How the viral protein LMP1 and the human gene MYC drive EBV-linked B-cell cancers
Roles of LMP1 and MYC in EBV-induced B-cell tumors
This project looks at how a viral protein called LMP1 and the human MYC gene cause Epstein-Barr virus (EBV)-related B‑cell lymphomas to help people with EBV-positive lymphomas.
Quick facts
| Grant type | U01 cooperative agreement |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Wisconsin-Madison NIH-funded |
| Lab location | 1 site (Madison, United States) |
| Project ID | NIH-11169879 on NIH RePORTER |
What this research studies
Researchers use a newly made EBV virus missing a key regulator to infect normal human B cells in lab cultures and model systems so they can recreate the forms of EBV infection seen in human lymphomas. They will study how LMP1 (a viral protein) and MYC (a human cancer gene) interact to drive different B‑cell tumor types and patterns of viral latency. The team combines experiments in human cells, molecular analyses, and model organisms to trace which gene changes lead to tumor growth. This work addresses a gap because existing models usually show a different, more immunogenic type of EBV latency than is seen in many human tumors.
Who could benefit from this research
Good fit: People with EBV-positive B‑cell lymphomas (for example, EBV+ Burkitt lymphoma, Hodgkin lymphoma, or EBV+ diffuse large B‑cell lymphoma) or patients willing to donate tumor or blood samples for research would be most relevant.
Not a fit: Patients with EBV-negative lymphomas or those needing immediate clinical treatment are unlikely to get direct or near-term benefit from this basic laboratory research.
Why it matters
Potential benefit: If successful, this work could explain why different EBV-linked B‑cell lymphomas form and point to new markers or targets that may lead to better tests or treatments for people with these cancers.
How similar studies have performed: Prior EBV research has largely produced models with a highly immunogenic (type III) latency, so creating stable models for the type I and II latency seen in many human tumors is a novel and partly untested approach.
Where this research is happening
Madison, United States
- University of Wisconsin-Madison — Madison, United States (Active)
Researchers
- Principal investigator: Kenney, Shannon Celeste — University of Wisconsin-Madison
- Study coordinator: Kenney, Shannon Celeste
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.