Abstract

Background: Osimertinib is a third generation EGFR inhibitor approved as first-line treatment for patients with exon 19 or specific exon 21 variants. While this therapy has proven efficacy, resistance to treatment inevitably occurs in patients. One reported resistance mechanism following first-line osimertinib treatment is an acquired TRIM24-BRAF fusion. While molecular studies to identify this and other genomic alterations have been performed, no actionable in vivo model of this resistance mechanism has been widely available for testing.

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