Authors: Frederico O. Gleber-Netto, Deborah Silverman, Tongxin Xie, Shamima Akhter, Nicole R. Vaughn, Adewale Adebayo, Kala Chand Debnath, Shorook Naara, Shajedul Islam, Erik Knutsen, Emily Lorin Ashkin, Simone Anfossi, Sara Leahey, Patrick Hwu, Sebastien Talbot, Erica K Sloan, Robert Saddawi-Konefka, Roberto Rangel, Jeffrey N. Myers, George A. Calin, and Moran Amit
Advanced Science, 10 February 2026
Researchers use the Maestro Edge system with the Impedance Module to show β-adrenergic signaling enhances immune cell–mediated killing of TP53-deficient HNSCC cells.
Head and neck squamous cell carcinoma (HNSCC) remains difficult to treat, in part due to therapeutic resistance and a lack of reliable biomarkers to monitor response. With approximately 75% of HNSCC cases harboring TP53 mutations, understanding how p53 status influences tumor–immune interactions is critical for improving treatment strategies. In this study, researchers investigated how β-adrenergic signaling affects immune cell function and tumor susceptibility in TP53-deficient HNSCC models.
To quantify immune-mediated tumor cell killing, the team used Axion BioSystems’ multimodal Maestro Edge platform equipped with the Impedance Module to monitor real-time cytolysis in co-cultures of tumor and immune cells. This label-free approach enabled continuous tracking of cell viability and immune activity. The researchers found that β-adrenergic stimulation significantly increased T cell–mediated cytotoxicity in TP53-deficient cells compared to TP53 wild-type controls, with elevated cytolysis observed in the early hours of co-culture.
These findings reveal a functional link between p53 status and β-adrenergic signaling in regulating immune response, highlighting a potential mechanism that could be leveraged to enhance immunotherapy in HNSCC. The study also demonstrates the value of impedance-based assays for capturing dynamic immune–tumor interactions in real time.
