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Scientists may have found a way to help the body’s immune cells fight cancer for longer, potentially making some treatments more effective.
Researchers at the UCLA Health Jonsson Comprehensive Cancer Center found that temporarily boosting a protein called p53 helped specially prepared immune cells stay stronger and kill more melanoma cells in laboratory experiments.
The study, published in Frontiers in Immunology, focused on T cells, which are immune cells that help the body fight disease.
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Some cancer treatments take a patient’s T cells, modify them in a lab so they can recognize cancer, and then return them to the body to attack tumors.
One challenge is that these cells can eventually become “exhausted,” making them less effective at fighting cancer, the UCLA researchers said.
Scientists at UCLA found that temporarily boosting a protein called p53 could help immune cells fight cancer more effectively in laboratory experiments. (iStock)
To address that problem, researchers treated human T cells with an experimental drug called navtemadlin, which temporarily increases the activity of p53, a protein known for helping to prevent cancer.
The treated T cells showed fewer signs of exhaustion, had more energy and developed characteristics that could help them last longer. When tested against melanoma cells in the lab, they were also significantly more effective at killing the cancer cells than untreated T cells, according to the research.
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Kien Vuu, a Los Angeles-based triple board-certified physician and former UCLA assistant clinical professor, confirmed that T-cell exhaustion is one of the biggest challenges encountered with these treatments.
“After repeated encounters with cancer, they become ‘exhausted’ and lose their ability to multiply and attack,” Vuu, who was not involved in the research, told Digital.
Scientists tested an experimental drug called navtemadlin to determine whether it could help T cells resist exhaustion. (iStock)
Vuu said the approach could offer a relatively simple way to strengthen existing treatments.
“The practical appeal is simplicity,” he said. “Rather than adding another genetic modification, this approach adds a drug during the manufacturing step, when a patient’s T cells are being prepared in the lab.”
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If the approach works in further research, Vuu said it could potentially help T cells remain effective for longer, particularly when treating solid tumors.
The findings are still preliminary, however.
The findings remain preliminary, with researchers emphasizing that the experiments involved human cells in a laboratory rather than patients. (iStock)
“This is early, laboratory-stage research,” Vuu acknowledged. “The experiments were done with human cells in a dish against melanoma cells, not in animals or people.”
Researchers will need to test the approach in animals and other types of cancer before moving into clinical trials, according to Vuu.
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The amount of the drug will also need to be carefully studied. The UCLA researchers found that higher doses caused more T cells to die, while lower doses produced the desired effects without substantially reducing the number of healthy cells.
“Dosing is especially important,” Vuu said. “The researchers found that too much p53 activation actually killed more of the T cells, so getting the balance right will be critical.”
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“Patients shouldn’t expect this in the clinic soon, but it’s a promising new direction worth following.”
Digital reached out to the researchers for comment.
