RAF1 extrachromosomal DNA amplification confers acquired erlotinib resistance in NSCLC cell model

Despite their clinical significance, EGFR-directed therapies inevitably encounter drug resistance. This study demonstrates that ecDNA-mediated RAF1 amplification reactivates MAPK signaling independently of mutant EGFR, contributing to erlotinib resistance in EGFR-mutant NSCLC cell models. This finding identifies oncogenic amplification by ecDNA as a novel mechanism leading to erlotinib resistance, opening new avenues for therapeutic strategies in NSCLC.

• Type: Cancer Genomics
• Archiver: European Genome-phenome Archive (EGA)