How kidney cancer hides from the immune system
Official title: Genetic Mechanisms Controlling Kidney Cancer Immune Escape
Funded at Emory University · NIH-11299576 · Data updated 2026-11-12
Researchers are looking for genetic changes in kidney tumors that let the cancer hide from immune cells in people with clear cell kidney cancer.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Emory University NIH-funded |
| Lab location | 1 site (Atlanta, United States) |
| Project start | April 1, 2024 |
| Project end | March 31, 2029 |
| Funding year | 2026 |
| Award (this year) | $409,045 |
| NIH project number | 5R01CA280069-03 |
| Project ID | NIH-11299576 on NIH RePORTER |
Who could benefit from this research
✓Could help
People with clear cell renal cell carcinoma who can provide tumor tissue from surgery (particularly T3-stage tumors) are the most suitable candidates.
✕Less likely to help
Patients with non-clear-cell kidney cancers, those without available tumor tissue, or those not undergoing surgical treatment are unlikely to be directly included or to benefit immediately.
What this research studies
Researchers will sort pure cancer cells from human clear cell kidney tumors and read their RNA to find gene changes linked to weak immune responses. They focus on small immune niches at the tumor border that support TCF1+ stem-like CD8 T cells, which help keep an ongoing attack on the cancer. By comparing tumor-cell gene activity from many patients, the team aims to find cancer-acquired changes that prevent these immune niches from forming. The findings could point to ways to restore the niche or make immunotherapy work better for more patients.
Why it matters
Potential benefit: If successful, this work could identify tumor genes that block immune-supporting niches and suggest new targets to improve responses to immunotherapy in kidney cancer.
How similar studies have gone: Prior studies showed the TCF1+ CD8 immune niche and its link to outcomes, but using purified tumor-cell RNA from a large patient set to find the genetic causes of niche loss is a newer approach.
Where this research is happening
-
Emory University
Atlanta, United States Active
Researchers
- Principal investigator: Kissick, Haydn — Emory University
- Study coordinator: Kissick, Haydn
Related research
Other NIH-funded projects on the same topics.
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Maximizing anti-tumor immune responses in kidney cancer
A cutting-edge program at UT Southwestern aims to speed up better immunotherapy options for kidney cancer by studying how to activate both innate and adaptive immune responses.
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Kidney Cancer Career Enhancement Program (CEP) at DF/HCC
A career-boosting program supports junior investigators studying kidney cancer to help them advance in basic, translational, and clinical work.
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Kidney Cancer Development Program at DF/HCC
A funded program at Dana-Farber/Brigham and Women’s Kidney Cancer Center supports new ideas from researchers to improve understanding and treatment of kidney cancer.
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Personalized antigens for kidney cancer therapy
This grant explores identifying and targeting tumor-specific antigens in kidney cancer to develop more effective, personalized immunotherapies.
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Optimizing Anti-PD1 Therapy for High-Risk and Metastatic Kidney Cancer
A large cancer research grant is testing how best to use anti-PD-1 therapy to help people with high-risk and metastatic kidney cancer live longer and with fewer side effects.
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Targeting the HIF2 Pathway in Kidney Cancer
A cancer treatment program aims to see if a drug called belzutifan can help people with a specific kind of kidney cancer whose growth is driven by the HIF2 pathway.
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.