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    12ms
    Genomic correlates of response and resistance to the irreversible FGFR1-4 inhibitor futibatinib based on biopsy and circulating tumor DNA profiling. (PubMed, Ann Oncol)
    In this largest and most systematic analysis of acquired resistance to an FGFR inhibitor from prospective clinical trials, emergence of secondary FGFR2 kinase domain mutations was observed in most patients receiving clinical benefit to futibatinib. ctDNA analysis shows clinically relevant potential as a noninvasive method for assessing genomic profiles, identifying patients who may benefit from FGFR inhibitor treatment, and exploring acquired resistance mechanisms.
    Journal • Circulating tumor DNA • Biopsy
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    TP53 (Tumor protein P53) • FGFR2 (Fibroblast growth factor receptor 2) • FGFR3 (Fibroblast growth factor receptor 3) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B)
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    FGFR1 amplification • FGFR2 mutation • FGFR2 fusion • FGFR2 amplification • FGFR1 rearrangement • FGFR3 amplification • FGFR2 N550K
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    Lytgobi (futibatinib)