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E. Felip

Moderator of

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    4th ESO Lung Cancer Observatory: Innovation and care in the next 12 months (ID 49)

    • Event: ELCC 2017
    • Type: Special session
    • Track:
    • Presentations: 7
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      Developments in medical oncology: What practice changing studies will mature in 2018? (ID 144)

      16:45 - 18:15  |  Author(s): E. Felip

      • Abstract
      • Presentation

      Abstract not provided

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      Prevention: Are we progressing in anti-tobacco campaigns in the world? (ID 135)

      16:45 - 18:15  |  Author(s): C. Adams

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      Radiation oncology: Will guidelines change? (ID 142)

      16:45 - 18:15  |  Author(s): F. Mornex

      • Abstract
      • Presentation

      Abstract not provided

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      Screening: Where will it be in 2018? (ID 140)

      16:45 - 18:15  |  Author(s): H. de Koning

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      Surgery or radiation: When is it a choice? (ID 141)

      16:45 - 18:15  |  Author(s): U. Pastorino

      • Abstract
      • Presentation

      Abstract not provided

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      The patient’s perspective (ID 145)

      16:45 - 18:15  |  Author(s): F. Johansson

      • Abstract
      • Presentation

      Abstract not provided

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      What to ask your pathologist today and in 2018? (ID 143)

      16:45 - 18:15  |  Author(s): K. Kerr

      • Abstract
      • Presentation

      Abstract not provided

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Author of

  • +

    4th ESO Lung Cancer Observatory: Innovation and care in the next 12 months (ID 49)

    • Event: ELCC 2017
    • Type: Special session
    • Track:
    • Presentations: 1
    • +

      Developments in medical oncology: What practice changing studies will mature in 2018? (ID 144)

      16:45 - 18:15  |  Author(s): E. Felip

      • Abstract
      • Presentation

      Abstract not provided

      Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.

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    Immunotherapies and targeted therapies in advanced NSCLC (ID 39)

    • Event: ELCC 2017
    • Type: Proffered Paper session
    • Track:
    • Presentations: 1
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      84O - Atezolizumab as first-line (1L) therapy for advanced non-small cell lung cancer (NSCLC) in PD-L1–selected patients: Efficacy data from the BIRCH trial (ID 367)

      14:45 - 16:15  |  Author(s): E. Felip

      • Abstract
      • Slides

      Background:
      Atezolizumab (atezo) inhibits binding of PD-L1 to its receptors, PD-1 and B7.1, restoring tumor-specific T-cell immunity and leaving the PD-L2/PD-1 interaction intact. This single-arm Phase II study (BIRCH; NCT02031458) was designed to evaluate atezo monotherapy in PD-L1–selected patients with advanced NSCLC. A previous analysis (median follow-up, 8.5 months) demonstrated clinical activity in chemotherapy-naive 1L and 2L+ PD-L1–selected patients. Here we present updated efficacy data for 1L patients.

      Methods:
      Eligible patients had PD-L1–selected advanced-stage NSCLC, with no prior chemotherapy or CNS metastases. PD-L1 was centrally evaluated using the VENTANA SP142 IHC assay. Enrolled patients expressed PD-L1 on ≥ 5% of tumor cells (TC) or tumor-infiltrating immune cells (IC), ie, TC2/3 or IC2/3. Those with EGFR mutation or ALK rearrangement must have had prior treatment with an appropriate TKI. Atezo was administered (1200 mg IV q3w) until radiographic disease progression or unacceptable toxicity. The primary endpoint was independent review facility (IRF)–assessed ORR; secondary endpoints included investigator (INV)-assessed ORR, DOR, PFS (RECIST v1.1) and OS.

      Results:
      With a median duration of survival follow-up of 22.5 months, INV-assessed ORR was 25% in TC2/3 or IC2/3 (all treated) patients and 34% in TC3 or IC3 patients (Table). Median OS was 23.5 months in all treated patients and 26.9 months in the TC3 or IC3 subgroup. Responses were observed in both EGFR and KRAS mutant and wild-type tumors. The safety profile was consistent with previous atezo NSCLC studies.

      Conclusions:
      With a median follow-up of 22.5 months, atezo continued to demonstrate durable clinical benefit in 1L NSCLC, in both EGFR and KRAS mutant and wild-type tumors. These results support ongoing Phase III trials evaluating atezo vs chemotherapy in 1L NSCLC.rnTable: 84Orn

      rnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrn
      Endpoint (95% CI)TC3 or IC3[a] (n = 65)TC2/3 or IC2/3[b] (n = 138)
      INV ORR, %34%25%
      (22.6-46.7)(18.4-33.5)
      EGFR mutant/wild type, ORR, %25%/31%31%/22%
      KRAS mutant/wild type, ORR, %38%/30%31%/22%
      Median DOR, moNE16.5
      (8.5-NE)(9.9-NE)
      Median OS, mo26.923.5
      (12.0-NE)(18.1-NE)
      12-mo OS rate, %61.5%66.4%
      (49.0-74.0)(58.1-74.6)
      Median PFS, mo7.37.3
      (4.9-12.0)(5.7-9.7)
      12-mo PFS rate, %36.5%32.5%
      (24.0-48.9)(24.2-40.8)
      rnNE, not estimable.rnaTC ≥ 50% or IC ≥ 10% PD-L1–expressing cells.rnbTC or IC ≥ 5% PD-L1–expressing cells.rn

      Clinical trial identification:
      NCT02031458

      Legal entity responsible for the study:
      F. Hoffmann-La Roche Ltd/Genentech Inc., a member of the Roche Group

      Funding:
      F. Hoffmann-La Roche Ltd/Genentech Inc, a member of the Roche Group

      Disclosure:
      M.C. Garassino: Honoraria, Consulting, Speaker\'s Bureau, research funding, expert testimony, travel expenses: MSD, BMS, AZ, Lilly, Roche. D. Christoph: Honoraria, Speaker\'s Bureau: BI, BMS, Chugai, Novartis, Merck, MSD, Pfizer, Roche; Consulting: BI, BMS, Novartis, Pfizer, Roche; Expert testimony: BI, BMS, Novartis, Pfizer, Roche. J. Chaft: Advisor for Genentech and Astra Zeneca. M.L. Johnson: Consulting: Genentech, Celgene, BI; Research funding: OncoMed, BerGenBio, Lilly, EMD Serono, Kadmon, Janssen, Mirati, Genmab, Pfizer, AZ, Roche/Genentech, Stemcentrix, Novartis, Checkpoint, Array, Regeneron. S. Mocci: Employee, stock: Roche/Genentech. S.N. Gettinger: Consulting: BMS; Research funding: Roche/Genentech, BMS, ARIAD, Incyte, Celldex. E. Felip: Advisory Boards: Lilly, Pfizer, BI, MSD, Roche; Speaker\'s Bureau: AZ, BMS, Novartis. All other authors have declared no conflicts of interest.

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    Poster Display Session (ID 63)

    • Event: ELCC 2017
    • Type: Poster Display Session
    • Track:
    • Presentations: 2
    • Moderators:
    • Coordinates: 5/07/2017, 12:30 - 13:00, Hall 1
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      102P - LUX-Lung 8 phase III trial: Analysis of long-term response to second-line afatinib in patients with advanced squamous cell carcinoma (SCC) of the lung (ID 355)

      12:30 - 13:00  |  Author(s): E. Felip

      • Abstract

      Background:
      In LUX-Lung 8, afatinib (A; 40mg/day) significantly improved OS (median 7.9 vs 6.8 months, p = 0.008) and PFS (2.6 vs 1.9 months, p = 0.010) versus erlotinib (E; 150mg/day) in pts with pretreated SCC of the lung (n = 795). 12-month (36 vs 28%; p = 0.016) and 18-month survival (22 vs 14%; p = 0.013) were significantly higher with A than E, indicating that some pts derive prolonged benefit from A. This is a post-hoc analysis of baseline characteristics and efficacy/safety of A in long-term responders (LTRs; treatment for ≥12 months). Archived tumor samples and serum were analyzed to identify potential biomarkers.

      Methods:
      Tumor samples were retrospectively analyzed using next-generation sequencing (NGS); EGFR expression was determined by IHC. Pre-treatment serum samples were analyzed with VeriStrat[®] and classified as VeriStrat-Good or VeriStrat-Poor.

      Results:
      21/398 pts treated with A were LTRs. Six pts were still on treatment at the time of data cut-off. The median duration of treatment was 17.6 months (range: 12.3–27.6). Baseline characteristics were similar to the overall dataset (median age: 64 y [range: 54–81]; male: 76%; Asian: 29%; ECOG 0/1: 33%/67%; best response to chemotherapy CR or PR/SD: 48%/52%; current and ex-smokers: 90%). Median PFS was 16.6 months (range: 2.8–25.8); median OS was 21.1 months (12.9–31.6). The most common treatment-related AEs (all grade/grade 3) were: diarrhea (81%/5%); rash/acne (71%/5%); stomatitis (29%/5%). AEs generally occurred soon after treatment onset. Six pts had dose reductions due to related AEs. NGS data in ten LTRs will be presented. Genomic aberrations in the ErbB gene family were identified in 50% of these pts (overall dataset: 26.5%). Of 17 pts assessed by VeriStrat, 88% were VeriStrat-Good (overall dataset: 62%). IHC data were available for only one LTR (EGFR-).

      Conclusions:
      Baseline characteristics of LTRs to A were similar to the overall dataset. A conferred median OS of almost 2 years in this subgroup. A was well tolerated with predictable, transient AEs. Though biomarker data look promising, the cohort was too small to identify any clear NGS/VeriStrat predictive signals; further studies are required.

      Clinical trial identification:
      LUX-Lung 8: EudraCT No: 2011-002380-24

      Legal entity responsible for the study:
      Boehringer Ingelheim

      Funding:
      Boehringer Ingelheim

      Disclosure:
      J.C-H. Yang: Ad board and honoraria: BI, Lilly, Bayer, Roche/Genentech/Chugai, Astellas, MSD, Merck Serono, Pfizer, Novartis, Clovis, Celgene, Merrimack, Yuhan Pharmaceuticals, BMS, Ono pharmaceutical Daiichi, Sankyo, and AZ. G. Goss: Participated on advisory boards for AstraZeneca, Boehringer Ingelheim, Pfizer, Eli Lilly, Bristol-Myers Squibb, and Celgene. E. Felip: Participated on advisory boards for Eli Lilly, Pfizer, Roche, MSD, and Boehringer Ingelheim. Felip has receieved lecture fees from AstraZeneca, Bristol-Myers Squibb, and Novartis. A. Ardizzoni: Received honoraria and participated on advisory boards for Bristol-Myers Squibb, MSD, Eli-Lilly, and Boehringer Ingelheim. Ardizzoni has received honoraria from Pfizer and Bayer. S.M. Gadgeel: Participated on advisory boards for Boehringer Ingelheim, Pfizer, Genentech, ARIAD, AstraZeneca, Bristol-Myers Squibb, and Roche. N. Dupuis: Employee of and owns stock in Biodesix. E. Ehrnrooth: Employee of Boehringer Ingelheim. J-C. Soria: Astrazeneca, Astex, GSK, Gammamabs, Lilly, MSD, Merus, Pfizer, Pharmamar, Pierre Fabre, Roche, Sanofi, Servier, Symphogen, Takeda. All other authors have declared no conflicts of interest.

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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): E. Felip

      • 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.