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Thongbliew - Prempree



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    P2.03 - Chemotherapy/Targeted Therapy (ID 704)

    • Event: WCLC 2017
    • Type: Poster Session with Presenters Present
    • Track: Chemotherapy/Targeted Therapy
    • Presentations: 1
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      P2.03-026 - Managing EGFR T790M Mutation in Advanced Non-Small Cell Lung Cancers in THAILAND (ID 8898)

      09:30 - 16:00  |  Presenting Author(s): Thongbliew - Prempree

      • Abstract

      Background:
      Acquired Resistance to EGFR-TKI is inevitable to occur to most of NSCLC treated by first generation TKI such as Gefitinib or Erlotinib. There have been many secondary resistance mutations discovered to date including, L747S, D761Y, T790M and T854A . But in our series, the most common secondary resistance mutations was T790M type and was studied in details as to the occurrence, the treatment and the response to the treatment.

      Method:
      42 patients from our own series of advanced Non-small cell lung cancer(NSCLC) , were identified as having EGFR mutations for which TKI was used for the treatment initially. Resistance to first generation TKI was found due to Mutation T790M in exon 20 of EGFR gene . A total of 21 patients 50%(from 42) harbored T790M mutation. Interestingly enough, only 5 cases from classical mutated exon19 EGFR ( 5/22) , 6 cases from classical mutated exon 21 L858R (6/7) and 10 cases from non –classical mutated exon 19 and 21(10/13). The treatment of those who harbored T790M was uniformly given: 1. Multi-targeted method , Bevacizumab and Afatinib second generation TKI 2.Osimertinib, third generation TKI to all patients when failed Afatinib.

      Result:
      At one year time, all 21 patients survived the treatment. Beyond one year with closed follow-up, the results showed, 1. All 5 cases from classical mutated exon 19 and 6 cases from mutated exon 21 survived the disease and continued the treatment with Osimertinib. 2. 1 case from non-classical mutated exon 19 and 21 survived The overall success rate was 5+6+1 = 12/ 21 = 57% All 9 cases who failed the treatment showed progression of cancer .

      Conclusion:
      Patients who harboured T790M mutation from classical mutated exon 19 and exon 21 EGFR continued to respond to the treatment very well clinically. Obviously, Osimertinib was specific for T790M mutation and no further acquired resistance mutation in their cancer cells. But for those who failed Osimertinib treatment they must have additional acquired resistance mutation along with T790M. Future Plan : Consider Immune Checkpoint Treatment