How metabolism and gene packaging drive cyclin E–high ovarian cancer
Metabolic and epigenetic reprogramming in cyclin E high ovarian cancer
['FUNDING_R01'] · WISTAR INSTITUTE · NIH-11379425
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
| Phase | ['FUNDING_R01'] |
|---|---|
| Study type | Nih_funding |
| Sex | All |
| Sponsor | WISTAR INSTITUTE (nih funded) |
| Locations | 1 site (PHILADELPHIA, UNITED STATES) |
| Trial ID | NIH-11379425 on ClinicalTrials.gov |
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.
Who could benefit from this research
Good fit: 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.
Not a fit: 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.
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 performed: 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
PHILADELPHIA, UNITED STATES
- WISTAR INSTITUTE — PHILADELPHIA, UNITED STATES (ACTIVE)
Researchers
- Principal investigator: AIRD, KATHERINE MARIE — WISTAR INSTITUTE
- Study coordinator: AIRD, KATHERINE MARIE
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 below.
Conditions: Cancer Genes, Cancer Patient