How two types of CALR mutations drive myeloproliferative blood cancers
The Pathophysiology of Type 1 Versus Type 2 Mutant Calreticulin-Drivenmyeloproliferative Neoplasms
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 ID | NIH-11189677 on NIH RePORTER |
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.
Who could benefit from this research
Good fit: 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.
Not a fit: 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.
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 performed: 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
Salt Lake City, United States
- 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
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 below.