Abstract

Introduction: Chemotherapy represents the backbone of treatment of advanced NSCLC; a platinum-based doublet is standard in first-line treatment. But resistance limits the effectiveness of anticancer drugs and is the major cause of relapse and cancer mortality. Cisplatin activates membrane-integrated proteins, like the EGFR. As in more than 60% of NSCLC s EGFR is overexpressed and in about 10% activated by a driver mutation, EGFR is a further target. We tested whether EGFR TKIs influence cisplatin resistance (CR).

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