Chemical changes to the glucocorticoid receptor that drive drug resistance in prostate cancer
Posttranslational modifications of glucocorticoid receptor associated with drug-resistance in prostate cancer
This project looks at whether a chemical change (phosphorylation) on the glucocorticoid receptor helps advanced prostate cancer resist androgen-blocking treatments and whether targeting AKT1 can stop that resistance.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | State University of New York at Buffalo NIH-funded |
| Lab location | 1 site (Amherst, United States) |
| Project ID | NIH-11306660 on NIH RePORTER |
What this research studies
Researchers will examine tumor samples from advanced prostate cancer and laboratory models to see how phosphorylation changes the glucocorticoid receptor. They will use protein-mapping (proteomics), gene editing (CRISPR), and drug tests to determine when and where this phosphorylation occurs. The team will test whether blocking the AKT1 protein or preventing GR phosphorylation reduces glucocorticoid-receptor-driven resistance to androgen receptor blockers like enzalutamide in cell and animal models. Findings could point to new drugs or tests to help patients whose cancers stop responding to standard hormone therapies.
Who could benefit from this research
Good fit: Ideal candidates are men with advanced or castration-resistant prostate cancer who have progressed on androgen-receptor-targeted therapies such as enzalutamide.
Not a fit: Patients with early-stage prostate cancer controlled by initial therapy, or those whose tumors do not show glucocorticoid-receptor changes, may not receive direct benefit from this work.
Why it matters
Potential benefit: If successful, this work could identify ways to prevent or reverse resistance to androgen-blocking drugs in advanced prostate cancer.
How similar studies have performed: Previous laboratory and clinical studies have shown that glucocorticoid-receptor activation can cause resistance and that broad AKT inhibition can reduce GR activity, but specifically targeting AKT1-driven GR phosphorylation is a newer approach with limited prior testing.
Where this research is happening
Amherst, United States
- State University of New York at Buffalo — Amherst, United States (Active)
Researchers
- Principal investigator: Adelaiye-Ogala, Remi — State University of New York at Buffalo
- Study coordinator: Adelaiye-Ogala, Remi
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.