Our findings suggest that TIGIT and CD96 could be markers of the clinical stage and treatment response of HNSCC. Therefore, administering anti-TIGIT and anti-CD96 after radiotherapy may provide a novel approach for incorporating immunoradiotherapy into HNSCC treatment.
Parallel analyses in human HNSCC cells overexpressing the H3K36M oncohistone reveal conserved disruptions to the epigenome and chromatin architecture. Together, these results establish H3K36 methylation as a pivotal regulator of chromatin state and genomic structure.
These findings establish CCR7 as a key regulator of IL-16-mediated neutrophil recruitment and N2 polarization in HNSCC, highlighting its potential as a therapeutic target to remodel the immunosuppressive tumour microenvironment.