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N. Pardo



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    Poster Display Session (ID 63)

    • Event: ELCC 2017
    • Type: Poster Display Session
    • Track:
    • Presentations: 1
    • Moderators:
    • Coordinates: 5/07/2017, 12:30 - 13:00, Hall 1
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      106P - Brain metastases (BM) development in molecular selected non-small cell lung cancer (NSCLC) patients included in clinical trials (ID 305)

      12:30 - 13:00  |  Author(s): N. Pardo

      • Abstract

      Background:
      The molecular profiling of patients (p) with advanced NSCLC identifies several oncogenic drivers that can be targeted with selective inhibitors. We aimed to assess the characteristics and brain development of p with molecular alterations at our center treated with targeted agents.

      Methods:
      EGFR, KRAS, HER2 mutated p and ALK, ROS1 and RET rearrangements positive p enrolled onto clinical trials between 2009 and 2015 at our center were included in this analysis. A cohort of wild type (WT) adenocarcinoma p was selected as comparator. Overall survival (OS) was estimated by the Kaplan Meier method.

      Results:
      200 p were collected (76 WT, 45 EGFR, 51 ALK, 21 KRAS, 3 ROS1, 2 HER2 and 2 RET). Median age 57 years (26-82), 52% men, 60% performance status (PS) 1, 59% smokers, 98% stage IV and 92% adenocarcinoma. First treatment was selective inhibitor in 73% of EGFR and 58% of ALK p. Median follow up was 23 months (m) (95% CI 1.6-104.6). The OS (immature with 58% of deaths) was 33m for all p and 57m EGFR, 40m ALK, 31m KRAS and 19m WT. We found differences in OS for molecular selected population vs WT (55m vs 19 m p < 0.001), women (55m vs 23m, p = 0.002), PS 0/1 vs PS2 (21 vs 7m, p < 0.001) and non-smokers (51 vs 23 m smokers, p = 0.002). Brain metastases were detected in 86 p (36 ALK, 25 WT, 14 EGFR, 8 KRAS, 2 ROS and 1 RET) and 87% received local therapy. BM were more frequent in women, non-smokers and ALK p (p < 0.001). BM developed at a median of 6m from diagnosis of NSCLC (6m molecular selected and 5m WT, p = 0.44) and median OS after development of BM was 14m (28m EGFR, 26m ALK and 8m WT, p < 0.001). No differences in OS were detected in p with or without BM (p > 0.05). Independently of target agent, we did not found significant differences in OS p with BM treated with local therapy vs systemic treatment (p > 0.005). P who initiated the EGFR and ALK inhibitors after diagnosis of BM had greater benefit than those p who began treatment before diagnosis of BM (86m vs 57m for EGFR and 55m vs 35m for ALK respectively, p > 0.05 in both).

      Conclusions:
      Molecular selected p treated with targeted agents have prolonged survival. Brain metastases is a frequent site of disease progression, but the prognosis of these p is impressive independently of local therapies.

      Clinical trial identification:
      not aplicable

      Legal entity responsible for the study:
      N/A

      Funding:
      N/A

      Disclosure:
      All authors have declared no conflicts of interest.