Inhibiting the DNA damage repair of HNSCC cells in combination with normo-fractionated radiotherapy influences clonogenicity, senescence and expression of NK cell activation markers.

Interestingly, UD-SCC-2 cells exhibited a decreasing trend in activation marker expression across all treatments—RT alone, RT + ATMi, and RT + ATRi—demonstrating a divergent response compared to the other cell lines, consistent with their distinct senescence profile (Fig. 2 ).

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