Environmental chemicals turning on dormant viral genes in germ cells that may raise cancer risk in children
Environmental chemicals impair epigenetic suppression of the endogenous retrovirus HML-2 in human primordial germ cells, predisposing the next generation to malignancies through HML-2 reactivation
This research looks at whether common environmental pollutants can switch on dormant viral genes in early human germ cells and potentially increase cancer risk in the next generation.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Massachusetts General Hospital NIH-funded |
| Lab location | 1 site (Boston, United States) |
| Project ID | NIH-11299049 on NIH RePORTER |
What this research studies
Researchers will use human pluripotent stem cell–derived primordial germ cell–like cells and lab models to see if exposures to chemicals such as benzo(a)pyrene disrupt the normal silencing of the HML-2 endogenous retrovirus. They will expose these germ cell models to toxicants and use sequencing methods (like ATAC-seq) and CRISPR-based tools to track chromatin changes and viral gene activation. The team will also use reconstituted testis models to study whether impaired silencing persists during germ cell development and could be passed to offspring. Findings will help link molecular changes in germ cells to later cancer risk in descendants.
Who could benefit from this research
Good fit: Adults concerned about past or ongoing exposure to environmental polycyclic aromatic hydrocarbons (for example, occupational or heavy urban exposure to benzo[a]pyrene) or those interested in inherited cancer risk would be most relevant to this topic.
Not a fit: People seeking immediate treatment for an existing cancer or those without concern about environmental or germline exposure are unlikely to gain direct benefit from this laboratory-focused work.
Why it matters
Potential benefit: If confirmed, this work could explain a pathway by which parental chemical exposures raise cancer risk in children and suggest ways to prevent or detect that risk early.
How similar studies have performed: Prior studies have shown HML-2 activation in some cancers and that toxicants can alter epigenetic marks, but directly linking germline HML-2 mis-silencing to increased cancer in offspring is a novel and not yet proven area.
Where this research is happening
Boston, United States
- Massachusetts General Hospital — Boston, United States (Active)
Researchers
- Principal investigator: Shioda, Toshihiro — Massachusetts General Hospital
- Study coordinator: Shioda, Toshihiro
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.