A new $11.7 million Washington University MPN grant will help researchers investigate a question that matters to patients: can targeting inflammation help keep an MPN from getting worse?
The award, announced September 29, 2026, comes from the National Heart, Lung, and Blood Institute, part of the National Institutes of Health. Stephen T. Oh, MD, PhD, leads the work at WashU Medicine, where investigators also care for patients at Siteman Cancer Center.
For people living with polycythemia vera (PV), essential thrombocythemia (ET), or myelofibrosis (MF), the important point is the research direction. Scientists want to understand the processes behind disease progression and identify better ways to interrupt them. The grant announcement does not establish a new treatment or a change to anyone’s care plan.
Why researchers are looking at inflammation
Inflammation is part of the body’s normal response to injury or illness. In MPNs, persistent inflammatory signals can also influence cancer cells and the surrounding bone marrow, where blood cells are made.
Understanding those signals may help explain why disease behaves differently from one person to another. Researchers are looking beyond the abnormal cells themselves to study their interactions with neighboring cells.
That distinction matters. A treatment can help someone feel better without answering every question about what happens to the disease over time. This research asks whether particular inflammatory pathways could become targets for approaches designed to alter their course.
What the Washington University MPN grant will study
The award supports four related research projects and shared resources that help the teams work together.
Blocking harmful signals
Oh’s team will examine DUSP6 and RSK1, molecules involved in cellular signaling. Using mouse models and human samples, researchers will test whether disrupting their downstream effects can reduce inflammation and limit progression.
Understanding competing stem cells
Grant A. Challen, PhD, will study how inflammation from MPN cells affects other groups of stem cells in the marrow. These groups, called clones, descend from individual cells. The question is whether inflammatory conditions give certain mutated clones an advantage, potentially contributing to leukemia.
Mapping the bone marrow
Daniel C. Link, MD, will use spatial imaging to examine where different cells sit and how they interact. These maps could reveal features of the marrow environment that encourage progression or help restrain it.
Investigating blood clot risk
Jorge A. Di Paola, MD, will focus on TNF-alpha, an inflammatory molecule linked to clotting. His project examines interference with this pathway. Blood clots are an important concern for MPN patients, making this work relevant beyond leukemia research.
Three shared cores support the projects: administration, led by Oh; biospecimens and pathology, led by Mark Watson, MD, PhD; and bioinformatics and biostatistics, led by Obi L. Griffith, PhD.
How this connects to PMD-026 research
There is already a related clinical effort, but its funding is separate from the new grant.
A 2025 laboratory study identified RSK1 as a potential treatment target in MPNs and secondary acute myeloid leukemia. Experiments with PMD-026, which inhibits several RSK proteins, supported further investigation. Laboratory results provide a reason to test a drug; they do not establish that it works for patients.
Amy W. Zhou, MD, now leads a phase I PMD-026 trial at Siteman for selected patients with myelofibrosis. Its goals include assessing safety, tolerability, dosing, and preliminary activity. It includes eligibility requirements involving prior JAK inhibitor treatment and disease risk. Having PV or ET alone does not make someone eligible.
Excerpt from WashU Medicine’s September 29, 2026 announcement. This broad description needs context: AML progression risk varies by MPN subtype, age, and individual disease features. The encouraging part is the focus on questions patients live with: why disease changes, whether complications can be reduced, and how treatment might eventually do more. Still, there is no established timetable for new therapies from this grant. It does not show that blocking TNF-alpha prevents clots in patients or that PMD-026 prevents transformation to leukemia. Those possibilities require appropriate clinical evidence. At your next visit, you could ask your MPN specialist what your current treatment is intended to accomplish and whether a clinical trial fits your situation. Any medication changes should be discussed with your healthcare team. The Washington University MPN grant gives researchers resources to pursue important answers. For patients, it is a meaningful research investment worth following as findings emerge, with the distinction between promising ideas and proven benefits kept clear. David Wallace is a nationally recognized myeloproliferative neoplasm (MPN) patient advocate, writer, and the founder and publisher of PV Reporter. He also founded MPN Cancer Connection, a 501(c)(3) nonprofit organization, and serves as its executive director. Diagnosed with polycythemia vera in 2009 and now in complete molecular remission, David has spent more than a decade helping patients understand MPN research, treatment options, and the questions to ask their healthcare teams. His work brings the patient voice into discussions with clinicians, researchers, and industry leaders. This article is for educational purposes only and is not medical advice. It does not replace consultation with a qualified hematologist or MPN specialist. Discuss all diagnosis and treatment decisions with your healthcare team.
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