How telomeres and DNA repair shape cancer genomes
Genome instability in cancer: telomeres and DNA repair
['FUNDING_OTHER'] · ROCKEFELLER UNIVERSITY · NIH-11178735
This work looks at how shortening chromosome ends (telomeres) and broken DNA-repair processes drive cancer, especially in tumors linked to BRCA1 problems.
Quick facts
| Phase | ['FUNDING_OTHER'] |
|---|---|
| Study type | Nih_funding |
| Sex | All |
| Sponsor | ROCKEFELLER UNIVERSITY (nih funded) |
| Locations | 1 site (NEW YORK, UNITED STATES) |
| Trial ID | NIH-11178735 on ClinicalTrials.gov |
What this research studies
Researchers study telomeres (the ends of chromosomes) and how double-strand DNA breaks are fixed to understand why many cancers carry large-scale genome damage. They use genetic experiments, whole-genome sequencing analyses, cell models, and gene-editing tools to track events like breakage-fusion-bridge cycles, chromothripsis, kataegis, and the creation of new telomeres at DNA breaks. The lab examines the role of proteins such as BRCA1 and 53BP1 and how telomerase activity and birth-set telomere length influence tumor development. These mechanistic findings aim to explain which tumors become genomically unstable and why some BRCA1-deficient cancers respond to PARP inhibitors.
Who could benefit from this research
Good fit: People with BRCA1-linked breast or ovarian cancer or patients whose tumors show marked genomic instability or telomere dysfunction would be most directly connected to this research.
Not a fit: Patients whose cancers are driven primarily by non-genomic mechanisms or who lack telomere or DNA-repair defects may not see direct benefit from these findings.
Why it matters
Potential benefit: If successful, this work could improve prediction of which tumors will become aggressive and guide more effective use of targeted treatments such as PARP inhibitors for BRCA1-related cancers.
How similar studies have performed: Previous research has linked telomere shortening and BRCA1 defects to genome instability and PARP inhibitor responses, while specific mechanisms like neotelomere formation and CST–Polα/primase-mediated fill-in are more recently described.
Where this research is happening
NEW YORK, UNITED STATES
- ROCKEFELLER UNIVERSITY — NEW YORK, UNITED STATES (ACTIVE)
Researchers
- Principal investigator: DE LANGE, TITIA — ROCKEFELLER UNIVERSITY
- Study coordinator: DE LANGE, TITIA
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: Breast Cancer 1 Gene, Breast Cancer 1 Gene Product, Breast Cancer Type 1 Susceptibility Gene, Breast Cancer Type 1 Susceptibility Protein, Breast-Ovarian Cancer Protein