MYC-driven vulnerability in myelofibrosis could guide new therapies
Official title: MYC-alarmin axis as a novel therapeutic vulnerability in myelofibrosis
Funded at H. Lee Moffitt Cancer Ctr & Res Inst · NIH-11329078 · Data updated 2026-11-12
A new project is exploring how the MYC protein contributes to myelofibrosis and whether it can be targeted to help people with this blood cancer.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | H. Lee Moffitt Cancer Ctr & Res Inst NIH-funded |
| Lab location | 1 site (Tampa, United States) |
| Project start | June 1, 2024 |
| Project end | May 31, 2029 |
| Funding year | 2026 |
| Award (this year) | $1,659,122 |
| NIH project number | 4R01CA280116-03 |
| Project ID | NIH-11329078 on NIH RePORTER |
Who could benefit from this research
✓Could help
Patients with myelofibrosis or related bone marrow disorders who could contribute samples or participate in future translational trials.
✕Less likely to help
Patients without myelofibrosis or related bone marrow conditions would not be direct beneficiaries.
What this research studies
This research will study how MYC may drive disease features in myelofibrosis and test strategies to disrupt this pathway. Teams will use lab models and patient-derived samples to understand the link between MYC and bone marrow fibrosis, inflammation, and progression to AML. The findings could point to new treatment approaches for MF patients, including those who do not respond to current JAK inhibitors. The work aims to translate basic insights into potential therapeutic strategies that could be tested in future human studies.
Why it matters
Potential benefit: If successful, the project could lead to new therapies that slow or halt disease progression for myelofibrosis patients.
How similar studies have gone: Previous work suggests MYC plays a role in myeloid cancers, but its role in MF is not well defined, making this an exploratory but promising approach.
Where this research is happening
-
H. Lee Moffitt Cancer Ctr & Res Inst
Tampa, United States Active
Researchers
- Principal investigator: Yun, Seongseok — H. Lee Moffitt Cancer Ctr & Res Inst
- Study coordinator: Yun, Seongseok
Related research
Other NIH-funded projects on the same topics.
-
Strategies to deplete myelofibrosis stem cells using HDM2/p53 pathway
A patient-focused program tests a therapy that may selectively reduce disease-causing blood stem cells in people with myelofibrosis.
-
Megakaryocyte changes in myelofibrosis and its progression to leukemia
A scientist-guided project will study how abnormal megakaryocytes and signals like TGF-β and IL-13 may drive progression from myelofibrosis toward acute leukemia, with potential implications for future treatments.
-
Molecular clues and new therapies for myelofibrosis and related blood cancers
This grant supports research to understand what drives myelofibrosis and related disorders and to develop new treatment ideas for patients.
-
Myelofibrosis and the bone marrow environment: how inflammation changes blood production
A doctor-researcher is studying how inflammation in the bone marrow affects the blood-forming system in people with myeloproliferative neoplasms (MPNs) to find ways to prevent scarring and leukemia.
-
Early detection of treatment response in myelofibrosis using a new imaging technology
A new, quick imaging method could tell patients with myelofibrosis early whether a treatment is working.
-
MRI markers to monitor bone marrow in myelofibrosis
Advanced MRI scans will be used to see bone marrow changes in people with myelofibrosis so doctors can tell sooner whether new targeted drugs are working.
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.