Mutant calreticulin in certain blood cancers (MPN)
Official title: Functional and Molecular Dissection of Mutant Calreticulin in Myeloproliferative Neoplasms
Funded at Palo Alto Veterans Instit for Research · NIH-11189783 · Data updated 2026-11-12
Looking for new treatments that target a mutant protein called calreticulin to help people with CALR‑mutant myeloproliferative neoplasms.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Palo Alto Veterans Instit for Research NIH-funded |
| Lab location | 1 site (Palo Alto, United States) |
| Project start | May 20, 2024 |
| Project end | September 30, 2026 |
| Funding year | 2026 |
| Award (this year) | $355,000 |
| NIH project number | 5R01HL131835-10 |
| Project ID | NIH-11189783 on NIH RePORTER |
Who could benefit from this research
✓Could help
People diagnosed with CALR‑mutant myeloproliferative neoplasms (for example essential thrombocythemia or primary myelofibrosis), including those with concurrent ASXL1 mutations, are the ideal candidates.
✕Less likely to help
Patients whose MPN is driven by other mutations (for example JAK2 or MPL without CALR) or unrelated blood disorders may not directly benefit from therapies developed here.
What this research studies
This project focuses on blood cancers called myeloproliferative neoplasms (MPN) driven by mutations in the calreticulin (CALR) protein. The research team will study how CALR mutations change blood stem cell behavior, including protein handling pathways such as N‑glycosylation and secretion, and how co‑mutations like ASXL1 alter chromatin to drive disease. They will use laboratory models, molecular analyses, and patient‑derived cells or samples to find biochemical vulnerabilities in CALR‑mutant cells. The ultimate aim is to turn those vulnerabilities into new therapies that could modify or possibly cure CALR‑mutant MPN.
Why it matters
Potential benefit: If successful, this work could produce more precise, disease‑modifying treatments for people with CALR‑mutant MPN.
How similar studies have gone: Existing drugs target related pathways (such as JAK inhibitors) but directly targeting mutant CALR is a newer approach that remains largely preclinical.
Where this research is happening
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Palo Alto Veterans Instit for Research
Palo Alto, United States Active
Researchers
- Principal investigator: Mullally, Ann — Palo Alto Veterans Instit for Research
- Study coordinator: Mullally, Ann
Related research
Other NIH-funded projects on the same topics.
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Myeloproliferative Neoplasm Research Consortium
A large research collaboration across multiple centers aims to improve survival for patients with myelofibrosis and related myeloproliferative neoplasms through coordinated laboratory, translational, and clinical work.
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Understanding how different CALR mutations drive certain blood cancers
This grant explores how two CALR mutation types cause myeloproliferative neoplasms and could lead to better treatments for people with these blood cancers.
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Cell Competition in Myeloproliferative Neoplasms
This NIH grant explores how healthy and mutant blood stem cells interact in certain blood cancers to understand why some patients progress and how future therapies might help.
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Targeting ERK’s brake pedals to slow cancer progression
Aims to block the parts of ERK signaling that speed up cancer progression, by guiding drugs to the substrate-binding domains that act like accelerator pedals in myeloproliferative neoplasms and related cancers.
-
Biomarker work to predict pancreatic IPMN cancer risk
A Duke University researcher is testing biomarkers to tell which pancreatic IPMN cysts are likely to become invasive 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.