Complement and clotting in JAK2V617F myeloproliferative neoplasms
Official title: Contribution of complement activation to JAK2V617F myeloproliferative neoplasm thrombosis
Funded at University of Minnesota · NIH-11437026 · Data updated 2026-11-12
A short, patient-friendly study will look at how a specific mutation in blood cells may trigger the body’s complement system to cause clots in people with myeloproliferative neoplasms.
Quick facts
| Grant type | R03 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Minnesota NIH-funded |
| Lab location | 1 site (Minneapolis, United States) |
| Project start | August 1, 2026 |
| Project end | July 31, 2028 |
| Funding year | 2026 |
| Award (this year) | $231,000 |
| NIH project number | 1R03HL187206-01 |
| Project ID | NIH-11437026 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates are adults with myeloproliferative neoplasms carrying the JAK2V617F mutation or related blood disorder models.
✕Less likely to help
People without the JAK2V617F mutation or without thrombosis risk related to MPN may not benefit from this specific mechanism-focused work.
What this research studies
This project uses lab models to explore whether the JAK2V617F mutation drives abnormal complement activation that leads to inflammation and clotting. It builds on existing data showing links between inflammation, coagulation, and the complement system, and will focus on pathways involving ProS-MerTK, C4BP, C1q, factor H, and VWF. The work will use animal models and biochemical assays to understand how these interactions might be targeted to prevent thrombosis in patients with MPNs. Findings could inform future therapies to reduce clot risk beyond current cell-count–reducing treatments.
Why it matters
Potential benefit: If successful, this research could guide development of new approaches to prevent blood clots in people with MPNs.
How similar studies have gone: Preliminary data and existing literature support a link between complement activation and thrombosis in MPNs, suggesting this approach is promising.
Where this research is happening
-
University of Minnesota
Minneapolis, United States Active
Researchers
- Principal investigator: Beckman, Joan Denise — University of Minnesota
- Study coordinator: Beckman, Joan Denise
Related research
Other NIH-funded projects on the same topics.
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Endothelial contribution to blood-clotting in myeloproliferative neoplasms
This project explores how the lining of blood vessels may drive dangerous clots in people with myeloproliferative neoplasms (MPNs).
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Hypoxia-inducible factors and neutrophil diversity in blood clotting in myeloproliferative neoplasms
A physician-scientist is training over five years to uncover how low-oxygen signals and diverse neutrophils drive dangerous clots in people with myeloproliferative neoplasms, with the goal of finding new treatment targets.
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Understanding blood clotting mechanisms in certain blood cancers
This study is looking into how blood clots form in people with myeloproliferative neoplasms (a type of blood cancer) to find new ways to help prevent serious complications, and it’s designed for patients who want to learn more about their condition and potential treatments.
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Understanding how blood vessel cells contribute to blood clots in certain blood cancers
This study is looking at how certain cells in your blood vessels might contribute to blood clots in people with myeloproliferative neoplasms (MPNs), especially those with a specific mutation, and it aims to understand how current medications can help, with the possibility of you providing blood samples to assist in thi
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Inherited genetic risks shaping myeloid cancer initiation
A research project at Boston Children’s Hospital is exploring how inherited genetic differences may push blood stem cells toward the start of myeloproliferative neoplasms, with potential implications for earlier detection and prevention.
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Understanding why some myeloproliferative neoplasm patients resist interferon therapy
Researchers are studying why interferon-alpha works for some blood cancer patients but not others, by looking closely at stem cells from CALR-mutated myeloproliferative neoplasms.
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.