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- W2896277158 abstract "While the elucidation of the mechanisms of acquired resistance to 1st and 3rd generation EGFR-TKI progresses, there have been few clinical investigations into the mechanisms of acquired resistance to 2nd generation EGFR-TKI, afatinib. We analyzed 20 patients with advanced lung adenocarcinoma who acquired resistance to afatinib including EGFR-TKI re-challenge. We examined EGFR T790M, C797S, BRAF V600E, MET amplification by MBP-QP method and droplet digital PCR using ctDNA and re-biopsy samples at pre and post afatinib treatment. Just before afatinib treatment, 15 patients were T790M negative, and 5 were positive with ctDNA. Among T790M negative patients, 40.0% (6/15) turned to positive at PD to afatinib. T790M positive patients showed synchronous change of T790M allele frequency with treatment efficacy of afatinib. C797S was not detected just before afatinib treatment, and it appeared in 3 patients with very low level of allele frequency. Two of 3 patients were both C797S and T790M positive, who achieved PR to osimertinib. However, PFS with these patients was a trend shorter than T790M only. BRAF V600E was detected in one patient at PD to afatinib. MET amplification was never detected in this study. T790M was related with acquired resistance to afatinib like 1st generation EGFR-TKI, but the frequency is relatively lower. The influence of C797S for resistance to afatinib would be less than T790M, but existence of C797S possibly causes shorter PFS of osimertinib." @default.
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- W2896277158 date "2018-10-01" @default.
- W2896277158 modified "2023-09-30" @default.
- W2896277158 title "P3.13-18 Mechanisms of Acquired Resistance to Afatinib Clarified with Liquid Biopsy" @default.
- W2896277158 doi "https://doi.org/10.1016/j.jtho.2018.08.1858" @default.
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