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R. Tsuzuki



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    P3.02b - Poster Session with Presenters Present (ID 494)

    • Event: WCLC 2016
    • Type: Poster Presenters Present
    • Track: Advanced NSCLC
    • Presentations: 1
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      P3.02b-036 - The Predictive Factors for Post-Progression Survival after EGFR-TKI Failure in Advanced EGFR-Mutant Lung Cancer Patients (ID 4822)

      14:30 - 14:30  |  Author(s): R. Tsuzuki

      • Abstract

      Background:
      The treatment strategy of EGFR-mutant non-small-cell lung cancer (NSCLC) with acquired tolerance for epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) is crucial. In that situation, we have various treatment options in clinical practice. We think predictive factors affecting for post-progression survival (PPS) after the failure of EGFR-TKI will provide useful information to clinicians regarding decision of next treatments. However, there were quite a few studies assessing predictive factors associated with PPS.

      Methods:
      We enrolled 85 consecutive advanced or recurrent NSCLC patients with harboring an EGFR mutation treated with EGFR-TKIs (gefitinib, erlotinib or afatinib) and experienced progressive disease (PD) at our institution between February 2004 and May 2016. We evaluated the patient characteristics, progression sites and the treatments following EGFR-TKIs. Progression sites were divided into two groups at each site, the appearance of new lesions (NLs) or the progression of existing lesions (ELs). PPS was calculated from the date of PD after initiation of EGFR-TKIs to the date of patient’s death.

      Results:
      Among 85 patients, 78 (91.8%) had major EGFR mutation and 64 (75.3%) received EGFR-TKIs as their first-line treatment. The progression sites (NLs, ELs) were lung (18.8%, 28.2%), central nerve system (CNS) (18.8%, 15.3%), bone (7.1%, 10.6%) and others (5.9%, 3.5%). Next treatments following EGFR-TKIs failure were continuation of the same EGFR-TKI; 27 (31.8%), switch to another EGFR-TKI; 24 (28.2%), switch to cytotoxic agents; 19 (22.4%), addition of cytotoxic non-platinum agents to EGFR-TKI; 8 (9.4%) and best supportive care; 7 (8.2%), respectively. Local therapies such as radiotherapies were included in each treatment. Median PPS was 342 days. The patients over 70 years old were comparable with those in younger patients (median PPS: ≥ 70 vs. < 70 years = 338.7 vs. 333.5 days, p = 0.705). Major EGFR mutation was associated with significantly longer PPS (297.9 vs. 85.7 days, p = 0.021). The patients who exhibited CNS-NLs progression showed the tendency for longer PPS (median PPS: NLs vs. ELs vs. non-progression of CNS = 619.0 vs. 237.1 vs. 300.2 days, p = 0.080).

      Conclusion:
      Major EGFR mutation and the new appearance of CNS lesions may be predictive factors for longer PPS after the failure of EGFR-TKIs.