Researchers found that imbalanced p53–RB signaling activates cGAS–STING-mediated immunity, delaying oral cancer progression
Genetic alterations in TP53 and CDKN2A can shape the immune response during early oral cancer development. Researchers from 91̽ reveal that imbalanced p53–RB signaling activated the cGAS–STING pathway, allowing increased inflammatory signaling and infiltration of cytotoxic T cells and natural killer cells. This immune response was associated with delayed progression to invasive oral cancer. The findings highlight how specific tumor-suppressor alterations can influence antitumor immunity and progression during early carcinogenesis.
How a combination of genetic alterations triggers antitumor immunity during early oral carcinogenesis