Understanding how ERCC1-XPF is turned on to fix damaged DNA in cancer-related pathways
Official title: P2 - Elucidating ERCC1-XPF activation in damaged nucleotide response pathways
Funded at University of Calif-Lawrenc Berkeley Lab · NIH-11423279 · Data updated 2026-11-12
A researchers team is studying how a DNA-cutting enzyme (ERCC1-XPF) is activated in damaged DNA repair pathways to better understand cancer and responses to chemotherapy.
Quick facts
| Grant type | P01 program project |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Calif-Lawrenc Berkeley Lab NIH-funded |
| Lab location | 1 site (Berkeley, United States) |
| Project start | September 27, 2001 |
| Project end | August 31, 2031 |
| Funding year | 2026 |
| Award (this year) | $529,672 |
| NIH project number | 2P01CA092584-26 |
| Project ID | NIH-11423279 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates are patients with cancers where ERCC1-XPF–related repair pathways influence treatment response or where DNA repair defects are known to play a role.
✕Less likely to help
Patients without cancers affected by ERCC1-XPF–related repair pathways or those not participating in related translational studies may see no direct benefit.
What this research studies
This project aims to reveal the molecular switches that activate ERCC1-XPF in different DNA repair contexts, with a focus on preventing excessive DNA damage and toxicity. The work will explore how ERCC1-XPF interacts with partners like XPA, TFIIH, and RPA in repair processes such as NER, interstrand crosslink repair, and LINE1 activity. Researchers will use biochemical and cellular approaches to map activation mechanisms, aiming to connect these insights to cancer predisposition and chemotherapy resistance. Findings could inform the development of more precise anti-cancer strategies that exploit DNA repair pathways while minimizing harm to patients.
Why it matters
Potential benefit: Better understanding of DNA repair activation could lead to more effective cancer treatments with fewer side effects and overcome drug resistance.
How similar studies have gone: Previous work shows that ERCC1-XPF is a key regulator of DNA repair and a biomarker for cisplatin response, supporting potential translational value.
Where this research is happening
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University of Calif-Lawrenc Berkeley Lab
Berkeley, United States Active
Researchers
- Principal investigator: Chazin, Walter J. — University of Calif-Lawrenc Berkeley Lab
- Study coordinator: Chazin, Walter J.
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.