Plate Nº 81 · recorded October 16, 2026
Health & Medicine ResearchReported finding
Turning a Cancer-Driving Protein into an Immune Ally
Cold Spring Harbor Laboratory researchers reported on October 16, 2026 that activating PPARD in immune cells boosted cancer fighting across multiple tumor types in preclinical experiments.
By Priya Raman3 min read607 words
In brief
- Published October 16, 2026 in Nature Immunology by researchers at Cold Spring Harbor Laboratory
- Colorectal cancer has become the leading cause of cancer-related death among people under 50
- Modified CAR T cells slowed or stopped tumor growth in models of colorectal, breast, ovarian cancers and melanoma
- Endometriosis, the next research target, affects approximately one in 10 women worldwide
- The study was led by Semir Beyaz, an assistant professor at Cold Spring Harbor Laboratory
On October 16, 2026, researchers at Cold Spring Harbor Laboratory reported in Nature Immunology that they can flip a protein long known to fuel cancer growth into a weapon against tumors by activating it inside the immune cells that attack them.
The finding carries weight for colorectal cancer patients in particular. The malignancy has become the leading cause of cancer-related death among people under 50, and those with difficult-to-treat forms of the disease have limited options when chemotherapy and newer immunotherapy treatments fail.
What did the scientists actually change?
Semir Beyaz, an assistant professor at CSHL, led the work centered on peroxisome proliferator-activated receptor delta, abbreviated PPARD. This protein governs how cells burn fat for energy by switching genes on or off, a category of regulator researchers call a transcription factor.
The team began with mice carrying colorectal cancer. They observed that cancer cells used PPARD to support their own growth, yet switching the same protein on in nearby immune cells produced the opposite effect. The surrounding tissue shifted in favor of immune attack rather than tumor tolerance.
"We hypothesized that the fitness determinants of cancer and our immune cells may not be so different," Beyaz said. "They're in the same universe. They're constrained by the same chemical and physical rules. So, it's not surprising they'd end up evolving the same way."
Could this strengthen existing immunotherapies?
To test the idea against human cancer, the researchers engineered CAR T cells, a type of immune cell already used as a living drug against certain blood cancers. CAR stands for chimeric antigen receptor, a laboratory-built surface protein that lets the cell recognize a specific target on cancer.
The team activated PPARD inside these modified cells and tested them against three experimental models of human colorectal cancer:
- Organoids, miniature tumors grown from patient tissue
- Cultured cancer cells in laboratory dishes
- Tumors implanted into mice
Across these experiments, the modified CAR T cells slowed or stopped tumor growth. The approach has not yet been proven in patients, and the researchers describe the work as preclinical.
"It's all about cell fitness," Beyaz explained. "What cells eat affects who they are. When immune cells burn more fat, they become more fit for fighting cancer."
Could this reach beyond colorectal cancer?
Colorectal cancer drew the team first because of its growing toll on younger adults. The same approach also showed promising results in models of three additional cancers:
- Breast cancer
- Ovarian cancer
- Melanoma, a serious form of skin cancer
Beyaz described the findings as the "tip of the iceberg" for new ways to strengthen cancer immunotherapy. He suggested that any condition in which the immune system fails to clear diseased cells could benefit.
"Boosting immune cell fitness may also help with other conditions where the immune system fails to clear diseased cells," Beyaz said.
His laboratory is now investigating the approach in endometriosis, a chronic inflammatory condition that affects approximately one in 10 women. Current treatments often fail to provide lasting relief, much like the resistant colorectal tumors that motivated the cancer work.
How can one protein do both?
Beyaz compared PPARD to the Force in Star Wars. The same underlying power can support disease progression in cancer cells, much like Darth Vader serving the Emperor. When activated in immune cells, however, it resembles Anakin Skywalker returning to the light side, turning destruction against the disease itself.
"It's the classic fight between good and evil," Beyaz said. "How can good ultimately prevail? Activating PPARD in immune cells could be the way."
The next test will be whether this cellular flip works inside patients.
via cshl.edu (Original)
More from Priya Raman
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Senior reporter covering people, launches and day-to-day practice in general science news at SciBeat.
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