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H.L. Liu



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    P3.01 - Advanced NSCLC (ID 621)

    • Event: WCLC 2017
    • Type: Poster Session with Presenters Present
    • Track: Advanced NSCLC
    • Presentations: 1
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      P3.01-083 - Clinical Characteristics and Survival Outcomes for Non-Small Cell Lung Cancer Patients with Epidermal Growth Factor Receptor Double Mutations (ID 8047)

      09:30 - 09:30  |  Author(s): H.L. Liu

      • Abstract
      • Slides

      Background:
      Multiple randomized clinical trials have demonstrated that epidermal growth factor receptor (EGFR) exon 19 deletion (19Del) and exon 21 L858R mutation (L858R) are highly correlated with sensitivity to epidermal growth factor receptor tyrosine kinase inhibitorsinhibitor (EGFR-TKIs)TKI) treatment in non-small -cell lung cancer (NSCLC). A mutation in exon 20 (T790M) is reportedly associated with resistance to EGFR-TKIs. However, there are few studies have focused on those patients harboring double mutations in these three3 mutation sites.

      Method:
      Between March 2007 toand November 2016, 2546 Chinese patients with non-small cell lung cancer,NSCLC underwent EGFR mutation detections in tumor tissues at three3 medical institutions and were enrolled in this retrospectivelyretrospective study. Clinical characteristics of these patients, including the response to EGFR-TKIs and progression -free survival outcomesoutcome for EGFR-TKIsTKI treatment (PFS-TKIs) of these patientsTKI), were analyzed.

      Result:
      Forty-five patients (45/2546, 1.7%) harbored double mutations of 19Del, L858R, and T790M. Patients with EGFR double mutations were more likely to be non-smoker, PS smokers, have a performance status of 0-1, have adenocarcinoma, and be at stage III-IV. Twenty-four patients with EGFR double mutations received EGFR-TKIsTKI therapy. The objective response rate (ORR), disease control rate (DCR)), and median PFS-TKIsTKI were 25% (6/24), 62.5% (15/24) and 5.95 months, respectively. The ORR, DCR, and median PFS-TKIsTKI in patients with double mutations of 19Del and T790M were 50% (4/8), 75% (6/8)), and 16.5 months, respectively. In those patients with 19Del and L858R, the ORR, DCR, and median PFS-TKIsTKI were 18.2% (2/11), 45.5% (5/11)), and 3.3 months, respectively. The ORR, DCR, and median PFS-TKIsTKI were 0% (0/5), 80% (4/5)), and 3.0 months, respectively, in patients with concomitant mutations of L858R and T790M.

      Conclusion:
      The ORR, DCR, and median PFS-TKIsTKI in patients harboring EGFR double mutations were lower than in patients with a single EGFR -activating mutation. The differences ofin ORR and DCR were statistically insignificant between the three3 groups. Patients with double mutations of 19Del and T790M had longer PFS-TKIs than patients in the other two2 groups.

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