Epithelial–mesenchymal transition (EMT) drives immunotherapy resistance in lung cancer through three interconnected axes: antigen/checkpoint dysregulation, chemokine remodeling, and metabolic reprogramming. We highlight partial EMT (pEMT) as a clinically prevalent hybrid state and biomarker candidate, and metabolic rewiring as an actionable immunometabolic vulnerability. EMT signatures may complement programmed death receptor ligand-1 (PD‑L1), but require treatment-by-biomarker interaction testing. Integrating these axes enables resistance-subtype stratification and precision combination therapy.
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Jin et al. (2026) studied this question.
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