Virtual Library

Start Your Search

R. Palmero



Author of

  • +

    Poster Display session (Friday) (ID 65)

    • Event: ELCC 2018
    • Type: Poster Display session
    • Track:
    • Presentations: 1
    • Moderators:
    • Coordinates: 4/13/2018, 12:30 - 13:00, Hall 1
    • +

      159P - Clinical activity of afatinib in a cohort of patients with lung adenocarcinoma harbouring uncommon EGFR mutations: A Spanish retrospective multicentre study (ID 269)

      12:30 - 13:00  |  Author(s): R. Palmero

      • Abstract

      Background:
      Uncommon EGFR mutations (u-EGFRm) in exons 18–21 account for 12–15% of overall EGFR mutations in non-small cell lung cancer (NSCLC). Afatinib has shown activity against some u-EGFRm, especially G719X, L861Q, and S768I; although other u-EGFRm (Ins20, de novo T790M) have a lower likelihood of response. U-EGFRm are a heterogeneous group of molecular alterations and have also been reported as co-mutations with other EGFR mutations (complex mutations). We examined the molecular and clinical characteristics and efficacy of afatinib in a cohort of patients with advanced NSCLC patients carrying u-EGFRm in Spanish clinical practice.

      Methods:
      Medical records of 67 NSCLC patients with u-EGFRm treated with afatinib between 2012 and 2017 at 23 Spanish institutions were reviewed. U-EGFRm were analysed as complex mutations (Group A), Ins20 (Group B), or single mutations (Group C). Efficacy data were evaluated in terms of tumour response and overall survival (OS).

      Results:
      Of the 67 patients, 96% were Caucasian, all were adenocarcinoma, 46% were never smokers and 37% were former smokers, 79% were Stage IV at diagnosis, 79% had ECOG PS 0–1. Group A complex u-EGFRm consisted of double mutations of G719X + E709F, G719X + S768I, G719X + L861Q, L858R + T790M, L858R + S768I, Del19 + S768I, Del19 + L747S, or R776C + L861Q. No differences in clinical characteristics were found between Group A (n = 20), Group B (n = 23), and Group C (n = 24). Afatinib was administered as 1st line therapy in 80% of patients. Median time on therapy was 4.2 months (range 2.0–12.9). Eighteen percent of patients started afatinib at a reduced dose and 24% of patients required a dose reduction. Response to afatinib was significantly higher in Group A and C (70% and 54%, respectively), compared with Group B (13%; pairwise comparison p < 0.001 and 0.013, respectively, Table). Median OS (mOS) for the entire cohort was 19.9 months (9.7–30.1). Hazard ratio for OS were 0.27 (95% CI 0.10-0-71; p = 0.009) and 0.40 (95% CI 0.17–0.95; p = 0.037) for Group A and C compared to Group B, respectively.

      u-EGFRmGroup A (complex)n = 20Group B (Ins20)n = 23Group C (other)n = 24
      Response to afatinib, n (%)
      Complete response1 (5.0)0 (0)1 (4.2)
      Partial response13 (65.0)3 (13.0)12 (50.0)
      Stable disease3 (15.0)8 (34.8)5 (20.8)
      Progressive disease0 (0)10 (43.5)3 (12.5)
      Not evaluable3 (15.0)2 (8.7)3 (12.5)
      mOS (95% CI), months28.8 (20.7–36.8)10.7 (6.2–15.3)19.9 (10.8–29.0)
      p = 0.014


      Conclusions:
      In clinical practice, afatinib was active in u-EGFRm NSCLC, particularly in complex and single mutations. Further strategies are needed for patients with ins20, a subgroup u-EGFRm with a lower clinical benefit from afatinib.

      Clinical trial identification:


      Legal entity responsible for the study:
      Hospital Germans Trias i Pujol, Badalona, Barcelona, Spain

      Funding:
      Has not received any funding

      Disclosure:
      All authors have declared no conflicts of interest.