HLA-Independent CD8+ T Cell Immunotherapy for AML using β-Catenin and NKG2D
Official title: Harnessing β-Catenin and NK2GD to enable HLA-Independent CD8+ T Cell immunotherapy Against AML
Funded at Upstate Medical University · NIH-11448445 · Data updated 2026-11-12
A new AML immunotherapy aims to boost patients’ CD8+ T cells by increasing NKG2D activity through stabilizing β-catenin, helping kill leukemia cells even when HLA is reduced.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Upstate Medical University NIH-funded |
| Lab location | 1 site (Syracuse, United States) |
| Project start | September 1, 2026 |
| Project end | August 31, 2031 |
| Funding year | 2026 |
| Award (this year) | $724,196 |
| NIH project number | 1R01CA308325-01A1 |
| Project ID | NIH-11448445 on NIH RePORTER |
Who could benefit from this research
✓Could help
Patients with acute myeloid leukemia whose leukemia cells exhibit reduced HLA class I expression or those eligible for adoptive CD8+ T cell therapies.
✕Less likely to help
Patients whose AML does not rely on HLA-related escape or who cannot mount a CD8+ T cell response may see no direct benefit.
What this research studies
This project tests a novel approach to enhance the natural ability of a patient’s CD8+ T cells to attack AML cells that hide from the immune system. By activating β-catenin through a small molecule, the treatment is designed to increase NKG2D expression and empower CD8+ T cells to kill leukemia cells without relying on traditional HLA recognition. The research uses a combination of genetic, molecular, and pharmacologic methods in both mouse and human T cells to map the underlying pathways. It also evaluates how well this strategy works in reducing leukemia cell survival, while monitoring T cell exhaustion and safety. If successful, this could inform a translational path toward a new immunotherapy option for AML patients.
Why it matters
Potential benefit: If successful, patients with AML could have a new T cell–based therapy that works even when leukemia cells downregulate HLA.
How similar studies have gone: Prior approaches targeting NK-like receptors on T cells have shown promise in preclinical models, but this exact β-catenin/NKG2D pathway in AML is exploratory.
Where this research is happening
-
Upstate Medical University
Syracuse, United States Active
Researchers
- Principal investigator: Karimi, Mobin — Upstate Medical University
- Study coordinator: Karimi, Mobin
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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.