ArticleOncogene2026
Imbalanced p53-RB signaling triggers cGAS-STING-mediated immune activation in early oral cancer development.
Article in Oncogene, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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11 authors.
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Abstract
Combined alterations of TP53 and CDKN2A are frequently observed in head and neck squamous cell carcinoma (HNSCC); however, their cooperative roles in oral carcinogenesis remain unclear. To investigate their interaction under carcinogenic stress, we generated Cdkn2a knock-in (KI) mice harboring a human-relevant R80X truncating mutation, along with Trp53 loss-of-function (LOF) mutants and exposed them to 4-nitroquinoline-1-oxide (4NQO). Partial loss of Cdkn2a combined with Trp53 heterozygosity was associated with increased STING-related inflammatory signaling and enhanced T-cell/NK-cell-associated immune infiltration, coinciding with delayed malignant progression. Enhanced production of proinflammatory cytokines and chemokines further indicated selective activation of the cGAS-STING-NF-κB axis. Analysis of the TCGA-HNSC cohort showed that combined TP53/CDKN2A alterations significantly separated overall survival and were associated with distinct survival patterns. These findings reveal a previously unrecognized mechanism by which imbalanced p53-RB signaling triggers tumor immunity during the early stages of oral carcinogenesis.
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