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Shun Futamura



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    P2.03 - Biology (ID 162)

    • Event: WCLC 2019
    • Type: Poster Viewing in the Exhibit Hall
    • Track: Biology
    • Presentations: 1
    • Now Available
    • Moderators:
    • Coordinates: 9/09/2019, 10:15 - 18:15, Exhibit Hall
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      P2.03-13 - Acquired Resistance to Afatinib in Non-Small Cell Lung Cancer with EGFR G719X Mutation (Now Available) (ID 1057)

      10:15 - 18:15  |  Author(s): Shun Futamura

      • Abstract
      • Slides

      Background

      The frequency of EGFR mutations is said to be relatively high within East Asian population. The most common EGFR mutations such as exon 19 deletions and exon 21 L858R mutation are strong predictors of good response to EGFR-TKIs in non-small-cell lung cancer. Exon 20 T790M mutation which accounts for a large part of 1st and 2nd generation EGFR-TKI resistance, is well known to be detected after failure of prior EGFR-TKI therapy. Furthermore, T790M mutation is a predictor of good response to osimertinib, 3rd generation EGFR-TKI. Meanwhile, other uncommon EGFR mutations are identified, such as exon 18 G719X mutation, exon 20 S768I mutation, and exon 21 L861Q mutation. LUX-Lung study reported afatinib may be effective for these uncommon EGFR mutations, however, their treatments are still controversial and their resistance-gaining mechanisms to EGFR-TKI are also unknown.

      Method

      We evaluated the characteristics of patients with G719X single mutation and their effectiveness of afatinib treatment. Furthermore, we analyzed the mechanism of acquired resistance to afatinib from their re-biopsied samples.

      Result

      Eighteen patients had G719X single mutation, which include fifteen patients with smoking history. Of all patients with G719X mutation, ten patients were treated with afatinib, which response rate was 40% (4/10). Eight patients of those treated with afatinib underwent re-biopsy after failure of the therapy, and their results revealed that G719X mutation was disappeared in six samples, and T790M mutation was not detected after afatinib treatment.

      Conclusion

      As previously reported, the presence of G719X mutation might be used as a predictor of sensitivity to afanitib therapy. Our data suggest that the loss of cancer cells with G719X mutation could be the main mechanism of acquired resistance to afanitib. Furthermore, patients with smoking history were seen frequently in those with G719X mutation. Considering that G719X mutation negative cancer cells may coexist with G719X mutation positive cells in NSCLC patients, smoking might be associated with development of its heterogeneity.

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