How metabolism and gene packaging drive cyclin E–high ovarian cancer
Official title: Metabolic and epigenetic reprogramming in cyclin E high ovarian cancer
Funded at Wistar Institute · NIH-11379425 · Data updated 2026-11-12
This work aims to find out whether blocking a cancer cell pathway that makes acetyl‑CoA-driven changes can help treatments like PARP inhibitors work better for people with cyclin E–high high‑grade serous ovarian cancer.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Wistar Institute NIH-funded |
| Lab location | 1 site (Philadelphia, United States) |
| Project start | May 1, 2021 |
| Project end | April 30, 2027 |
| Funding year | 2025 |
| Award (this year) | $212,508 |
| NIH project number | 7R01CA259111-06 |
| Project ID | NIH-11379425 on NIH RePORTER |
Who could benefit from this research
✓Could help
The ideal patients would be people with high‑grade serous ovarian cancer whose tumors show high cyclin E (CCNE1) expression and who have limited benefit from PARP inhibitors.
✕Less likely to help
Patients whose tumors do not have high cyclin E expression or who have other ovarian cancer subtypes are less likely to benefit from findings tied to this specific pathway.
What this research studies
From a patient perspective, the team will study tumors that make too much cyclin E to see how a metabolic chemical called acetyl‑CoA changes how DNA is packaged and repaired. They will track where acetyl‑CoA is made and how it leads to extra chemical tags on histone proteins that help cancer cells fix DNA damage. The researchers will use lab-grown cancer cells and preclinical models to test whether interrupting this pathway can make PARP inhibitor therapies more effective against these resistant tumors. If promising, the work could point toward new drug combinations to try in people with this type of ovarian cancer.
Why it matters
Potential benefit: If successful, this could make PARP inhibitors or new drug combinations work better for the ~20% of high‑grade serous ovarian cancer patients whose tumors have high cyclin E and are resistant to current PARP therapy.
How similar studies have gone: Related preclinical studies linking metabolism, histone acetylation, and DNA repair show promise, but targeting acetyl‑CoA–driven histone changes in cyclin E–high tumors with PARP inhibitors is largely untested in patients.
Where this research is happening
-
Wistar Institute
Philadelphia, United States Active
Researchers
- Principal investigator: Aird, Katherine Marie — Wistar Institute
- Study coordinator: Aird, Katherine Marie
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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.