New VHL tumor-suppressor signaling in kidney cancer
Official title: New Von Hippel Lindau (VHL) tumor suppressor signaling in renal cancer
Funded at Ut Southwestern Medical Center · NIH-11380777 · Data updated 2026-11-12
This project looks at why a common kidney cancer (ccRCC) resists treatment and how changes in a gene called VHL and a chemical tag on RNA might open new ways to fight it.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Ut Southwestern Medical Center NIH-funded |
| Lab location | 1 site (Dallas, United States) |
| Project start | August 7, 2024 |
| Project end | July 31, 2029 |
| Funding year | 2026 |
| Award (this year) | $1,591,046 |
| NIH project number | 4R01CA294636-03 |
| Project ID | NIH-11380777 on NIH RePORTER |
Who could benefit from this research
✓Could help
Patients whose kidney cancer shows loss of VHL function and related molecular features may be most relevant.
✕Less likely to help
Patients whose tumors do not involve VHL-related pathways may see limited direct benefit.
What this research studies
Patients with clear cell renal cell carcinoma often respond poorly to today’s therapies. The research will explore how loss of the VHL gene affects cancer behavior through RNA methylation (m6A) and its impact on the PI3K pathway. By comparing kidney cancer cells with and without VHL, scientists will map changes in gene expression and identify VHL-dependent vulnerabilities. The study uses techniques like m6A RIP-Seq and RNA-Seq to uncover regulatory networks that could reveal new therapeutic targets. If successful, these findings could guide development of treatments for patients whose tumors rely on this VHL-m6A axis.
Why it matters
Potential benefit: It could lead to new targets and strategies to treat VHL-deficient kidney cancer and overcome therapy resistance.
How similar studies have gone: Preliminary data suggest m6A RNA modifications and VHL interactions may influence renal cancer biology, with some related findings supporting this approach but the exact mechanism is being explored.
Where this research is happening
-
Ut Southwestern Medical Center
Dallas, United States Active
Researchers
- Principal investigator: Zhang, Qing — Ut Southwestern Medical Center
- Study coordinator: Zhang, Qing
Related research
Other NIH-funded projects on the same topics.
-
Profilin as a Target to Normalize Tumor Vessels in Kidney Cancer
A new approach aims to curb blood vessel growth in a common kidney cancer by targeting a protein called Profilin 1 to improve how blood vessels form in tumors.
-
Overcoming obesity-related resistance to immunotherapy in kidney cancer
A study aims to understand why obesity affects how well immunotherapy works for people with advanced kidney cancer and how to improve treatments for those patients.
-
Copper-driven metabolism in clear cell kidney cancer relapse
This grant studies how copper metabolism affects the growth and relapse of clear cell renal cell carcinoma to identify new ways to help patients after surgery.
-
Targeting epigenetic drivers in clear cell kidney cancer
A doctor-scientist at Johns Hopkins is exploring how epigenetic changes shape kidney cancer and whether new therapies can target these changes.
-
Targeting profilin to normalize blood vessels in kidney cancer
This work tests whether blocking a protein called profilin can normalize tumor blood vessels and help people with clear cell kidney cancer.
-
Copper and kidney cancer progression
Researchers are looking at whether copper changes how clear cell kidney cancer cells make energy and helps tumors grow or come back.
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.