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Xingyang Xue

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    P1.13 - Targeted Therapy (Not CME Accredited Session) (ID 945)

    • Event: WCLC 2018
    • Type: Poster Viewing in the Exhibit Hall
    • Track:
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/24/2018, 16:45 - 18:00, Exhibit Hall
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      P1.13-24 - EGFR-KDD is Rare and Demonstrates Variable Anti-Tumor Response to Tyrosine Kinase Inhibitors in East Asian NSCLC Population (ID 13253)

      16:45 - 18:00  |  Author(s): Xingyang Xue

      • Abstract
      • Slides


      The kinase domain duplication of epidermal growth factor receptor (EGFR-KDD) has been identified and implicated to be oncogenic in non-small cell lung cancer (NSCLC). However, its frequency and clinical outcomes in lung cancer patients are largely uncertain.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      We conducted a multi-center record review of 8064 East Asian NSCLC patients who underwent genetic testing using next-generation sequencing (NGS) targeting the whole exons of EGFR gene as well as introns involved in EGFR-KDD and gene rearrangements. Patients’ demographic and clinical data, including age, gender, histology type, pathological stage, and their responses to tyrosine kinase inhibitor (TKI) treatments were analyzed.

      4c3880bb027f159e801041b1021e88e8 Result

      EGFR-KDD was identified in 11 patients, which is approximately 0.012% of the total NSCLC population reviewed (N=8064), and also consists of 0.05% of all patients with EGFR aberrations (N=2289). Nine patients were identified with the canonical EGFR-KDD form involving the duplication of exon 18 throughout exon 25, while the remaining two cases harbor EGFR exon 14-26 and exon 17-25 duplication, respectively, which have not been previously described. Importantly, all these patients were not identified with any other co-existing known driver mutations, highlighting the potential oncogenic role of this alteration. Three out of five patients with exon 18-25 KDD who received TKI treatments showed partial anti-tumor responses to the therapy, while the other two patients progressed shortly. Our data further indicated that EGFR T790M mutation and EGFR amplification may represent the major resistance mechanisms against targeted therapy in tumors bearing EGFR-KDD.

      8eea62084ca7e541d918e823422bd82e Conclusion

      EGFR-KDD is rare in East Asian NSCLC population with different duplication variants. Tyrosine kinase inhibitors demonstrated variable anti-tumor efficacy in patients harboring EGFR-KDD alteration.


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