Understanding genetic dependencies when Fanconi anemia pathway is lost
Official title: Characterizing genetic dependencies induced by Fanconi anemia pathway loss
Funded at Columbia University Health Sciences · NIH-11421557 · Data updated 2026-11-12
A study to find other genes or pathways that cancer cells rely on when the Fanconi anemia repair system is broken, with the aim of guiding future treatments.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Columbia University Health Sciences NIH-funded |
| Lab location | 1 site (New York, United States) |
| Project start | July 1, 2026 |
| Project end | June 30, 2031 |
| Funding year | 2026 |
| Award (this year) | $586,864 |
| NIH project number | 1R01CA315098-01 |
| Project ID | NIH-11421557 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates are patients or tumors with known FA pathway gene mutations or deficiencies, such as BRCA1/2-related contexts.
✕Less likely to help
Patients without FA pathway defects or BRCA-related mutations may not benefit from these findings.
What this research studies
This project looks at how cancer cells cope when the Fanconi anemia DNA repair pathway is defective. Researchers will map which other genes become essential for survival in these cells and test potential vulnerabilities. The work builds on prior high-throughput screening to uncover synthetic lethal interactions that could be targeted by new therapies. Insights from this study could help tailor treatments for patients with tumors that carry FA pathway defects.
Why it matters
Potential benefit: Could reveal new targets for therapy in cancers with Fanconi anemia pathway defects, potentially improving outcomes for patients.
How similar studies have gone: Previous high-throughput studies identified several candidate dependencies; this work extends those findings in mammalian systems.
Where this research is happening
-
Columbia University Health Sciences
New York, United States Active
Researchers
- Principal investigator: Ciccia, Alberto — Columbia University Health Sciences
- Study coordinator: Ciccia, Alberto
Related research
Other NIH-funded projects on the same topics.
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In vivo gene repair to restore healthy hematopoiesis in Fanconi anemia
A study aims to repair faulty genes inside patients’ blood-forming cells to help people with Fanconi anemia regain healthy blood cell production.
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Innovative cell and gene therapy approaches to treat Fanconi anemia
A Stanford-led project aims to develop safer cell and gene therapies to help people with Fanconi anemia who have bone marrow failure.
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How cells detect DNA damage and activate ATR, ATM, and Fanconi anemia repair systems
Researchers are using high-resolution structural imaging to show how key repair proteins sense DNA damage, with relevance for people whose cancers come from DNA repair defects.
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In vivo gene therapy for Fanconi anemia
A patient-focused overview of a potential in vivo gene therapy approach to correct Fanconi anemia, aiming to reduce the need for donor transplants.
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Fanconi anemia: what happens inside cells
Researchers want to learn how proteins called REV7 and CHAMP1 change DNA repair in people with Fanconi anemia and related genetic syndromes.
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Understanding how cells detect and respond to DNA damage
This study is looking at how our cells detect and fix damage to their DNA, which is really important for stopping cancer, and it aims to understand how certain proteins work together to repair serious DNA problems, with the hope that this knowledge can help develop new treatments to improve DNA repair in cancer cells.
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.