How disrupted body clocks can increase cancer growth
Establishing a mechanistic basis for enhanced tumorigenesis under chronic circadian disruption
This work looks at whether long-term disruption of daily light–dark cycles makes KRAS-driven lung tumors grow faster by increasing activity of a stress protein called HSF1.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Scripps Research Institute, the NIH-funded |
| Lab location | 1 site (La Jolla, United States) |
| Project ID | NIH-11231243 on NIH RePORTER |
What this research studies
Researchers will use genetically engineered mice that develop lung tumors driven by the KRASG12D mutation and expose them to light schedules that mimic chronic jet lag or shift work. They will compare tumor formation in animals with normal HSF1 levels to animals where HSF1 has been deleted to see if HSF1 is required for the tumor-promoting effects of circadian disruption. The team will perform molecular analyses to measure heat-shock response genes and other pathways linking gene activity changes to tumor growth. The approach aims to connect disrupted sleep–light cycles to a specific molecular mechanism that could suggest prevention or treatment strategies.
Who could benefit from this research
Good fit: People with KRAS-mutant lung cancer and individuals who experience chronic circadian disruption (for example, long-term night-shift workers) are most relevant to this research.
Not a fit: People with cancers not driven by KRAS mutations or those without chronic circadian disruption may be less likely to directly benefit from these findings.
Why it matters
Potential benefit: If confirmed, the findings could point to HSF1 as a target to reduce cancer risk linked to chronic circadian disruption and inform protection strategies for people who work night shifts.
How similar studies have performed: Prior animal studies have shown that altered light cycles can increase tumor growth and have linked HSF1 to cancer, but directly testing whether HSF1 is required for KRAS-driven tumor promotion under circadian disruption is a newer, less-tested approach.
Where this research is happening
La Jolla, United States
- Scripps Research Institute, the — La Jolla, United States (Active)
Researchers
- Principal investigator: Lamia, Katja a — Scripps Research Institute, the
- Study coordinator: Lamia, Katja a
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.