Investigating the role of IL-1 signaling in myelofibrosis
Official title: Targeting of IL-1 Signaling in Myelofibrosis
Funded at University of Virginia · NIH-10804665 · Data updated 2026-11-12
This study is looking at how a protein called IL-1 affects myelofibrosis, a serious blood condition, in hopes of finding new ways to treat it and help patients feel better.
Quick facts
| Grant type | R21 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Virginia NIH-funded |
| Lab location | 1 site (Charlottesville, United States) |
| Project start | April 1, 2023 |
| Project end | March 31, 2026 |
| Funding year | 2024 |
| Award (this year) | $215,179 |
| NIH project number | 5R21CA274430-02 |
| Project ID | NIH-10804665 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates for this research are patients diagnosed with myelofibrosis or related myeloproliferative neoplasms.
✕Less likely to help
Patients with other types of blood disorders not related to myelofibrosis may not benefit from this research.
What this research studies
This research focuses on understanding how IL-1 signaling contributes to myelofibrosis, a severe blood disorder characterized by the overproduction of blood cells. The study aims to explore new therapeutic targets by examining the effects of IL-1 on bone marrow fibrosis and blood counts in a mouse model. By targeting IL-1 signaling, the researchers hope to develop novel treatments that could improve patient outcomes. The approach includes genetic manipulation and analysis of blood and bone marrow samples to assess the impact of IL-1 inhibition.
Why it matters
Potential benefit: If successful, this research could lead to new therapies that significantly improve the management and outcomes for patients with myelofibrosis.
How similar studies have gone: Preliminary studies have shown promising results in mouse models, indicating that targeting IL-1 signaling may be a viable approach for treating myelofibrosis.
Where this research is happening
-
University of Virginia
Charlottesville, United States Active
Researchers
- Principal investigator: Mohi, Golam — University of Virginia
- Study coordinator: Mohi, Golam
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.
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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.
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Myelofibrosis and the bone marrow environment: how inflammation changes blood production
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.
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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.
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.