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Molecular mechanisms of ETV1 resistance to EGFR tyrosine kinase inhibitors in SCLC transformation. ETV1 mutations stimulated EGFR signaling during gefitinib and osimertinib treatment and indirectly promoted ASCL1 overexpression, which contributed to neuroendocrine differentiation. EGFR, epidermal growth factor receptor; SCLC, small cell lung cancer; NSCLC, non-small cell lung cancer; ETV1, ETS variant transcription factor 1; ASCL1, achaete-scute homolog 1.
