Researchers believe they have found a “kill switch” that can trigger the death of cancer cells in new research.
Scientists at the UC Davis Comprehensive Cancer Center in Sacramento, California, identified a protein on the CD95 receptor, a protein within a cell that receives and transmits signals, that can “program” cancer cells to die, as detailed in a study published in the journal Cell Death & Differentiation last month.
A press release from UC Davis reports that CD95 receptors, also referred to as Fas, have gained the nickname “death receptors” because they send a signal that causes cancer cells to “self-destruct.”
“Previous efforts to target this receptor have been unsuccessful. But now that we’ve identified this epitope (target), there could be a therapeutic path forward to target Fas in tumors,” Jogender Tushir-Singh, an associate professor in the Department of Medical Microbiology and Immunology and senior author of the study, said in the release.
Experts hope that future cancer drugs could boost the activity of these receptors in order to better combat cancer and cancerous tumors, which have been treated historically with surgery, chemotherapy and radiation therapy, all of which are extremely hard on the human body.
Immune-based therapies, such as chimeric antigen receptor T-cell therapy, have been shown to be effective for a subset of patients but have had limited effectiveness against many cancer types.
“Despite being decently successful in liquid tumors, such as leukemia spectrum cancers, long-term remission remains the biggest challenge for CAR T-cell therapies,” Tushir-Singh told Fox News.
However, CAR T-Cell therapy, which typically costs $500,000 or more, has only shown “meager success” in treating solid tumors, which the new discovery could theoretically solve for, making it “a potential one-two punch against tumors.”
“Our study strongly provides a comprehensive takeaway and potential solution to transform the meager success of CAR-T therapies into potentially successful [therapies for] solid tumors,” researchers wrote.
So far, no CD95-boosting drugs have made it into clinical trials
“Despite many breakthroughs in the cancer immunotherapeutic field, targeting Fas remains neglected, primarily due to fear of retaliation against immune-system T-cells,” Tushir-Singh told Fox News.
The study also had several limitations, with limited data from clinical trials. However, Tushir-Singh pointed out that cancer researchers can now go back and collect human tumor samples from clinical trials and perform new analyses in light of these findings.
“It is evident that the success of CAR-T therapy relies on off-target killing by Fas,” he told Fox News. “With the current information, we researchers and doctors should screen potential cancer patients — who would be undergoing CAR-T therapy — to check for the comprehensive presence of Fas on their tumors.”
“If a patient lacks Fas expression in his or her tumors, we need to find ways to safely manipulate these tumors and start making them Fas before giving costly CAR therapies. The latter would likely make the CARs more potent in long-term efficacy,” he wrote.
Looking ahead, Tushir-Singh said he is hopeful for the future of cancer treatments.
“Due to the advent of cancer immunotherapy and other targeted therapies, cancer rates overall in the past decades have decreased significantly,” he said. “I read every day the outstanding research that is happening in the U.S. to beat cancer. People should stay positive.”
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