MnSOD modification drives a stem-cell like switch in some ER-positive breast cancers
Official title: MnSOD-K68-Ac reprograms a lineage plasticity switch / stemness in ER+ breast malignancies
Funded at University of Cincinnati · NIH-11543353 · Data updated 2026-11-12
A small study in ER-positive breast cancer looks at how a specific mitochondrial change (MnSOD-K68 acetylation) may push cancer cells toward a more stem-like, therapy-resistant state.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Cincinnati NIH-funded |
| Lab location | 1 site (Cincinnati, United States) |
| Project start | January 9, 2021 |
| Project end | December 31, 2026 |
| Funding year | 2025 |
| Award (this year) | $101,321 |
| NIH project number | 7R01CA253678-06 |
| Project ID | NIH-11543353 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates are patients with ER-positive breast cancer exhibiting mitochondrial/metabolic alterations and/or endocrine therapy resistance, or available patient-derived samples for related analyses.
✕Less likely to help
Patients whose cancer does not involve MnSOD K68 acetylation–related pathways may see no direct benefit.
What this research studies
This project focuses on breast cancer cells that rely on estrogen signaling. It explores how altering MnSOD acetylation at lysine 68 changes cell metabolism and increases reactive oxygen species, potentially driving plasticity and stemness. Using cell and possibly tumor models, the researchers will examine signaling pathways linked to stem cell markers like SOX2 and Oct4 and their connection to therapy resistance. The goal is to understand whether this mitochondrial change helps tumors switch identities and resist standard endocrine therapies. Findings could point to new strategies to prevent or overcome resistance in ER-positive breast cancer.
Why it matters
Potential benefit: If successful, the work could reveal new targets to prevent stem-like resistance in ER-positive breast cancers and improve responses to therapy.
How similar studies have gone: Previous work has linked MnSOD signaling and ROS to cancer cell behavior, but this approach explores a specific acetylation state and its link to lineage plasticity, making it relatively novel.
Where this research is happening
-
University of Cincinnati
Cincinnati, United States Active
Researchers
- Principal investigator: Gius, David — University of Cincinnati
- Study coordinator: Gius, David
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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.