How cancer cells hijack gene switches
Official title: Identification of chromatin regulators required for enhancer hijacking in cancer genomes
Funded at Salk Institute for Biological Studies · NIH-11368273 · Data updated 2026-11-12
Researchers will use CRISPR gene-editing screens to find proteins that let cancer cells' gene switches be wrongly turned on, aiming to help people whose tumors have DNA rearrangements.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Salk Institute for Biological Studies NIH-funded |
| Lab location | 1 site (La Jolla, UNITED STATES) |
| Project start | May 4, 2026 |
| Project end | April 30, 2031 |
| Funding year | 2026 |
| Award (this year) | $795,143 |
| NIH project number | 1R01CA304705-01A1 |
| Project ID | NIH-11368273 on NIH RePORTER |
Who could benefit from this research
✓Could help
People with tumors known to contain structural DNA rearrangements that create enhancer hijacking—such as some leukemias, sarcomas, and brain tumors—would be most likely to benefit from any therapies that come from this work.
✕Less likely to help
Patients whose cancers are driven mainly by simple point mutations or other non-structural mechanisms may not see direct benefit from this specific line of research.
What this research studies
This project uses genome-wide CRISPR/Cas9 knockout screens in engineered cells to see which genes allow an enhancer to inappropriately activate an oncogene. The team focuses on chromatin regulators and 3-D genome structure, including factors such as STAG1 and STAG2. Experiments use cell models with enhancer-hijacking reporters to identify proteins that enable promiscuous gene regulation after DNA rearrangements. Results could point to molecular targets for therapies that stop enhancers from turning on cancer-driving genes.
Why it matters
Potential benefit: If successful, this work could reveal drug targets that block a common mechanism cancers use to turn on growth genes, potentially helping patients across many tumor types.
How similar studies have gone: Related CRISPR screening and genome-editing work has previously linked chromatin factors like STAG1 and STAG2 to gene regulation, but applying these methods specifically to enhancer hijacking across many cancers is relatively new.
Where this research is happening
-
Salk Institute for Biological Studies
La Jolla, United States Active
Researchers
- Principal investigator: Dixon, Jesse R — Salk Institute for Biological Studies
- Study coordinator: Dixon, Jesse R
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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.