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EHA 2026 | Insights into the evolving treatment landscape for MPNs: current state and future directions
Ruben Mesa, MD, Levine Cancer Institute, Atrium Health Wake Forest Baptist Comprehensive Cancer Center, Winston Salem, NC, shares insights into the current state and future directions of myeloproliferative neoplasms (MPNs) treatment. Dr Mesa highlights the benefits of single-agent JAK inhibitors and notes that upcoming developments include more active or specific inhibitors targeting driver mutations, such as calreticulin and JAK2 inhibitors, as well as new mechanisms of action and additional modifiers, such as hepcidin mimetics and inhibitors. This interview took place at the 31st Congress of the European Hematology Association (EHA) in Stockholm, Sweden.
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Transcript
I think we’re learning much about how do we kind of continue to move forward in the MPNs. You know, where we stand now is we have the single agent JAK inhibitors that have made a benefit. I think they have helped to alleviate suffering, improve symptoms, and I think they have had some impact on survival, but clearly with opportunity for greater impact. I think what comes next, and we’re very much seeing it at this year’s EHA meeting, is first, more active or specific inhibitors for the driver mutations...
I think we’re learning much about how do we kind of continue to move forward in the MPNs. You know, where we stand now is we have the single agent JAK inhibitors that have made a benefit. I think they have helped to alleviate suffering, improve symptoms, and I think they have had some impact on survival, but clearly with opportunity for greater impact. I think what comes next, and we’re very much seeing it at this year’s EHA meeting, is first, more active or specific inhibitors for the driver mutations. In particular, those inhibitors of calreticulin and kind of evolving Phase I data from those trials and what does that impact look like to the type two inhibitors of JAK2 from AJAX that cause a lot of buzz at the meeting regarding, you know, deep responses for spleen and symptoms, varying allele frequency in the hopes of really kind of deeper responses. I think we are seeing numerous additional new mechanisms of action that are going to be used alone or in combination with these agents. And then I think we’re seeing this other kind of class of additional modifiers, I would really frame them, the hepcidin mimetics for PV, the hepcidin kind of inhibitors for myelofibrosis that, again, I think will probably be used, you know, alone in certain circumstances or perhaps in combination with these other options. So for me, it leaves me quite excited. You know, as I’m at this meeting and I see the maturation of, well, the portfolio of drugs that are available for lymphoma, for Hodgkin’s disease, for multiple myeloma in particular. I think we will see kind of an evolving multi-drug approach to patients with MPNs, driven by driver mutations, modified by additional somatic mutations. Things such as improvement in symptoms are very, very relevant, but I think it’s a lens of a more holistic assessment of disease biology, progression-free survival, as well as maintaining those core aspects of efficacy that we’ve usually tracked.
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