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Luís Cirnes



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    EP1.01 - Advanced NSCLC (ID 150)

    • Event: WCLC 2019
    • Type: E-Poster Viewing in the Exhibit Hall
    • Track: Advanced NSCLC
    • Presentations: 2
    • Moderators:
    • Coordinates: 9/08/2019, 08:00 - 18:00, Exhibit Hall
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      EP1.01-24 - Lung Adenocarcinoma: Mutational Profile in Ever Smokers and Non-Smokers Patients (ID 2847)

      08:00 - 18:00  |  Author(s): Luís Cirnes

      • Abstract
      • Slides

      Background

      Lung cancer occurring in never-smokers had become a distinct entity. This study aims to evaluate the mutational profile in ever smokers and non-smokers patients with pulmonary adenocarcinoma.

      Method

      Retrospective analysis (Oct-2016 to Aug-2017) of patients diagnosed with pulmonary adenocarcinoma in our pulmonology department.

      Next generation sequencing (NGS) was used to identify different mutations and translocations. Pathological variants of genes and variants of uncertain clinical significance were included.

      Result

      60 patients were enrolled in this study: 18 (30%) non-smokers and 42 (70%) ever smokers.

      In 72.2% of non-smokers and 57.1% of ever smokers were identified at least one mutation. Despite this, ever smokers had an overall higher frequency of mutations (72.6% vs 27.4%) because many patients had concomitant mutations.

      Although not statistically significant, ever smokers had more mutations that are variants of uncertain clinical significance (40% vs 23.5%; p=0,227)

      Table 1. Frequency of mutations

      ___ Non-smoker Ever smokers
      Mutated gene

      Pathological variants

      (n)

      Variants of uncertain clinical significance (n)

      Pathological variants

      (n)

      Variants of uncertain clinical significance (n)
      KRAS 3 0 18 0
      EGFR 5 0 4 5
      ERBB4 0 0 0 1
      MET 0 1 0 3
      PTEN 0 0 1 1
      HER2 1 2 0 7
      PI3KCA 0 1 1 1
      BRAF 0 0 1 0
      ROS 1 0 1 0
      ALK 3 0 1 0
      Total 13 4 27 18
      Conclusion

      Although not statistically significant, smokers and non-smokers appear to have a different mutational profile. Smokers have a higher rate of concomitant mutations, although some of them are variants of uncertain clinical significance. NGS will help to increase knowledge about the mutational profile in these patients.

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      EP1.01-80 - Progressive Disease with T790M Mutation vs Non-T790M Mutation in EGFR Positive Patients Treated with Tyrosine Kinase Inhibitors (ID 2781)

      08:00 - 18:00  |  Author(s): Luís Cirnes

      • Abstract
      • Slides

      Background

      Patients with metastatic non-small cell lung cancer (NSCLC) with a sensitizing EGFR mutation are candidates for treatment with a tyrosine kinase inhibitor (TKI), but acquired resistance is inevitable. The most frequent mechanism of acquired resistance to TKI is the T790M mutation.

      Method

      Retrospective analysis of patients with EGFR mutation treated with TKI who progressed from November 2016 to July 2018, for whom the T790M mutation testing was done through liquid or tissue biopsy.

      Result

      Progression disease was observed in 18 patients. The mean age was 67.1 ± 14.4 years. Twelve patients (66.7%) were female. Ten patients (55.5%) presented the T790M mutation as a resistance mechanism to TKI.

      T790M positive T790M negative p value

      Non-smokers

      Ever smokers

      9 (90%)

      1 (10%)

      2 (25 %)

      6 (75 %)

      0.005

      EGFR mutation

      Exon 18

      Exon 19

      Exon 21

      0 (0%)

      8 (80%)

      2 (20%)

      1(12.5%)

      5(62.5%)

      2 (25%)

      0.604

      Initial TKI

      Gefitinib

      Afatinib

      Erlotinib

      2 (20%)

      0 (0%)

      8 (80%)

      2 (25%)

      3(37.5%)

      3(37.5%)

      0.146

      Response evaluation

      Stable disease

      Partial response

      3 (30%)

      7 (70%)

      6 (75%)

      2 (25%)

      0.119
      PFS with initial TKI - months (mean ± SD) 11 ± 5.3 10 ± 6.9 0.586
      Months treated with initial TKI after disease progression due to clinical benefit (median - IQR) 2 - 5 4 - 3 0.409

      Progressive disease

      Increase of primary lesion size

      Increase of metastasis size

      New intrathoracic lesions

      New extrathoracic ± intrathoracic lesions

      3 (30%)

      3 (30%)

      2 (20%)

      2 (20%)

      3(37.5%)

      2 (25%)

      0 (0%)

      3(37.5%)

      0.465

      Conclusion

      The T790M mutation was the most frequent mechanism of TKI resistance. Non-smokers developed the mutation more often than ex-smokers, although this result was not statistically significant. In the other analyzed variables there were no statistically significant differences.

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