In a significant breakthrough, scientists in California at the UC Davis Comprehensive Cancer Center in Sacramento claim to have uncovered a ‘kill switch’ capable of triggering the death of cancer cells. The researchers identified a protein on a receptor, specifically CD95 receptors, also known as Fas, which, when activated, releases a signal causing the self-destruction of cells residing on cell membranes—a phenomenon known as death receptors.
The therapeutic approach employed is termed CAR T-cell therapy. This process involves extracting T cells from the patient’s blood, genetically modifying them in a laboratory to generate receptors known as chimeric antigen receptors (CARs), and subsequently reintroducing these modified cells into the patient’s bloodstream.
Jogender Tushir-Singh, an associate professor in the Department of Medical Microbiology and Immunology and the senior author of the study, highlighted the discovery of the critical epitope for cytotoxic Fas signaling and CAR T-cell bystander anti-tumor function.
Although the therapy has shown promising efficacy against liquid cancers such as leukemia and other blood cancers, its success against solid tumors like breast, lung, and bowel cancer has been limited, constituting a major challenge. The researchers acknowledge this limitation but express optimism that the therapy can evolve to target solid cancers in the future.
Tushir-Singh notes that modulating Fas could potentially extend the benefits of CAR T-cell therapy to solid tumors like ovarian cancer. Past attempts to target this receptor have faced obstacles, but with the identification of this epitope, there is now potential for a therapeutic path forward to target Fas in tumors, according to the team’s statement.
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