Clinical Pearls for Community Oncologists Treating Myelofibrosis

EP: 1.Diagnosis and Risk Stratification of Myelofibrosis

EP: 2.Differences Between Types of Myelofibrosis

EP: 3.The JAK/STAT Pathway and Myelofibrosis

EP: 4.Clinical Scenario: Patient with Primary Myelofibrosis

EP: 5.Approved Treatments for Myelofibrosis

EP: 6.Therapy Strategies for Primary Myelofibrosis

EP: 7.Treatments for Myelofibrosis Based on Platelet Counts

EP: 8.Clinical Scenario: Myelofibrosis Treatment in the Second-Line Setting

EP: 9.Approaches to Switching Treatments for Myelofibrosis

EP: 10.Considering Toxicities when Choosing Appropriate Treatment for Myelofibrosis

EP: 11.Assessing Response to Treatment in Myelofibrosis

EP: 12.Sequencing Treatments for Myelofibrosis

EP: 13.Unmet Needs in Myelofibrosis Treatment

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EP: 14.Clinical Pearls for Community Oncologists Treating Myelofibrosis

John Mascarenhas, MD: To end today’s session, we’ll go around, and I’ll ask each of you for a clinical pearl that you could share with the community and oncologists regarding treating myelofibrosis. Aaron, I’ll start with you. What’s 1 clinical pearl from today that you could share?

Aaron Gerds, MD: Partnering with someone makes a lot of sense. There are a handful of us across the country who are interested in this disease, have gathered experience treating this disease, and are up to date on all the nuances going on. Partnering with someone like that can be incredibly helpful in determining which JAK inhibitor to start or which trial to consider. That could be a key to helping patients do better over time.

John Mascarenhas, MD: Excellent. Srdan, a clinical pearl?

Srdan Verstovsek, MD, PhD: I’d hope that we can move from controlling only the symptoms and the spleen to survival benefit as the ultimate goal. Even with our current JAK inhibitors, through optimizing the dose or the way we treat patients, whether this is ruxolitinib, fedratinib, pacritinib, or even momelotinib in the future, if these clinical benefits are provided in an optimal way, it may make people live longer. As John pointed out, there’s already 1 study that looks for a survival benefit. I’d try to emphasize that the clinical spectrum of studies and the number of studies have changed, but we’re ready to move the bar through combinations and novel approaches and focus on what’s most important: good quality of life for much longer. That’s survival benefit.

John Mascarenhas, MD: Raajit, [do you have] a clinical pearl?

Raajit Rampal, MD, PhD: I have 2 points. Building on what Srdan said, we’ve moved the needle, but now we have to do better. I agree with Srdan: survival has to be what we ultimately try to do to help these patients. That’s the biggest thing. We have a lot of new studies, and building on Aaron’s message, I’d strongly advise partnership with referral centers that have trials. Almost all patients with MPNs [myeloproliferative neoplasms] should be considered for clinical trials. Of course, not everyone is eligible or willing. That’s the first thing.

The second thing is that, to me, the mantra with current therapy is always “the right tools for the right job.” Not every patient who has myelofibrosis needs a JAK inhibitor. No. 2, the type of JAK inhibitor you use depends. We’ve had a robust discussion about that today. No. 3, we have to think about other agents that we have: for example, ESAs [erythropoiesis-stimulating agents] for treating anemia. Use the right tools for the right job. You have to think about what the patient needs.

John Mascarenhas, MD: I agree with all of you. I’ll add my last clinical pearl. Myelofibrosis is very heterogeneous and variable in its presentation and clinical course. To Aaron’s point, that’s why there’s an advantage to consulting with someone who focuses on this, like the 4 of us. Because it’s very heterogeneous, we’re looking at different ways of categorizing patients with myelofibrosis. We discussed the spectrum of the cytopenic to the proliferative patient and how that might impact treatment decision-making.

Lastly, as you guys have said very eloquently, in the near future, we’re probably going to be combining these drugs with the available JAK inhibitors and other alternative agents that hit other relevant pathways to hopefully improve upon the responses in this very heterogeneous group. It probably isn’t going to be 1 drug fits all. It’s going to be using a lot of drugs and creative ways with data to support it that will hopefully improve the outcomes of our patients.

With that, I want to thank Dr Gerds, Dr Rampal, and Dr Verstovsek for joining us in this lively discussion on MF. This is brought to you by CancerNetwork®. I want to thank our viewing audience for tuning in. We hope you found this interactive discussion to be informative and beneficial to your clinical practice. Thanks very much.

Trancript edited for clarity.