, when starting ruxolitinib, discuss with the patient in terms of expectations, that yes, your numbers may drop. But if you feel better, maybe that’s still overall a net benefit. I always emphasize that when I’m discussing that issue with patients who are potentially starting ruxolitinib.

The other sort of flip side with regard to anemia, I think with all of these prognostication schemes we talked about, anemia is a big factor. I think that has been understood off for many years, but it’s even more being appreciated. For instance, just tying it back to some of the data that have come out of the momelotinib studies showing that achievement of transfusion independence seems to be associated with prolonged survival. I think that while on the one hand we can use supportive care, transfusions for anemia, and we also have had limited options for treating anemia historically, there are agents that hopefully will be coming to the fore in the near future, momelotinib, pelabresib, with some hint of anemia benefits, that we may be able to impact that in a positive way.

Ruben Mesa, MD: Very helpful, and I leave the pearl that I think our therapies are helping prolong survival in myelofibrosis. I saw my first patient with MF in 1991, and in the pre-JAK inhibitor era, I know what that experience was like. In the post-JAK inhibitor era, people are living longer. There is no question in my mind, and I think that’s due to a range of things. I think it’s the impact of therapy, less debilitation, fewer complications from the disease, probably a lower rate of progression overall as a population, although there can be exceptions. I do think this next wave where we really impact cytopenic MF will help extend that even further. I think there are many issues related to the difficulties for cytopenic MF that somewhat compound some of the difficulties we’ve had with other things before, and I’m really looking forward to seeing that impact.

This transcript has been edited for clarity.