How age-related inflammation and gene-control changes let mutated blood stem cells grow and start leukemia
Assessing the Interplay Between Inflammatory Signaling and Epigenetic Dysregulation in Age-associated Clonal Hematopoiesis and Leukemia Initiation
Researchers are looking at whether inflammation that increases with age and changes in gene regulation help mutated blood stem cells expand and lead to acute myeloid leukemia, especially in older adults.
Quick facts
| Grant type | U01 cooperative agreement |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Jackson Laboratory NIH-funded |
| Lab location | 1 site (Bar Harbor, United States) |
| Project ID | NIH-11091460 on NIH RePORTER |
What this research studies
This project focuses on common age-associated mutations in blood-forming stem cells (for example, DNMT3A, TET2, ASXL1) and asks how aging-related inflammation and altered gene control give these cells a growth advantage. The team compares mutant cell behavior in aged versus young mouse models and examines human blood samples to connect findings back to people. They measure inflammatory signals and epigenetic (gene-control) changes to pinpoint which molecular shifts drive clonal expansion and leukemia initiation. The goal is to find molecular targets that could be used to prevent progression from clonal hematopoiesis to AML.
Who could benefit from this research
Good fit: Ideal candidates would be older adults with clonal hematopoiesis identified on genetic testing—especially those carrying DNMT3A, TET2, or ASXL1 mutations—or people considered at higher risk for AML.
Not a fit: People without clonal hematopoiesis mutations, those with unrelated diseases, or patients seeking immediate leukemia treatment are unlikely to receive direct benefit from this research.
Why it matters
Potential benefit: Could reveal ways to prevent or slow the progression from clonal hematopoiesis to acute myeloid leukemia in older adults.
How similar studies have performed: Previous work has linked inflammation and CH mutations to increased AML risk in both human data and mouse models, but turning those findings into proven prevention or treatment approaches is still unproven.
Where this research is happening
Bar Harbor, United States
- Jackson Laboratory — Bar Harbor, United States (Active)
Researchers
- Principal investigator: Trowbridge, Jennifer Jean — Jackson Laboratory
- Study coordinator: Trowbridge, Jennifer Jean
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.