Myelofibrosis and the bone marrow environment: how inflammation changes blood production
Official title: Myelofibrosis impacts the hematopoietic niche through TNF-a
Funded at Washington University · NIH-11385368 · Data updated 2026-11-12
A doctor-researcher is studying how inflammation in the bone marrow affects the blood-forming system in people with myeloproliferative neoplasms (MPNs) to find ways to prevent scarring and leukemia.
Quick facts
| Grant type | Career grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Washington University NIH-funded |
| Lab location | 1 site (Saint Louis, United States) |
| Project start | July 1, 2024 |
| Project end | June 30, 2029 |
| Funding year | 2026 |
| Award (this year) | $170,948 |
| NIH project number | 5K08HL166969-03 |
| Project ID | NIH-11385368 on NIH RePORTER |
Who could benefit from this research
✓Could help
Adults with myeloproliferative neoplasms or related bone marrow disorders who could contribute marrow samples or participate in future studies.
✕Less likely to help
Patients without MPNs or related bone marrow issues may not benefit from this specific research.
What this research studies
This project looks at how signals like TNF-alpha from blood cells influence the cells that form the bone marrow niche. By studying patient samples and mouse models, the team aims to map the pathways that cause fibrosis and disrupt normal blood cell development. The goal is to identify targets that could be blocked to restore healthy marrow function and prevent progression to leukemia. The work could lay the groundwork for new treatments that protect the bone marrow environment in people with MPNs.
Why it matters
Potential benefit: If successful, the research could lead to therapies that preserve healthy bone marrow function and reduce the risk of progression to acute leukemia in MPN patients.
How similar studies have gone: Previous work showed that blocking TGF-β signaling may reverse fibrosis in models, and this study seeks additional signals like TNF-α and PDGF that disrupt the niche.
Where this research is happening
-
Washington University
Saint Louis, United States Active
Researchers
- Principal investigator: Oetjen, Karolyn Ann — Washington University
- Study coordinator: Oetjen, Karolyn Ann
Related research
Other NIH-funded projects on the same topics.
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Strategies to deplete myelofibrosis stem cells using HDM2/p53 pathway
A patient-focused program tests a therapy that may selectively reduce disease-causing blood stem cells in people with myelofibrosis.
-
Megakaryocyte changes in myelofibrosis and its progression to leukemia
A scientist-guided project will study how abnormal megakaryocytes and signals like TGF-β and IL-13 may drive progression from myelofibrosis toward acute leukemia, with potential implications for future treatments.
-
Molecular clues and new therapies for myelofibrosis and related blood cancers
This grant supports research to understand what drives myelofibrosis and related disorders and to develop new treatment ideas for patients.
-
Early detection of treatment response in myelofibrosis using a new imaging technology
A new, quick imaging method could tell patients with myelofibrosis early whether a treatment is working.
-
MYC-driven vulnerability in myelofibrosis could guide new therapies
A new project is exploring how the MYC protein contributes to myelofibrosis and whether it can be targeted to help people with this blood cancer.
-
MRI markers to monitor bone marrow in myelofibrosis
Advanced MRI scans will be used to see bone marrow changes in people with myelofibrosis so doctors can tell sooner whether new targeted drugs are working.
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page.