Author of

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  P76 - Targeted Therapy - Clinically Focused - EGFR (ID 253)

  • Event: WCLC 2020
  • Type: Posters
  • Track: Targeted Therapy - Clinically Focused
  • Presentations: 1
  • Moderators:
  • Coordinates: 1/28/2021, 00:00 - 00:00, ePoster Hall

  • 36338

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    P76.01 - Impact of Clinicopathological Features on Efficacy of Osimertinib in Advanced NSCLC Patients With EGFR Mutations (ID 681)

    00:00 - 00:00  |  Presenting Author(s): Yubo Wang
    • Abstract
    • Slides

    Introduction
    

    Osimertinib, a third-generation EGFR-TKI, has been emerged as the standard selection of NSCLC patients with T790M positive who progressed on prior EGFR-TKI treatments. However, the efficacy of osimertinib varies from different patients. Whether the clinicopathological features of patients can predict the efficacy of osimertinib still remains unclear.

    Methods
    

    We retrospectively enrolled 173 advanced EGFR mutated NSCLC patients from Jan 2015 to May 2018 who received osimertinib treatment after progressed on prior first-generation EGFR-TKI treatment. Clinicopathological features and clinical outcomes were analyzed. Plasma samples were obtained from 46 patents at the time of progression after first-generation EGFR-TKI treatment and analyzed by NGS.

    Results
    

    In the 173 patients treated with osimertinib, we found out that there was no significantly relationship between age, gender, smoking history and the PFS of osimertinib (all p>0.05). However, patients with less lesions (number of lesions ≤4) and smaller lesions (volume of lesions ≤14.3 cm²) had longer PFS of osimertinib (both p<0.05). Patients who reached PR or CR after 2 months of osimertinib treatment seemed to have longer PFS of osimertinib than those who didn’t reach, although the difference wasn’t significant (15.2m vs 10.0m, p=0.1505). It was also interestedly found out that patients who had benefited longer from prior first-generation EGFR-TKI treatment (PFS of first-generation EGFR-TKI >9 months) also had longer PFS of osimertinib markedly (11.3m vs 7.0m, p<0.0001). Moreover, cut-off values of active-EGFR mutant allele frequency (MAF), T790M MAF and T790M/active-EGFR MAF ratio were 2.7%, 3.1% and 0.3 calculated by X-tile, respectively. The median PFS of osimertinib in lower active-EGFR MAF (≤2.7%) group was remarkably longer than those in higher group (16.0m vs 7.0m, p=0.0006). Patients with lower T790M MAF (≤3.1%) also had longer median PFS of osimertinib than those in higher group (15.8m vs 6.8m, p<0.0001). However, patients with T790M/active-EGFR MAF ratio >0.3 seemed to benefit longer from osimertinib than those in MAF ratio ≤0.3 group (13.5m vs 11.0m, p=0.0114). Finally, we also discovered that less number of co-mutations (≤4), without TP53 mutation and EGFR amplification might result in longer PFS of osimertinib.

    Conclusion
    

    The longer PFS of prior first-generation EGFR-TKI might also result in the longer PFS of osimertinib. Moreover, active-EGFR MAF, T790M MAF and T790M/active-EGFR MAF ratio might be potential markers of outcome in patients treated with osimertinib.

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