How fat, nerves, and blood “chips” could drive AML growth
Official title: Loss of TET2 Promotes Leukemogenesis by Enhancing NPY-Mediated PRC2 Disruption and CTCFL Chromatin Remodeling
Funded at Indiana University Indianapolis · NIH-11454472 · Data updated 2026-11-12
This NIH grant looks at how obesity-related signals in the body might fuel the growth of certain blood cancer cells in people with or at risk for acute myeloid leukemia.
Quick facts
| Grant type | R21 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Indiana University Indianapolis NIH-funded |
| Lab location | 1 site (Indianapolis, United States) |
| Project start | September 18, 2026 |
| Project end | August 31, 2028 |
| Funding year | 2026 |
| Award (this year) | $407,543 |
| NIH project number | 1R21CA307781-01A1 |
| Project ID | NIH-11454472 on NIH RePORTER |
Who could benefit from this research
✓Could help
Adults with or at risk for AML, especially those with TET2 mutations or clonal hematopoiesis of indeterminate potential (CHIP).
✕Less likely to help
Patients without CHIP/TET2 mutations or those not affected by the studied pathways might not benefit from these findings.
What this research studies
Researchers will study how a protein messenger called neuropeptide Y, which is altered in obesity and diabetes, may create a bone marrow environment that lets cancer-prone blood cell clones grow faster. Using human samples and animal models, they will examine TET2-mutant cells to understand how NPY signaling changes the way these cells expand and transform into AML. The project aims to identify molecular pathways that could be targeted to slow or prevent leukemic progression in patients who have CHIP or early AML features. This is a focused, mechanism-driven project with potential implications for therapies that modify the inflammatory and metabolic signals in the bone marrow.
Why it matters
Potential benefit: If successful, this work could lead to new strategies that slow or prevent AML progression in at-risk patients by targeting obesity-related signals.
How similar studies have gone: Preliminary data show a link between TET2 mutations and altered NPY signaling in AML samples and mouse models, suggesting this approach could translate to human therapies.
Where this research is happening
-
Indiana University Indianapolis
Indianapolis, United States Active
Researchers
- Principal investigator: Kapur, Reuben — Indiana University Indianapolis
- Study coordinator: Kapur, Reuben
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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.