How the androgen receptor can switch between stopping and driving prostate cancer growth
Growth suppressive and oncogenic transcriptional programs controlled by the androgen receptor in prostate cancer
Researchers are looking at how the androgen receptor in prostate cells can flip between programs that slow growth and those that drive prostate cancer, with the goal of finding ways to turn the normal growth-blocking program back on for men with prostate cancer.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Weill Medical Coll of Cornell Univ NIH-funded |
| Lab location | 1 site (New York, United States) |
| Project ID | NIH-11291339 on NIH RePORTER |
What this research studies
If I have prostate cancer, this work is trying to understand why the androgen receptor (AR) sometimes keeps prostate cells calm and other times drives cancer growth. The team uses laboratory models and analyses of human tumor samples to change AR binding sites and find the factors that shift AR from a normal, growth-suppressive role to an oncogenic role. They study common AR alterations seen in advanced disease, like amplification and splice variants, to see how those changes affect gene programs. The goal is to identify targets or strategies that could restore the AR's normal behavior and slow tumor growth.
Who could benefit from this research
Good fit: Men with prostate cancer, including those with advanced or treatment-resistant disease and those willing to provide tumor tissue or clinical data, would be most relevant to this work.
Not a fit: People without prostate cancer or those whose tumors do not rely on androgen receptor signaling (for example AR-negative or neuroendocrine prostate cancers) are unlikely to benefit directly.
Why it matters
Potential benefit: If successful, this research could point to new ways to restore the AR's natural growth-suppressing program and slow or stop prostate cancer progression.
How similar studies have performed: Many approved therapies target AR signaling and benefit patients, but reactivating the AR's normal growth-suppressive gene program is a newer and less-tested approach that builds on prior AR-targeted successes.
Where this research is happening
New York, United States
- Weill Medical Coll of Cornell Univ — New York, United States (Active)
Researchers
- Principal investigator: Barbieri, Christopher E — Weill Medical Coll of Cornell Univ
- Study coordinator: Barbieri, Christopher E
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.