How repetitive DNA activity affects ATR inhibitor therapy for prostate cancer

Effect of DNA repeat silencing on efficacy of ATRi in prostate cancer treatment

NIH-funded research University of Pennsylvania · NIH-11307060

This work looks at whether turning on repetitive DNA sequences in prostate tumors makes ATR inhibitor drugs work better for men with advanced or castration-resistant prostate cancer.

Quick facts

Grant typeR01 grant
Study typeNIH-funded research
Funding institutionUniversity of Pennsylvania NIH-funded
Lab location1 site (Philadelphia, United States)
Project IDNIH-11307060 on NIH RePORTER

What this research studies

If you have advanced prostate cancer, researchers are trying to understand why ATR inhibitor drugs cause more DNA damage in some tumors than others. They are focusing on repetitive DNA sequences that are normally turned off but can become active in cancer, and on common changes in advanced prostate cancer such as loss of RB1 or p53, hypomethylation, and RNASEH2 problems. The team will use lab models and likely patient-derived samples to see how these changes affect repeat transcription and sensitivity to ATR inhibitors. Their methods aim to connect molecular tumor features with drug response to guide future treatments.

Who could benefit from this research

Good fit: Men with advanced or castration-resistant prostate cancer, especially those whose tumors have DNA repair gene changes (like BRCA2 or ATM) or signs of repeat derepression, would be most relevant.

Not a fit: People with early-stage prostate cancer or tumors lacking repeat derepression or related DNA repair defects are less likely to benefit directly from this work.

Why it matters

Potential benefit: If successful, this could help identify which prostate cancers are most likely to respond to ATR inhibitors and suggest combinations to make the drugs more effective.

How similar studies have performed: ATR inhibitors have shown promise in cancers with DNA repair defects in clinical trials, but using retroelement derepression to predict or boost response is a newer approach that is still being explored.

Where this research is happening

Philadelphia, United States

Researchers

About this research

  1. This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
  2. Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
  3. For full project details, budget, and progress reports, visit the official NIH RePORTER page below.
Conditions Breast Cancer 2 GeneBreast Cancer Type 2 Susceptibility GeneCancer TreatmentCancers
Last reviewed 2026-06-14 by the Find a Trial editorial team. Information on this page is for educational purposes and is not medical advice. Always consult qualified healthcare professionals about clinical trial participation.