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N. Reguart

Moderator of

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    Immunotherapies and targeted therapies in advanced NSCLC (ID 39)

    • Event: ELCC 2017
    • Type: Proffered Paper session
    • Track:
    • Presentations: 6
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      Invited Discussant 83O, 84O and 2O (ID 526)

      14:45 - 16:15  |  Author(s): L. Paz-Ares

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      Invited Discussant 85O_PR (ID 528)

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

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      2O - Favorable clinical outcome and response to immunotherapy share a common PD-L1/PD-1 based NSCLC immune contexture (ID 400)

      14:45 - 16:15  |  Author(s): G. Mazzaschi, D. Madeddu, G. Bocchialini, L. Gnetti, G. Armani, F. Sogni, M. Tiseo, A. Ardizzoni, F. Aversa, F. Quaini

      • Abstract
      • Presentation
      • Slides

      Background:
      The success of PD-1/PD-L1 immune checkpoint inhibitors strengthens the notion that tumor growth and regression are immune regulated. According to PD-L1 status and number of Tumor Infiltrating Lymphocytes (TILs), the cancer microenvironment can be classified into four types reflecting immune resistance, ignorance, induction and tolerance. However, an extended tissue characterization of the immune contexture and its predictive/prognostic value in NSCLC remain elusive. The aim of the present investigation was to determine whether immunologically defined classes of NSCLC differentially impact on clinical outcome.

      Methods:
      Histologic sections of NSCLC samples surgically removed to untreated 51 ADC and 69 SCC and 8 ADC and 10 SCC patients receiving Nivolumab were included. PD-L1 (clones 28-8 and SP142) was measured by immunoperoxidase (H-score) and immunofluorescence (QIF). The n/mm[2] and intra-, peri-tumor or invasive margin localization of TILs subpopulations were computed establishing cut off values relative to each phenotype. Immunohistochemical data and clinical records were subjected to Kaplan Meier analysis.

      Results:
      ADC cases had 2-fold higher CD3[pos] and 1.8-fold lower CD4[pos] cells compared to SCC and TILs-rich ADC had 10 months’ increase in OS vs –poor (p < 0.01). EGFR mutation conditioned a lower intratumor density of TILs. The frequency of type I (PD-L1[high] TILs[high]) contexture was low (14.6%) while > 1/3 of NSCLC samples displayed type II (PD-L1[low/neg] TILs[low]), reflecting immune exhaustion. The proportion of type III (PD-L1[high] TILs[low]) and IV (PD-L1[low/neg] TILs[high]) immune categories, with relatively increased Nks and Tregs, was similar. NSCLC type III had the highest OS (35.5 mos.) and PFS (25.7) while in type II immune ignorant cases OS and PFS were respectively 21.7 and 12. Independently from immune categories, patients with PD-1[low] and high CD8/CD3 ratio had 11 mos. gain in OS (p < 0.01) compared to the reverse counterpart. Accordingly, PD-L1[high] and PD-1[low] characterized 86% of patients responsive to nivolumab.

      Conclusions:
      In a dynamic PD-L1 milieu a concomitant intrinsic or therapeutically induced decay of PD-1 receptor allows TILs to escape from PD-L1 pressure and delays tumor progression, improving OS.

      Clinical trial identification:


      Legal entity responsible for the study:
      University Hospital of Parma, Medicine

      Funding:
      University of Parma

      Disclosure:
      All authors have declared no conflicts of interest.

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      83O - A phase II study of durvalumab (MEDI4736) for previously treated patients with stage IV squamous NSCLC (SqNSCLC): Lung-MAP Sub-study SWOG S1400A (ID 279)

      14:45 - 16:15  |  Author(s): V. Papadimitrakopoulou, M.W. Redman, H. Borghaei, S.N. Waqar, F. Robert, G.J. Kiefer, S. McDonough, R.S. Herbst, K. Kelly, D.R. Gandara

      • Abstract
      • Presentation
      • Slides

      Background:
      Durvalumab (MEDI4736) is an engineered human IgG1 mAb targeting programmed cell death ligand-1 (PD-L1). Treatment with other anti-PD-1/PD-L1 antibodies has demonstrated meaningful clinical benefit in patients with advanced NSCLC.

      Methods:
      As part of the Lung Master Protocol S1400, a National Clinical Trials Network group "umbrella" trial for second-line SqNSCLC we conducted a phase II study of durvalumab in patients with Stage IV squamous NSCLC (ECOG PS 0-2; ≥1 prior systemic treatment regimens, including one platinum-based), EGFR/ALK wild-type. The primary endpoint was overall response rate (ORR) (RECIST v1.1); secondary endpoints included duration of response (DoR), ORR among PD-L1 positive patients, disease control rate (DCR), investigator-assessed progression-free survival (PFS), overall survival (OS) and safety (CTCAE v4.03). The initial protocol was a randomized phase II/III comparison of durvalumab to docetaxel, and was amended to be a single arm phase II trial of single agent durvalumab. PD-L1 positive tumors were defined by ≥ 25% of tumor cells with membrane staining.

      Results:
      Of the 68 eligible patients (median [range] age 66 [35-92] years, PS 0/1/2 26%/62%/12%), 11 were responders (16% ORR, 95% Confidence Interval [CI] 7%, 25%). DCR was 54% (CI 43%, 66%), median OS was 11.5 months (CI 10.1-12.4 mos), and median PFS was 2.9 mos (CI 2.0-4.1 mos). Of the 11 responders, median time to response and DoR were 3.6 mos (CI 2.8-4.2 mos) and 18.6 months (95% CI 4.4-NR mos), respectively. Of the 14 PDL1-positive patients, 2 were responders (14% ORR, 95% CI 0%, 33%), DCR was 57% (CI 31%, 83%), median OS and PFS were 10.7 mos (CI 9.2-10.7 mos) and 2.3 mos (CI 1.4-4.9 mos), respectively. Durvalumab showed a manageable safety and tolerability profile; most adverse events (AEs) were low grade and resolved with treatment delay and/or immunosuppressive interventions. Grade ≥3 treatment-related AEs occurred in 23(34%) of patients. Drug-related AEs led to discontinuation in 6 patients (9%, 95% CI 2%, 16%).

      Conclusions:
      Durvalumab demonstrated clinical benefit and durable responses in a previously treated metastatic NSCLC population with manageable toxicity profile. Results are comparable with other anti-PD-1/PD-L1 therapies in metastatic, relapsed NSCLC.

      Clinical trial identification:
      NCT02766335

      Legal entity responsible for the study:
      Southwest Oncology Group/NCTN

      Funding:
      Lung-MAP supported in part by NIH/NCI grants CA180888, CA180819, CA180820, CA180821, CA180868, and by Amgen, AstraZeneca, Bristol-Myers Squibb Company Genentech and Pfizer through the Foundation for the National Institutes of Health, in partnership with Friends of Cancer Research.

      Disclosure:
      V. Papadimitrakopoulou: Advisory Role for: Eli Lilly&Co, Genentech, Janssen Global Sevices, Bristol-Myers Squibb, ARIAD, Astra Zeneca Pharmaceuticals, Novartis, Merck Corporate-sponsored research: Novartis, Astra Zeneca, Genentech, Merck, Janssen, ACEA, Bristol-Myers Squibb. H. Borghaei: Advisory: Bristol-Myers Squibb, Lilly, Genentech, Celgene, Pfizer, EMD-Serono, Boerhinger-Ingelheim, Trovagene, AstraZeneca, Research Support: Millenium, Merck, Celgene. K. Kelly: Advisory: Synta, AstraZeneca, Lilly, Clovis Oncology, ARIAD, Boehringer Ingelheim, Bristol-Myers Squibb, Genentech, G1 Therapeutics. Research: Millenium, Novartis, EMD Serono, Lilly, Genentech, Abbvie, Gilead, Celgene, Five Prime Therapeutics, Transgene. All other authors have declared no conflicts of interest.

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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): S. Peters, E. Carcereny Costa, M.C. Garassino, D. Christoph, T. Kurata, J. Chaft, M.L. Johnson, S. Mocci, S.N. Gettinger, 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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      85O_PR - Patient-reported symptoms and impact of treatment with osimertinib vs chemotherapy for advanced non-small cell lung cancer (ID 373)

      14:45 - 16:15  |  Author(s): C.K. Lee, S. Novello, A. Ryden, A. Templeton, K. Rüdell, H. Mann, S. Ghiorghiu, T. Mok

      • Abstract
      • Slides

      Background:
      We assessed self-reported symptoms of advanced non-small cell lung cancer patients treated with osimertinib 80mg or chemotherapy in the AURA3 phase III clinical trial (NCT02151981).

      Methods:
      Patients completed the European Organisation for Research and Treatment of Cancer QLQ-LC13 questionnaire on disease-specific symptoms and QLQ-C30 on general cancer symptoms, functioning and global health status. QLQ-LC13 was completed at baseline, weekly for 6 weeks, then 3-weekly up to end of study, and at progression. QLQ-C30 was completed at baseline, then 6-weekly up to end of study, and at progression. We compared for differences between treatments in time to deterioration and odds of improvement of symptoms (two assessments ≥18 days apart). A deterioration or improvement was defined as a change in score from baseline of ≥ +/-10. Hazard ratios (HR) and 95% confidence intervals (CI) were calculated using a log-rank test stratified by ethnicity. Odds ratios (OR) and 95% CIs were calculated using logistic regression adjusted for ethnicity.

      Results:
      At baseline, 215 − 228 of 279 (77 − 82%) patients on osimertinib and 106 − 114 of 140 (76 − 81%) on chemotherapy had QLQ-LC13 scores ≤90 (cut-off to have potential for deterioration) for cough, chest pain and dyspnoea. Time to deterioration of key symptoms was longer with osimertinib than with chemotherapy (Table). The proportion of patients with improvement in global health status was higher with osimertinib (80/215 [37%]) than with chemotherapy (23/105 [22%]; OR: 2.11; 95% CI: 1.24, 3.67; p = 0.007), as it was for appetite loss (OR: 2.50; 95% CI: 1.31, 4.84) and fatigue (OR: 1.96; 95% CI: 1.20, 3.22).rnTable: 85O_PRTime to deterioration of selected key symptomsrn

      rnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrn rnrn
      SymptomTreatmentNumber (%) of patients with eventHR (95% CI)p-value
      CoughO99 (46.0)0.74 (0.53, 1.05)0.090
      C58 (54.7)
      Chest painO99 (43.8)0.52 (0.37, 0.73)<0.001
      C66 (58.4)
      DyspnoeaO122 (53.5)0.42 (0.31, 0.58)<0.001
      C84 (73.7)
      rnC, chemotherapy; O, osimertinib.rn

      Conclusions:
      Time to deterioration of key symptoms was longer and more patients had an improvement in global health status with osimertinib treatment than with chemotherapy, demonstrating improved patient outcomes with osimertinib.

      Clinical trial identification:
      NCT02151981

      Legal entity responsible for the study:
      AstraZeneca

      Funding:
      AstraZeneca

      Disclosure:
      C.K. Lee: Served on advisory boards for AstraZeneca. S. Novello: Served on speaker bureaux for AstraZeneca, Boehringer Ingelheim, Bristol-Myers Squibb, Eli Lilly, Merck Sharp & Dohme Limited and Roche. A. Rydén, H. Mann, S. Ghiorghiu: Employees of AstraZeneca and are AstraZeneca shareholders. A. Templeton, K. Rüdell: Former employees of AstraZeneca and former shareholders. T. Mok: Grant/Research Support from AstraZeneca, BI, Pfizer, Novartis, SFJ, Roche, MSD, Clovis Oncology, BMS, Eisai, Taiho; Speaker’s fees with: AstraZeneca, Roche/Genentech, Pfizer, Eli Lilly, BI, MSD, Novartis, BMS; Major Stock Shareholder in: Sanomics Ltd.; Advisory Board for: AstraZeneca, Roche/Genentech, Pfizer, Eli Lilly, BI, Clovis Oncology, Merck Serono, MSD, Novartis, SFJ Pharmaceutical, ACEA Biosciences, Inc., Vertex Pharmaceuticals, BMS, geneDecode Co., Ltd., OncoGenex Technologies Inc., Celgene, Ignyta, Inc.; Board of Directors: IASLC, Chinese Lung Cancer Research Foundation Ltd., Chinese Society of Clinical Oncology (CSCO), Hong Kong Cancer Therapy Society (HKCTS).

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    SCLC: New insights (ID 25)

    • Event: ELCC 2017
    • Type: Educational session
    • Track:
    • Presentations: 4
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      Can brain control be improved beyond PCI? (ID 104)

      11:00 - 12:30  |  Author(s): E. Gkika

      • Abstract
      • Slides

      Abstract not provided

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      New therapies, new era? (ID 105)

      11:00 - 12:30  |  Author(s): N. Reguart

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      What can CDX models teach us? (ID 106)

      11:00 - 12:30  |  Author(s): C. Dive

      • Abstract
      • Slides

      Abstract not provided

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      What is the optimal thoracic radiotherapy in limited stage SCLC? (ID 103)

      11:00 - 12:30  |  Author(s): C. Faivre-Finn

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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    Targeted therapies and immunotherapies (ID 46)

    • Event: ELCC 2017
    • Type: Poster Discussion session
    • Track:
    • Presentations: 8
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      Invited Discussant 89PD, 90PD and 91PD_PR (ID 547)

      14:45 - 15:45  |  Author(s): S. Ekman

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      Invited Discussant 92PD, 93PD and 94PD (ID 548)

      14:45 - 15:45  |  Author(s): N. Reguart

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      89PD - Results from OAK subgroup analyses: A randomized Phase III study of atezolizumab vs docetaxel in patients (pts) with advanced NSCLC (ID 317)

      14:45 - 15:45  |  Author(s): D. Cortinovis, S.M. Gadgeel, A. Rittmeyer, F. Barlesi, M. Cobo Dols, T. Hida, P. He, M. Ballinger, D.R. Gandara, J. von Pawel

      • Abstract

      Background:
      Atezolizumab (atezo) prevents binding of PD-L1 to its receptors PD-1 and B7.1, restoring tumor-specific T-cell immunity. Primary analysis of the Phase III OAK study in previously treated NSCLC showed superior survival with atezo vs docetaxel (doc) in the ITT population (mOS, 13.8 vs 9.6 months; HR, 0.73) and in pts expressing ≥1% PD-L1 on TC or IC (TC1/2/3 or IC1/2/3; mOS, 15.7 vs 10.3; HR, 0.74). Here we present further subgroup analyses.

      Methods:
      OAK evaluated atezo vs doc in PD-L1 unselected NSCLC pts who had failed prior platinum-containing chemotherapy. Pts were stratified by PD-L1 expression, prior chemotherapy regimens and histology and randomized 1:1 to atezo (1200 mg) or doc (75 mg/m[2]) IV q3w. PD-L1 expression by IHC and mRNA was centrally evaluated by VENTANA SP142 IHC assay and Fluidigm, respectively. Data cutoff, July 7, 2016.

      Results:
      In the first 850 of 1225 randomized pts (primary study population), OS was improved with atezo vs doc regardless of histology, and this benefit was seen across PD-L1 subgroups within each histology (Table). Similar OS was seen regardless of PD-L1 expression as assessed by mRNA and IHC. ORR was 14.4% vs 15.2% in non-squamous (non-sq) pts and 11.6% vs 8.2% (atezo vs doc) in squamous (sq) pts. Improved OS was seen with atezo vs doc across subgroups, including pts with treated baseline brain metastases (n = 85; mOS, 20.1 vs 11.9 mo; HR, 0.54; 95% CI, 0.63, 0.89) and never smokers (n = 156; mOS, 16.3 vs 12.6 mo; HR, 0.71; 95% CI, 0.47, 1.08). Further secondary endpoints and exploratory biomarker analyses for these subgroups and by age and EGFR/KRAS status will be presented.

      Conclusions:
      OAK demonstrated clinically relevant improvements with atezo in the ITT population, including in both histology subgroups, regardless of PD-L1 expression (measured by IHC or tumor gene expression), and among other subgroups, including never smokers and pts with baseline brain metastases.rnTable: 89PDrn

      rnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrn rnrn
      rnOS
      AtezoDocHR[a] 95% CI
      nMedian, monMedian, mo
      Non-sq population
      TC3 or IC34922.5478.70.35 (0.21, 0.61)
      TC2/3 or IC2/38918.79911.30.61 (0.42, 0.88)
      TC1/2/3 or IC1/2/317117.616211.30.72 (0.55, 0.95)
      TC0 and IC014014.015011.20.75 (0.57, 1.00)
      All non-sq31315.631511.20.73 (0.60, 0.89)
      Sq population
      TC3 or IC32317.51811.60.57 (0.27, 1.20)
      TC2/3 or IC2/34010.4379.70.76 (0.45, 1.29)
      TC1/2/3 or IC1/2/3709.9608.70.71 (0.48, 1.06)
      TC0 and IC0407.6497.10.82 (0.51, 1.32)
      All sq1128.91107.70.73 (0.54, 0.98)
      rnaUnstratified HRs.rnTC, tumor cell; IC, tumor-infiltrating immune cell.rn

      Clinical trial identification:
      NCT02008227

      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:
      S.M. Gadgeel: Speaker\'s bureau from Astra-Zeneca, Genentech/Roche and Advisory Boards from Astra-Zeneca, Ariad, Pfizer, Bristol Myers- Squibb and Genentech/Roche. A. Rittmeyer: Grants as an advisor or speaker by Astra Zeneca, BMS, Boehringer Ingelheim, Eli Lilly, Pfizer and Roche Genentech. F. Barlesi: Honarium from Roche. T. Hida: Corporate-sponsored research from Chugai Pharmaceutical. P. He: Employee of Roche/Genentech, and has stocks for Roche and Amgen. Her husband has stocks for Allergan and Gilead. M. Ballinger: Genentech/Roche employee and has Roche stock. D.R. Gandara: Consultant for Genentech and clinical trial grant from Genentech. J. von Pawel: Adboard with fees paid to the institution from AbbVie, Pfizer, Bristol Myers Squibb, and Novartis. All other authors have declared no conflicts of interest.

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      90PD - Previously treated advanced NSCLC cohort from a multi-disease phase 1 study of ramucirumab (R) plus pembrolizumab (P): Efficacy and safety data (ID 169)

      14:45 - 15:45  |  Author(s): R.S. Herbst, J. Martin-Liberal, E. Calvo, N. Isambert, J. Bendell, P. Cassier, J. Jin, G. Mi, J. Rege, L. Paz-Ares

      • Abstract

      Background:
      R (anti-VEGFR2) and P (anti-PD-1) are active in previously treated advanced NSCLC. Median progression-free survival (PFS) reported in KEYNOTE-001 (previously treated; PD-L1 all comers) was 3.0 months (95%CI, 2.2-4.0) and ORR was 18%. This is the first study to combine R with P.

      Methods:
      Ongoing, multi-cohort, phase 1a/b trial enrolled pts with confirmed NSCLC with prior progression on systemic therapy, measurable disease, ECOG PS 0-1 and baseline tumor tissue. PD-L1 was classified strongly positive (tumor proportion score [TPS] ≥50%), weakly positive (TPS=1-49%), or negative (TPS <1%) using the DAKO PD-L1 22C3 IHC pharmDx assay. Primary objective- assess safety and tolerability of R + P; preliminary efficacy will be examined.

      Results:
      As of 21-Nov-2016, 27 pts with previously treated advanced NSCLC received R at 10 mg/kg on Day 1 with P 200 mg on Day 1 q3W. Median age was 65, 78% male, 96% had a history of smoking, 78% had adenocarcinoma and 15% had squamous-cell carcinoma. Sixteen (59%) pts received ≥2 and 4 (15%) received ≥3 prior treatment regimens for their disease. Median duration of treatment was 7.0 mo (IQR 3.0-12.4) and 8.3 mo (IQR 3.3-12.4) for R and P, respectively. Treatment related adverse events (TRAEs) occurred in 25 (93%) pts, most commonly hypertension (26%) and asthenia (19%). Five (19%) pts experienced grade 3 TRAEs (adrenal insufficiency, delirium, hypertension [n = 2], hyponatremia, infusion related reaction, proteinuria, and respiratory failure). No grade 4-5 TRAEs occurred. ORR was 30% with a median time to response of 2.1 mo. Duration of response has not been reached. Responses occurred in PD-L1 unknown (n = 1), negative (n = 2), and strong positive (n = 5) groups as well as both histologies. Median PFS was 9.7 mo (95% CI 4.6-11.5) and overall survival rate at 6 mo was 84.9%. Disease control rate was 85%. Ten (37%) pts remain on study treatment, including all responders.

      Conclusions:
      R + P demonstrated encouraging antitumor activity independent of PD-L1 and histology. The safety profile was consistent with monotherapy treatment for each drug, with no additive toxicities. The study was amended and is now enrolling pts with treatment naïve advanced NSCLC.

      Clinical trial identification:
      NCT02443324 JVDF

      Legal entity responsible for the study:
      Eli Lilly and Company, Indianapolis, IN

      Funding:
      Eli Lilly and Company, Indianapolis, IN

      Disclosure:
      R.S. Herbst: Personal fees from Eli Lilly, outside the submitted work. E. Calvo: Institutional research funding: multiple- available upon request; Travel expenses: Lilly, PsiOxus, Novartis; Consultant: Novartis, GSK, Astellas, Genentech, Lilly, Nanobiotich, Pfizer; SB: Novartis. N. Isambert: Honoraria: Pfizer, Novartis; Consulting/Advisory: Merck Serono. J. Bendell: Institutional research funding: From multiple and available upon request, including Lilly and Merck. P. Cassier: Personal fees from Roche/Genentech, Novartis, Astra-Zeneca, Amgen, Plexxikon; non-financial support from Roche/Genentech, Merck Sharp Dohme, Astra-Zeneca, Plexxikon; and grants from Merck Sharp Dohme and Astra-Zeneca, outside the submitted work. J. Jin, G. Mi, J. Rege: Employee and stock holder at Eli Lilly and Company. L. Paz-Ares: Consultant/Advisory role: Roche, Lilly, Novartis, MSD, BMS, Amgen, Clovis, AZ, BI, Pfizer. All other authors have declared no conflicts of interest.

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      91PD_PR - Response to salvage chemotherapy following exposure to PD-1/PD-L1 inhibitors in patients with NSCLC (ID 498)

      14:45 - 15:45  |  Author(s): S.I. Rothschild, P. Leger, E.L. Castellanos, R.N. Pillai, S.J. York, L. Horn

      • Abstract

      Background:
      Immune checkpoint inhibitors are active for patients with stage IV NSCLC who have progressed following platinum-based chemotherapy. We evaluated responses to chemotherapy in patients with NSCLC who had progressed on a checkpoint inhibitor.

      Methods:
      Eligible patients were adults with NSCLC who received salvage chemotherapy following PD-1/PD-L1 inhibitors (cases) versus no PD-1/PD-L1 inhibitors (controls). CT-imaging was done within 4 weeks of initiation of salvage chemotherapy and every 6 weeks thereafter. Revised RECIST guidelines were used to define response. Clinical and imaging data were abstracted from review of electronic medical records. Multivariate logistic regression analysis was used to calculate probability of response.

      Results:
      355 patients’ charts were reviewed and 82 patients met eligibility criteria. Among evaluable patients, 46 were males versus 36 females. 67 patients were classified as cases versus 15 controls. 56 patients received nivolumab, 7 pembrolizumab and 4 atezolizumab. 63 (77%) patients had adenocarcinoma, 18 (22%) squamous cell carcinoma and 1 (1%) large cell carcinoma. The mean number of chemotherapy regimens prior to salvage chemotherapy was 2.37 (95% CI: 2.10-2.64) in cases versus 1.93 (95% CI: 1.32-2.54) in controls. Salvage drugs used included docetaxel (62%), pemetrexed (20%), gemcitabine (12%) and paclitaxel (6%). 18 (27%) cases had partial response to chemotherapy versus 1 (7%) controls. 15 (22%) cases had progressive disease versus 6 (40%) controls. 34 (51%) cases had stable disease versus 8 (53%) controls. The odds ratio for achieving a partial response was 0.30 (95% CI: 0.18 to 0.50, p = 0.000). In multiple logistic regression model, age, gender, number of prior chemotherapy regimens, tumor histology, smoking status, different salvage chemotherapy regimens were not associated with the likelihood of achieving a partial response.

      Conclusions:
      The odds of achieving a partial response to salvage chemotherapy were significantly higher in patients with prior exposure to PD-1/PD-L1 inhibitors. This observed difference however warrants confirmation in larger cohorts. Ongoing investigations include the duration of response as well as evaluation of toxicity.

      Clinical trial identification:


      Legal entity responsible for the study:
      N/A

      Funding:
      N/A

      Disclosure:
      All authors have declared no conflicts of interest.

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      92PD - First-line afatinib for advanced EGFRm+ NSCLC: Analysis of long-term responders (LTRs) in the LUX-Lung (LL) 3, 6 and 7 trials (ID 299)

      14:45 - 15:45  |  Author(s): M. Schuler, L. Paz-Ares, L.V. Sequist, Y. Wu, S.L. Geater, A. Märten, J. Fan, K. Park, J.C. Yang

      • Abstract

      Background:
      In the Phase III LL3 and LL6 trials, first-line afatinib significantly improved PFS and ORR versus platinum-doublet chemotherapy in pts with EGFRm+ NSCLC. In the Phase IIb LL7 trial, afatinib significantly improved PFS, time to treatment failure, and ORR versus gefitinib in this setting. Here we present post-hoc analyses of afatinib LTRs (treated with afatinib ≥3 years) in LL3/6/7.

      Methods:
      Treatment-naïve pts with stage IIIB/IV EGFRm+ NSCLC who were randomized to 40 mg/day afatinib in LL3/6/7 were included.

      Results:
      24/229 (10%), 23/239 (10%) and 19/160 (12%) afatinib-treated pts in LL3, LL6 and LL7 were LTRs; 6, 9 and 14 LTRs were still on treatment at the time of analysis. In LL7, 4% of gefitinib-treated pts were LTRs. Baseline characteristics were generally consistent with the overall study populations, with the exception of greater proportions of women (LL3/6 only; 92/78% vs 64% in the overall populations) and Del19+ pts (63–79% vs 49–58% overall) among LTRs. The table shows treatment duration and outcomes. The median OS values for LL3/6 were >30 months longer than those reported in the overall populations. ORRs ranged from 70.8% in LL3 to 89.5% in LL7. Frequency and duration of subsequent therapy was similar to the overall population. Frequency of afatinib dose reduction due to TRAEs was broadly consistent with the overall populations; final afatinib doses of 20/30/40/50 mg were observed in 50/25/21/4% in LL3, 13/22/61/4% in LL6, and 32/21/47/0% in LL7.

      Conclusions:
      In the LL3/6/7 studies, 10–12% of afatinib-treated pts were LTRs (treated ≥3 years). Among these pts, greater proportions of women (LL3/6 only) and Del19+ NSCLC were observed. In LTRs, afatinib conferred a long-term survival benefit of ∼5 years and was well tolerated. Long-term treatment was independent of tolerability-guided dose adjustment, or the presence of brain metastases at time of enrolment, and had no detrimental impact on subsequent treatment.rnTable: 92PDrn

      rnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrn rnrn
      CharacteristicLL3 (n = 24)LL6 (n = 23)LL7 (n = 19)
      Median follow-up for OS, months64.657.042.1
      Median duration of treatment, months (range)50 (41–73)56 (37–68)42 (37–50)
      Median PFS (central review), months37.530.627.6
      Median OS, months63.255.340.8
      Overall response rate (CR+PR), n (%)17 (70.8)18 (78.3)17 (89.5)
      CR, n (%)1 (4.2)3 (13.0)1 (5.3)
      PR, n (%)16 (66.7)15 (65.2)16 (84.2)
      SD, n (%)5 (20.8)2 (8.7)2 (10.5)
      NN, n (%)2 (8.3)3 (13.0)–
      Median duration of response, months34.528.319.4
      rnCR, complete response; NN, not-PR/not-SD; PR, partial response; SD, stable diseasern

      Clinical trial identification:
      LUX-Lung 3: EudraCT No: 2008-005615-18 LUX-Lung 6: clinicaltrials.gov ref: NCT01121393 LUX-Lung 7: EudraCT No: 2011-001814-33

      Legal entity responsible for the study:
      Boehringer Ingelheim

      Funding:
      Boehringer Ingelheim

      Disclosure:
      M. Schuler: Advisory boards: AstraZeneca, Boehringer Ingelheim, Celgene, Eli Lilly, Novartis; Corporate-sponsored research: Boehringer Ingelheim, Bristol-Myers Squibb, Novartis; Honoraria: AstraZeneca, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Eli Lilly, Novartis, Roche, MSD, Alexion; Patents: University Duisburg-Essen. L. Paz-Ares: Honoraria from Pfizer, Bristol-Myer Squibb, MSD, Novartis, Roche, Eli Lilly, Boehringer Ingelheim, Clovis Oncology, AstraZeneca, and Amgen. L.V. Sequist: Participated on advisory boards for Boehringer Ingelheim, AstraZeneca, Novartis, Clovis Oncology, Genentech, Merrimack, Ariad, and Bristol-Myers Squibb. S.L. Geater: Participated in advisory boards for Novartis and Boehringer Ingelheim, and has also received honoraria from Roche, AstraZeneca, Boehringer Ingelheim, and Novartis. A. Märten: Employee of Boehringer Ingelheim. J. Fan: Boehringer Ingelheim Pharmaceuticals Inc. employee. K. Park: Participated on advisory boards for Astellas, AstraZeneca, Boehringer Ingelheim, Clovis Oncology, Eli Lilly, Hanmi, MSD, Novartis, and Roche. 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. All other authors have declared no conflicts of interest.

    • +

      93PD - Afatinib (A) vs gefitinib (G) in patients with EGFR mutation-positive (EGFRm+) NSCLC: Updated OS data from the phase IIb trial LUX-Lung 7 (LL7) (ID 301)

      14:45 - 15:45  |  Author(s): J. Corral, K. Park, J.C. Yang, T. Mok, E. Tan, K. O'Byrne, V. Hirsh, M. Boyer, J. Fan, L. Zhang

      • Abstract

      Background:
      A, an irreversible ErbB family blocker, and G, a reversible EGFR TKI, are approved for 1st-line treatment (tx) of advanced EGFRm+ NSCLC. In LL7, A (40 mg/d) significantly improved PFS (HR 0.73 [95% CI 0.57–0.95], p = 0.017), ORR (70 vs 56%, p = 0.008) and time to tx failure (TTF; HR 0.73 [0.58–0.92], p = 0.007) vs G (250 mg/d) in this setting; the primary OS analyses (data cut-off 8 Apr 16) showed a non-significant difference in OS between A and G (median 27.9 vs 24.5 mos; HR 0.86 [0.66–1.12], p = 0.258) that was consistent across subgroups. Here, we present updated OS data.

      Methods:
      LL7 assessed A vs G in tx-naïve pts with EGFRm+ (Del19/L858R) stage IIIb/IV NSCLC. Co-primary endpoints were PFS, TTF and OS. Other endpoints: ORR and AEs.

      Results:
      Data cut-off for the updated OS analysis was 12 Dec 16. Median follow-up for OS was 49.2 mos. 73/77% (A/G) of pts had ≥1 subsequent systemic anti-cancer tx after discontinuation of A/G. 48/56% (A/G) received a subsequent EGFR TKI; 31 (19%)/26 (16%) pts (A/G) received a 3[rd]-gen EGFR TKI. Updated median OS was 27.9 vs 24.5 mos with A vs G (HR 0.85 [0.66–1.09], p = 0.1950). Landmark 24-mo and 30-mo OS with A vs G was 61 vs 51% and 48 vs 40%, respectively; 48-mo OS was 28% with A vs 20% with G. In patients treated with A, ≥30-mo survival rates were generally similar across countries of origin and mean average dose received. Similar OS trends were observed with A vs G in pts with Del19 (30.7 vs 26.4 mos; HR 0.82 [0.59–1.15]) and L858R (25.0 vs 21.2 mos; HR 0.89 [0.61–1.31]) mutations. There was a trend towards improved OS with A vs G in pts who received a 3[rd]-gen EGFR TKI (NE vs 48.3 mos; HR 0.49 [0.20–1.19]). In patients treated with A, consistent OS outcomes were observed across age groups (median, mos: 28.9 [<60 years]; 30.1 [<65 years]; 28.9 [<75 years]; 27.9 [≥75 years]). Updated PFS, TTF and ORR (at primary OS data cut-off, 8 Apr 16) were similar to the primary analyses, and all were significantly improved with A vs G; the AE profile of A and G was virtually unchanged since the primary analysis.

      Conclusions:
      In this updated OS analysis, there was no significant difference in OS with A vs G. A trend favouring A, generally consistent across subgroups, was observed.

      Clinical trial identification:
      Clinical Trials.gov Identifier: NCT01466660

      Legal entity responsible for the study:
      Boehringer Ingelheim

      Funding:
      Boehringer Ingelheim

      Disclosure:
      K. Park: Participated on advisory boards for Astellas, AstraZeneca, Boehringer Ingelheim, Clovis Oncology, Eli Lilly, Hanmi, Merck & Co., Inc., Novartis, and Roche. 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, AZ. T. Mok: Receipt of grants/research supports: AstraZeneca, BI, Pfizer, Novartis, SFJ, Roche, MSD, Clovis Oncology, BMS. Receipt of honoraria or consultation fees: AstraZeneca, Roche/Genentech, Pfizer, Eli Lilly, BI, Merck Serono, MSD, Janssen, Clovis Oncology, BioMarin, GSK, Novartis, SFJ Pharmaceutical, ACEA Biosciences, Inc., Vertex Pharmaceuticals, BMS, AVEO & Biodesix, Prime Oncology, Amgen. Participation in a company sponsored speaker’s bureau: AstraZeneca, Roche/Genentech, Pfizer, Eli Lilly, BI, MSD, Amgen, Janssen, Clovis Oncology, GSK, Novartis, BMS, PrIME Oncology. Stock shareholder: Sanomics Limited. K. O\'Byrne: Ad board, speaker bureau, travel to international conferences and honoraria: AZ, BMS, Roche-Genentech, MSD, Pfizer, BI. Ad board and speaker bureau: Novartis. 3 Patents: 1 on novel drugs, 2 on biomarkers, IP held by Queensland University of Technology. V. Hirsh: Has received advisory board honoraria from Boehringer Ingelheim, AstraZeneca, Roche, Merck, Eli Lilly, Pfizer, Amgen, and Bristol-Myers Squibb. M. Boyer: Ad board: BMS, Merck Sharpe and Dohme, Pfizer Board of Directors: IASLC Research: Pfizer, Genentech, BI, AZ, Novartis, Merck Sharpe and Dohme, Clovis Honoraria: Merck Sharpe and Dohme, BI, BMS, AZ. J. Fan: Boehringer Ingelheim employee. All other authors have declared no conflicts of interest.

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      94PD - Adverse events self-reported by patients with advanced non-small cell lung cancer treated with osimertinib or chemotherapy (ID 353)

      14:45 - 15:45  |  Author(s): M. Sebastian, A. Ryden, A. Walding, S. Ghiorghiu, K. Rüdell, V. Papadimitrakopoulou

      • Abstract

      Background:
      The Patient-Reported Outcomes version of the Common Terminology Criteria for Adverse Events (PRO-CTCAE) complements standard adverse event (AE) reporting in oncology trials. We assessed patient-reported symptomatic AEs in individuals receiving osimertinib 80mg once daily or chemotherapy for advanced non-small cell lung cancer (NSCLC) in the AURA3 trial, using the PRO-CTCAE.

      Methods:
      AURA3 (NCT02151981) was a multinational, open-label, randomized phase III trial involving 419 patients.1 As part of exploratory analyses, individuals for whom validated local language versions were available (in English, German, Japanese or Spanish) were asked to complete the PRO-CTCAE by e-device, weekly for 18 weeks and then every 3 weeks.

      Results:
      In total, 161 patients (38%; 102 osimertinib, 59 chemotherapy) provided data for PRO-CTCAE analysis (mean age: 64 years; 63% women). The number of patients providing PRO-CTCAE data fluctuated between different items and time points, and decreased over the study period. Of patients on osimertinib providing information on acne/pimples, 37%, 38%, 32% and 29% reported having acne/pimples at baseline, 4 weeks, 12 weeks and 24 weeks, respectively, compared with 30%, 19%, 14% and 12% on chemotherapy. Most cases (>90%) were mild. Reported rates of diarrhoea changed little over time post-baseline and were higher with osimertinib than with chemotherapy (32% vs 36% at baseline, 47% vs 28% at 4 weeks, 53% vs 33% at 12 weeks, 45% vs 21% at 24 weeks). Most cases were mild or moderate. Fatigue (64% vs 72% at baseline, 72% vs 89% at 4 weeks, 55% vs 89% at 12 weeks, 60% vs 79% at 24 weeks) and decrease in appetite (54% vs 53% at baseline, 42% vs 75% at 4 weeks, 35% vs 69% at 12 weeks, 33% vs 46% at 24 weeks) were reported less commonly with osimertinib than with chemotherapy. Most cases were mild.

      Conclusions:
      Self-reported data from patients with NSCLC treated with osimertinib or chemotherapy showed changes over time in AE rates from start of treatment and differences in prevalence of patient-reported AEs (PRO-CTCAEs) with osimertinib versus chemotherapy.

      Clinical trial identification:
      NCT02151981

      Legal entity responsible for the study:
      AstraZeneca

      Funding:
      AstraZeneca

      Disclosure:
      M. Sebastian: Honoraria: Novartis, BMS, Roche, Lilly, Boehringer-Ingelheim, Pierre-Fabre, Pfizer, MSD, AstraZeneca. Consultant: Novartis, BMS, Roche, Lilly, Boehringer-Ingelheim, Pfizer, MSD, AstraZeneca, Celgene. V. Papadimitrakopoulou: Advisory: Eli Lilly&Co, Genentech, Janssen Global Sevices, Bristol-Myers Squibb, ARIAD, AstraZeneca Pharmaceuticals, Novartis, Merck Corporate-sponsored. Research: Novartis, AstraZeneca, Genentech, Merck, Janssen, ACEA, Bristol-Myers Squibb. A. Walding: AstraZeneca employee and shareholder. S. Ghiorghiu: AstraZeneca employee and shareholder. A. Ryden: AstraZeneca employee and shareholder. K. Rudell: Former AstraZeneca employee and shareholder. All other authors have declared no conflicts of interest.



Author of

  • +

    SCLC: New insights (ID 25)

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

      New therapies, new era? (ID 105)

      11:00 - 12:30  |  Author(s): N. Reguart

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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    Targeted therapies and immunotherapies (ID 46)

    • Event: ELCC 2017
    • Type: Poster Discussion session
    • Track:
    • Presentations: 1
    • +

      Invited Discussant 92PD, 93PD and 94PD (ID 548)

      14:45 - 15:45  |  Author(s): N. Reguart

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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