Understanding why some patients with blood cancers don't respond to interferon-alpha treatment
Official title: Elucidating Mechanisms of Therapy-Resistance to Interferon-alfa in Myeloproliferative Neoplasm Stem Cells - Diversity Supplement
Funded at Weill Medical Coll of Cornell Univ · NIH-11180710 · Data updated 2026-11-12
This study is looking at how certain blood cancer stem cells with CALR mutations react to a treatment called interferon-alpha, to help understand why some patients improve in their blood counts but not in tumor size, which could lead to better treatments for people with blood cancers.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Weill Medical Coll of Cornell Univ NIH-funded |
| Lab location | 1 site (New York, United States) |
| Project start | December 10, 2024 |
| Project end | May 31, 2025 |
| Funding year | 2025 |
| Award (this year) | $54,859 |
| NIH project number | 3R01HL167139-02S1 |
| Project ID | NIH-11180710 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates for this research are patients diagnosed with myeloproliferative neoplasms who have CALR mutations and are undergoing interferon-alpha treatment.
✕Less likely to help
Patients without CALR mutations or those not receiving interferon-alpha therapy may not benefit from this research.
What this research studies
This research investigates how certain blood cancer stem cells, particularly those with CALR mutations, respond to interferon-alpha therapy. By analyzing blood samples from patients, the study aims to uncover the molecular mechanisms that lead to therapy resistance. The researchers will use advanced techniques to examine the genetic and cellular changes in these stem cells before and after treatment, providing insights into why some patients see improvements in blood counts but not in tumor size. This could help tailor more effective treatments for patients with myeloproliferative neoplasms.
Why it matters
Potential benefit: If successful, this research could lead to improved treatment strategies for patients with myeloproliferative neoplasms, enhancing their response to interferon-alpha therapy.
How similar studies have gone: Previous research has shown that understanding the genetic basis of therapy resistance can lead to significant advancements in treatment, suggesting that this approach has the potential for success.
Where this research is happening
-
Weill Medical Coll of Cornell Univ
New York, United States Active
Researchers
- Principal investigator: Nam, Seung Ha — Weill Medical Coll of Cornell Univ
- Study coordinator: Nam, Seung Ha
Related research
Other NIH-funded projects on the same topics.
-
Complement and clotting in JAK2V617F myeloproliferative neoplasms
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Hypoxia-inducible factors and neutrophil diversity in blood clotting in myeloproliferative neoplasms
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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.
-
Genetic and epigenetic factors shaping response in advanced myeloproliferative neoplasms
This grant looks at how genetic and epigenetic differences influence how patients with advanced myeloproliferative neoplasms respond to therapies.
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.