Environmental contaminant 1,4-dioxane and cancer: how it may spur tumor progression through cell communication
Official title: Environmental toxicant 1,4-dioxane drives carcinogenesis through Nrf2-dependent extracellular vesicle biogenesis
Funded at State University New York Stony Brook · NIH-11431768 · Data updated 2026-11-12
A NIH grant is studying how exposure to the environmental toxin 1,4-dioxane could promote cancer by altering cell signals and small particles that influence cancer spread.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | State University New York Stony Brook NIH-funded |
| Lab location | 1 site (Stony Brook, United States) |
| Project start | September 1, 2026 |
| Project end | June 30, 2031 |
| Funding year | 2026 |
| Award (this year) | $492,022 |
| NIH project number | 1R01ES038941-01 |
| Project ID | NIH-11431768 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates would be individuals in areas with documented exposure to 1,4-dioxane or communities with environmental contamination impacting water supplies.
✕Less likely to help
People without exposure history or with non-cancerous outcomes may not benefit from this specific research.
What this research studies
Researchers will use animal models and cell-based systems to explore how 1,4-dioxane activates Nrf2 signaling and drives extracellular vesicle production. They will examine how these vesicles carry pro-cancer cargo that enhances EMT, movement, and metastasis, and how ablation of Nrf2 affects these processes. The work includes CRISPR-Cas9 approaches to modify specific genes and test their roles in vesicle biogenesis and cancer traits. Three aims will investigate RAB39B, SDC4, and the overall metastatic potential of 1,4-dioxane–induced vesicles. The findings could reveal new targets for preventing or mitigating environmentally linked cancer progression.
Why it matters
Potential benefit: If successful, the research could identify molecular targets to prevent or slow cancer progression linked to environmental toxins.
How similar studies have gone: Prior work shows that similar toxin-related signaling pathways can influence cancer-related vesicle production, but this exact mechanism is novel and exploratory.
Where this research is happening
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State University New York Stony Brook
Stony Brook, United States Active
Researchers
- Principal investigator: Chen, Fei — State University New York Stony Brook
- Study coordinator: Chen, Fei
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.