How two types of CALR mutations drive myeloproliferative blood cancers
Official title: The Pathophysiology of Type 1 Versus Type 2 Mutant Calreticulin-Drivenmyeloproliferative Neoplasms
Funded at Utah State Higher Education System--University of Utah · NIH-11189677 · Data updated 2026-11-12
This project compares how type 1 and type 2 CALR mutations change blood-cell behavior to help people with myeloproliferative neoplasms such as essential thrombocythemia, polycythemia vera, and myelofibrosis.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Utah State Higher Education System--University of Utah NIH-funded |
| Lab location | 1 site (Salt Lake City, United States) |
| Project start | August 1, 2024 |
| Project end | August 31, 2027 |
| Funding year | 2025 |
| Award (this year) | $463,672 |
| NIH project number | 5R01HL165119-04 |
| Project ID | NIH-11189677 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates would be people diagnosed with an MPN (essential thrombocythemia, polycythemia vera, or primary myelofibrosis) who are known to carry a CALR mutation or are willing to have their mutation status checked.
✕Less likely to help
People whose MPNs are driven by other mutations (for example JAK2) or those with unrelated blood conditions are less likely to get direct benefit from this specific CALR-focused work.
What this research studies
You or your donated blood or bone marrow samples would help researchers compare how type 1 and type 2 CALR mutations alter blood-cell development and signaling. The team will examine differences in calcium binding, interaction with the thrombopoietin receptor (MPL), and downstream JAK/STAT and endoplasmic-reticulum stress pathways using patient samples and laboratory models. They will combine molecular testing, cell-based experiments, and genetic tools to explain why type 1 mutations are linked more often to myelofibrosis while type 2 mutations produce different disease patterns. The work aims to spot mutation-specific weaknesses that could point to new targeted treatments.
Why it matters
Potential benefit: If successful, this work could identify mutation-specific targets that lead to better therapies tailored to CALR mutation type and potentially improve outcomes for MPN patients.
How similar studies have gone: Prior research established that CALR mutations activate MPL and JAK/STAT signaling and that JAK inhibitors relieve symptoms but are not curative, while directly comparing type 1 versus type 2 CALR mechanisms is a newer, less-explored area.
Where this research is happening
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Utah State Higher Education System--University of Utah
Salt Lake City, United States Active
Researchers
- Principal investigator: Elf, Shannon Elisabeth — Utah State Higher Education System--University of Utah
- Study coordinator: Elf, Shannon Elisabeth
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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.