Abstract
Immune checkpoint inhibitors (ICIs) have revolutionized the treatment of non-small cell lung cancer (NSCLC). KMT2C/TP53 co-mutations have been reported as a potential biomarker to predict responses to ICIs therapy in NSCLC. In the meantime, the tumor microenvironment (TME) also plays a central role in the efficacy and development of resistance to ICIs. But the correlation of KMT2C/TP53 co-mutations with immune signatures remains unclear.
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