Targeting c-Myc DNA with next-generation nucleic acid tools in aggressive B-cell lymphomas
Official title: Sequence-specific inhibition of c-Myc in vivo by next-generation nucleic acid analogs
Funded at University of Connecticut Storrs · NIH-11449412 · Data updated 2026-11-12
This grant tests a new way to slow or stop aggressive B-cell lymphomas by directly targeting the c-Myc gene in patients and model systems using advanced nucleic acid analogs.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Connecticut Storrs NIH-funded |
| Lab location | 1 site (Storrs-Mansfield, United States) |
| Project start | August 1, 2026 |
| Project end | July 31, 2031 |
| Funding year | 2026 |
| Award (this year) | $395,526 |
| NIH project number | 1R01CA303285-01A1 |
| Project ID | NIH-11449412 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates include adults with aggressive B-cell lymphomas where c-Myc plays a driving role, or those contributing to preclinical modeling and future clinical trial readiness.
✕Less likely to help
Patients with lymphomas driven by mechanisms independent of c-Myc may not benefit from this approach.
What this research studies
Researchers will use synthetic nucleic acid mimics called gamma Peptide Nucleic Acids (gPNA) linked to a nucleus-delivery tag to bind the c-Myc DNA in tumor cells, aiming to reduce c-Myc protein and tumor growth. The work includes testing these agents in cell cultures and animal models to show sequence-specific knockdown of c-Myc with reduced off-target effects. If successful, this approach could pave the way for a new class of antigene therapies for B-cell lymphomas. The project builds on prior findings that c-Myc drives poor outcomes and that gPNA can resist degradation, enabling in vivo activity.
Why it matters
Potential benefit: If successful, patients with aggressive B-cell lymphomas could benefit from a targeted therapy that reduces tumor growth by silencing a key cancer driver.
How similar studies have gone: Previous work showed about 50% reduction in c-Myc protein and decreased tumor growth in preclinical models using gPNA-based antigene strategies.
Where this research is happening
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University of Connecticut Storrs
Storrs-Mansfield, United States Active
Researchers
- Principal investigator: Bahal, Raman — University of Connecticut Storrs
- Study coordinator: Bahal, Raman
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.