Cell signaling and gene regulation in liver and gastrointestinal cancers
Cellular interactions between TGF-beta pathway members and epigenetic regulators in liver and gastrointestinal cancers
Researchers are looking at how signaling proteins and gene-regulating enzymes like SIRT6 interact to explain why fatty liver disease can turn into liver cancer.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Feinstein Institute for Medical Research NIH-funded |
| Lab location | 1 site (Manhasset, United States) |
| Project ID | NIH-11308736 on NIH RePORTER |
What this research studies
This work uses patient liver samples, lab-grown human liver cultures, and mouse models to study proteins (SIRT6, SMAD3, and the adaptor β2SP/SPTBN1) and TGF‑β signaling that may drive progression from fatty liver/NASH to hepatocellular carcinoma. The team examines how lower SIRT6 levels and a specific β2SP mutation alter cell signaling and fat-producing programs in liver cells. They combine genetically modified mice, human microfluidic liver cultures, and analysis of human tumor samples to connect lab findings to patient disease. The goal is to pinpoint molecular interactions that could become targets for future tests or treatments.
Who could benefit from this research
Good fit: Adults with non-alcoholic fatty liver disease (NAFLD)/NASH or hepatocellular carcinoma who are willing to provide tissue or blood samples or participate in linked clinical studies are the most relevant candidates.
Not a fit: People without liver disease or those seeking an immediate treatment benefit should not expect direct clinical benefit from this laboratory-focused research at this time.
Why it matters
Potential benefit: If successful, this research could point to new ways to prevent or treat the progression from NASH/fatty liver to liver cancer by targeting these signaling and epigenetic pathways.
How similar studies have performed: Previous studies have linked SIRT6 and TGF‑β/SMAD signaling to liver disease, but the specific role of β2SP/SPTBN1 mutations and their interaction with SIRT6 in NASH-to-HCC progression is a newer and still-emerging finding.
Where this research is happening
Manhasset, United States
- Feinstein Institute for Medical Research — Manhasset, United States (Active)
Researchers
- Principal investigator: Mishra, Lopa — Feinstein Institute for Medical Research
- Study coordinator: Mishra, Lopa
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.