How parts of a glioblastoma tumor stop the immune system from fighting cancer
The role of ECM-mediated mechanosignaling on regional immunosuppression in GBM
This project tests whether stiff, hyaluronic-acid–rich areas in glioblastoma make tumor cells change and attract immune-suppressing cells, which could matter for people with glioblastoma.
Quick facts
| Grant type | NIH-funded research |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Louisville NIH-funded |
| Lab location | 1 site (Louisville, United States) |
| Project ID | NIH-11096674 on NIH RePORTER |
What this research studies
Researchers will study glioblastoma tumor tissue and lab models to see how changes in the tumor’s extracellular matrix (especially hyaluronic acid stiffness) activate cancer-cell signals (CD44→STAT3/ZEB1) that may drive a mesenchymal change. They will measure how those changes affect recruitment or differentiation of monocytic myeloid-derived suppressor cells (M-MDSCs) and related cytokines like IL-6 and IL-17. Experiments will use molecular analyses, imaging, and controlled changes in matrix stiffness in cell and tissue models, and may include analysis of patient tumor samples. The team aims to map the pathway that links physical changes in the tumor to local immune suppression so future therapies can target it.
Who could benefit from this research
Good fit: Ideal participants would be people with glioblastoma who can provide tumor tissue or who are treated at centers collaborating with the University of Louisville and may be eligible for future trials targeting this pathway.
Not a fit: People without glioblastoma or whose tumors do not show the specific ECM/CD44-driven features studied here are unlikely to benefit directly from this project.
Why it matters
Potential benefit: If successful, this work could point to a new drug target or strategy to reduce local immune suppression in glioblastoma and help immune-based treatments work better.
How similar studies have performed: Prior laboratory studies have linked ECM stiffness, CD44 signaling, and STAT3-driven mesenchymal changes to immune suppression, but translating these findings into effective patient therapies is still early and largely unproven.
Where this research is happening
Louisville, United States
- University of Louisville — Louisville, United States (Active)
Researchers
- Principal investigator: Chen, Joseph — University of Louisville
- Study coordinator: Chen, Joseph
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.