Virtual Library

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    Targeted therapies and management of brain metastasis (ID 40)

    • Event: ELCC 2017
    • Type: Proffered Paper session
    • Track:
    • Presentations: 7
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      1O - ROS1 immunocytochemistry on cytological specimens in patients with non-small cell lung cancer (ID 503)

      16:45 - 18:15  |  Author(s): T. Vlajnic, S. Savic, L. Bubendorf

      • Abstract
      • Slides

      Background:
      Rearrangements of the ROS1 gene are found in 1-2% of non-small cell lung cancers (NSCLC) and are regarded as mutually exclusive oncogenic driver mutations. Since targeted therapy has recently been approved for ROS1-positive NSCLC, ROS1 testing is entering diagnostic routine. Fluorescence in situ hybridization (FISH) optionally selected for by immunohistochemistry (IHC) on histological material is regarded as gold standard for detection of ROS1 rearrangements. However, NSCLC is often diagnosed by cytology alone, requiring the option of predictive marker testing on cytological specimens. In this study, we explored the utility of ROS1 immunocytochemistry (ICC) on cytological specimens as a preliminary screening tool for detection of ROS1 rearrangements.

      Methods:
      ICC using the D4D6 antibody was prospectively performed in the routine diagnostic setting on ethanol-fixed and previously Papanicolaou-stained specimens from 296 patients with NSCLC, including adenocarcinomas (n = 243), NSCLC NOS (n = 47), and others (n = 6) and encompassing specimens from the lung (n = 107), locoregional lymph nodes (n = 87) and distant metastases (n = 102). Cytospin specimens of the cell line HCC-78, known to express ROS1, were used as positive control. Cytoplasmic staining of any intensity was considered positive.

      Results:
      ICC was positive in 12 cases with ROS1 rearrangements confirmed by FISH. Confirmation of 284 ICC-negative cases was available in 210 cases (FISH in 71 cases, mRNA based fusion NGS in 2 cases and detection of other known, mutually exclusive driver mutations in 137 cases). Only one ICC-negative case showed a ROS1 rearrangement by FISH (sensitivity 92%, specificity 100%, PPV 100%, NPV 99%).

      Conclusions:
      Our data show that ROS1 ICC is a highly accurate method for detection of ROS1 rearrangements in NSCLC. Given the high costs and technical challenges of FISH and the rarity of ROS1 rearrangements, ICC is cost effective and rapid and therefore well suited as a preliminary screening method. Cases with equivocal or positive findings on ICC can be confirmed by FISH or molecular tests (e.g. NGS).

      Clinical trial identification:


      Legal entity responsible for the study:
      University Hospital Basel

      Funding:
      University Hospital Basel

      Disclosure:
      All authors have declared no conflicts of interest.

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      86O - Afatinib (A) plus cetuximab (C) in the treatment of patients (pts) with NSCLC: The story so far (ID 311)

      16:45 - 18:15  |  Author(s): E. Smit, J. Soria, Y.Y. Janjigian, H.J.M. Groen, W. Pao, E. Calvo, A. Gazzah, J. Fan, M. Ould-Kaci, L. Horn

      • Abstract
      • Presentation
      • Slides

      Background:
      Constitutive EGFR signalling due to activating mutations (e.g. EGFRm+ NSCLC) or overexpression (e.g. squamous (sq) NSCLC) is a common mechanism of tumourigenesis. There is biological rationale for combining A + C in tumours with unmet medical need, e.g. EGFRm+ NSCLC with resistance to EGFR-TKIs, and in advanced sqNSCLC. Preclinically, A + C improved anti-tumour activity in EGFRm+ NSCLC vs A or C alone. Here we report outcomes from two Phase Ib studies of A + C: NCT01090011 (study 1) in pts with EGFRm+ NSCLC resistant to gefitinib/erlotinib (G/E); and NCT02020577 (study 2) in unselected pts with heavily pretreated advanced solid tumours, including sqNSCLC.

      Methods:
      Study 1 comprised a dose-finding phase to identify the maximum tolerated dose (MTD) of A + C, and an expansion phase (EP) in which 126 pts received the MTD of A 40 mg/day + C 500 mg/m[2] Q2W. In study 2, 9 pts received A + C in a dose-escalation phase, and a further 49 pts received the MTD of A 40 mg/day + C 250 mg/m[2]/week in an EP, including 12 pts with sqNSCLC.

      Results:
      Drug-related adverse events (DR-AEs; all grades) were reported in 99% of pts in the EP of study 1 (n = 126), and 98% of pts in study 2 (n = 58). Grade 3/4/5 DR-AEs were experienced by 44%/2%/2% of pts in study 1 and 31%/3%/0% in study 2. DR-AEs led to discontinuation of treatment in 14% of pts in study 1 and 12% in study 2. Efficacy in pts with NSCLC is shown in the table. In the study 1 EP, ORR was 29% and median PFS was 4.7 months; there were no significant differences in ORR or median PFS in pts with T790M+ vs T790M- tumours (32 vs 25% [p = 0.341] and 4.6 vs 4.8 months [p = 0.643], respectively). Median duration of OR was 5.7 months. In the study 2 EP, 75% of pts with sqNSCLC had SD, and median PFS was 11.9 weeks.

      Conclusions:
      Based on the demonstrated antitumour activity and a predictable/manageable safety profile, A + C may be a treatment option in pts with EGFRm+ NSCLC and acquired resistance to G/E (irrespective of T790M status) or with pre-treated advanced sqNSCLC. rnTable: 86OEfficacy outcomesrn

      rnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrn rnrn
      TrialEGFRm+ NSCLCsqNSCLC
      Study 1 expansion phase[1] (n = 126)Study 2 expansion cohort[2] (n = 12)
      Disease control (CR/PR/SD), n (%)89 (71)9 (75)
      OR (CR/PR), n (%)37 (29)0
      SD52 (41)9 (75)
      Unconfirmed OR5 (4)
      PD, n (%)27 (21)3 (25)
      Median duration of OR, months (range)5.7 (1.8–24.4)
      Median duration of disease control, weeks (standard deviation)17.9 (9.9)
      Median PFS (95% CI)4.7 months (4.3–6.4)11.9 weeks (5.1–19.4)
      rnCR, complete response; PR, partial response; SD, stable disease; PD, progressive disease;rnOR, objective response; PFS, progression-free survival 1. Janjigian YY, et al. Cancer Discov 2014;4:1036-45 2. Gazzah A, et al. Eur J Cancer 2016;68(Suppl. 1);S139:abstract 426rn

      Clinical trial identification:
      NIH study numbers: 1200.71: NCT01090011 1200.122: NCT02020577

      Legal entity responsible for the study:
      Boehringer Ingelheim

      Funding:
      Boehringer Ingelheim

      Disclosure:
      J-C. Soria: Astrazeneca, Astex, GSK, Gammamabs, Eli Lilly, MSD, Merus, Pfizer, Pharmamar, Pierre Fabre, Roche, Sanofi, Servier, Symphogen, Takeda. Y.Y. Janjigian: Employee of Memorial Sloan Kettering Cancer Center Advisory boards: ASCO GI Corporate-sponsored research: Merck, BMS Consultant: Pfizer Grant/research: BI, Bayer, Amgen, Genentech, Roche. H.J.M. Groen: Participated on advisory boards for Boehringer Ingelheim. W. Pao: Reports that patent rights on EGFR T790M were licensed by MSKCC to Molecular MD. J. Fan: Boehringer Ingelheim employee. M. Ould-Kaci: Employee of Boehringer Ingelheim. L. Horn: Consulting for AbbVie, BMS, Merck, Eli Lilly, Xcovery, Bayer. All other authors have declared no conflicts of interest.

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      Invited Discussant 1O and 86O (ID 535)

      16:45 - 18:15  |  Author(s): D.P. Carbone

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      3O - Innate resistance in EGFR mutant non-small cell lung cancer (NSCLC) patients by coactivation of receptor tyrosine kinases (RTKs) (ID 339)

      16:45 - 18:15  |  Author(s): R. Rosell, N. Karachaliou, I. Chaib, A. Drozdowskyj, A. Frías, C. Teixidó, S. Viteri, L. Santarpia, M.A. Molina-Vila, T.G. Bivona

      • Abstract
      • Slides

      Background:
      The MET ligand hepatocyte growth factor (HGF) in stromal cells provides an alternative signaling mechanism for EGFR by inducing inter-receptor cross talk with EphA2, CUB domain-containing protein-1 (CDCP1) or AXL. Src-homology 2 domain-containing phosphatase 2 (SHP2) also plays a role in RTK signaling and is required for MAPK activation.

      Methods:
      We studied the expression levels of stromal HGF and tumor RTKs: AXL, CDCP1, MET, and EphA2, as well as SHP2, and clinical outcome in baseline samples of 64 EGFR-mutant NSCLC patients (pts) treated with first-line EGFR TKI. Paraffin-embedded samples and the discrimination between tumor and stromal cells were performed by a pathologist. mRNA expression was analyzed by qRT-PCR.

      Results:
      AXL and CDCP1 were among the genes that most significantly influenced treatment outcome. Median progression-free survival (PFS) was 14 months (mo) and 23.4 mo for pts with high and low AXL mRNA, respectively (p = 0.03), (HR: 2.05, p = 0.03). Median PFS was 9 mo and 20.2 mo for pts with high and low CDCP1 mRNA, respectively (p = 0.01), (HR: 2.1, p = 0.02). There were no significant differences in PFS according to levels of EPHA2 and MET in the tumor, and HGF in the stroma. Median PFS was 11.4 mo and 24 mo for pts with high and low SHP2 mRNA, respectively (p = 0.09) (HR: 2.4, p = 0.01). Median overall survival (OS) was 19.1 mo and 40.7 mo for pts with high and low AXL mRNA, respectively (p = 0.009) (HR: 2.9, p = 0.001). Median OS was 19.1 mo and 34.9 mo for pts with high and low CDCP1 mRNA, respectively (p = 0.03) (HR: 2.2, p = 0.03). In addition, differences in OS were noted according to levels of EPHA2, MET and SHP2.

      Conclusions:
      AXL and CDCP1 are adverse predictive markers of PFS and OS. It has been reported that overexpression of several RTKs can substitute EGFR signaling in EGFR mutant NSCLC pts. The findings show the need to scrutinize RTK levels in EGFR mutant NSCLC patients and, henceforth, the importance of tailored combinatory therapy with AXL inhibitors, or with Src inhibitors, in those pts with elevated CDCP1 (CDCP1 triggers SFK activation).

      Clinical trial identification:


      Legal entity responsible for the study:
      Institut d’Investigació en Ciències Germans Trias i Pujol, Badalona, Spain Institut Català d’Oncologia, Hospital Germans Trias i Pujol, Badalona, Spain

      Funding:
      Institut d’Investigació en Ciències Germans Trias i Pujol, Badalona, Spain Institut Català d’Oncologia, Hospital Germans Trias i Pujol, Badalona, Spain

      Disclosure:
      All authors have declared no conflicts of interest.

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      87O - Brigatinib in ALK+ NSCLC pts with intracranial CNS metastases in 2 clinical trials (ID 241)

      16:45 - 18:15  |  Author(s): M. Tiseo, R.M. Huber, M.J. Hochmair, L.A. Bazhenova, S.I. Ou, W. Reichmann, J. Haney, D. Kerstein, D.R. Camidge, S.N. Gettinger

      • Abstract
      • Presentation
      • Slides

      Background:
      The investigational next-generation anaplastic lymphoma kinase (ALK) inhibitor brigatinib is being evaluated in patients (pts) with ALK-positive non–small cell lung cancer (ALK+ NSCLC) in a phase 1/2 trial (Ph1/2) and a pivotal phase 2 trial (ALTA); most of these pts had intracranial central nervous system (CNS) metastases at baseline.

      Methods:
      In Ph1/2 (NCT01449461), pts with advanced malignancies, including ALK+ NSCLC, received brigatinib (30–300 mg/d). In ALTA (NCT02094573), crizotinib-resistant pts with advanced ALK+ NSCLC received brigatinib at 90 mg qd in arm A or 180 mg qd with a 7-day lead-in at 90 mg in arm B. ALK+ NSCLC pts with baseline brain metastases were analyzed. CNS efficacy in both trials and safety in ALTA are shown.

      Results:
      In Ph1/2 and ALTA, 50/79 (63%) and 154/222 (69%) ALK+ NSCLC pts had baseline brain metastases based on independent review committee (IRC) and investigator assessment, respectively. Most pts had received chemotherapy (Table). In Ph1/2, 25/50 (50%) pts were receiving brigatinib as of 16 November 2015; in ALTA, 101/154 (66%) pts were receiving brigatinib as of 29 February 2016. In pts with measurable brain lesions, confirmed intracranial objective response rate was 53% in Ph1/2 and 42%/67% in ALTA A/B (Table). In pts with only nonmeasurable brain lesions, 35% (11/31) in Ph1/2 and 7% (4/54)/18% (10/55) in ALTA A/B had confirmed complete resolution of brain lesions. Further data are shown in the table. The most common treatment-emergent adverse events (TEAEs) in the 151 treated ALTA pts with baseline brain metastases were nausea (A/B, 32%/43%), headache (30%/30%), diarrhea (18%/36%), cough (21%/30%), and vomiting (25%/26%); the most common grade ≥3 TEAEs were increased blood creatine phosphokinase (1%/11%), hypertension (4%/7%), increased lipase (3%/3%), and pneumonia (1%/4%).

      Conclusions:
      Brigatinib yielded substantial clinical activity in ALK+ NSCLC pts with brain metastases in 2 trials.rnTable: 87OBaseline characteristics and IRC-assessed intracranial efficacy of brigatinib in ALK+ NSCLC Pts with brain metastases at baselinern

      rnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrnrn
      rnPh1/2 n = 50ALTA Arm A n = 80ALTA Arm B n = 74
      Median age, years534955
      Received prior chemotherapy, %767476
      Crizotinib-naive, %800
      Pts evaluable for intracranial efficacy by IRC, n[a]468073
      Median iPFS, months14.615.612.8
      Pts with measurable brain lesions, n152618
      iORR, n (%)8 (53)11 (42)12 (67)
      iDCR, n (%)13 (87)22 (85)15 (83)
      No rad/active[b] subset, n91915
      iORR, n (%)6 (67)8 (42)11 (73)
      iDCR, n (%)8 (89)16 (84)14 (93)
      rniDCR = intracranial disease control rate, iORR = intracranial objective response rate (confirmed), iPFS = intracranial progression-free survivalrnaLast scan date: 8 October 2015 in Ph1/2; 14 April 2016 in ALTArnbNo prior brain radiotherapy in Ph1/2; active (untreated or treated and progressed) brain lesions in ALTArn

      Clinical trial identification:
      NCT01449461 and NCT02094573

      Legal entity responsible for the study:
      ARIAD Pharmaceuticals, Inc.

      Funding:
      ARIAD Pharmaceuticals, Inc.

      Disclosure:
      M. Tiseo: Consulting or advisory role (AstraZeneca, BMS, Boehringer Ingelheim, Eli Lilly, Novartis, Otsuka, Pierre Fabre), research funding (ARIAD). R.M. Huber: Honoraria (ARIAD, AstraZeneca, BMS, Boehringer Ingelheim, Pfizer, Roche), consulting or advisory role (BMS, Boehringer Ingelheim, Celgene, Clovis Oncology, Eli Lilly, Novartis, Roche), research funding (Pierre Fabre). L.A. Bazhenova: Stock and other ownership interests (Epic Sciences), honoraria (Novartis), consulting or advisory role (AbbVie, AstraZeneca, BMS, Boehringer Ingelheim, Clovis Oncology, Genoptix, Heat Biologics, Pfizer, Roche/Genentech, Seattle Genetics, Trovagene), speakers bureau (AstraZeneca, Novartis, Pfizer, Roche/Genentech), research funding (AbbVie, ARIAD, Astellas, Astex, AstraZeneca/MedImmune, Boehringer Ingelheim, Chugai, Clovis Oncology, Eisai, Eli Lilly, Heat Biologics, Johnson & Johnson, Merck, Mirati, NanoCarrier, Novartis, Pfizer, Roche/Genentech). S-H.I. Ou: Advisory board (ARIAD). W. Reichmann, J. Haney, D. Kerstein: Employment, stock and other ownership interests (ARIAD). D.R. Camidge: Honoraria (ARIAD), research funding (ARIAD). S.N. Gettinger: Consulting or advisory role (ARIAD, BMS, Janssen), research funding (ARIAD, AstraZeneca/MedImmune, BMS, Boehringer Ingelheim, Incyte, Pfizer, Roche/Genentech). All other authors have declared no conflicts of interest.

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      88O - CNS activity of ensartinib in ALK+ non-small cell lung cancer (NSCLC) patients (pts) (ID 461)

      16:45 - 18:15  |  Author(s): K.L. Reckamp, H.A. Wakelee, S. Patel, G. Blumenschein, J.W. Neal, B. Gitlitz, S.N. Waqar, F. Tan, K. Harrow, L. Horn

      • Abstract
      • Presentation
      • Slides

      Background:
      Ensartinib (X-396) is a potent ALK small molecule TKI with additional activity against MET, ABL, Axl, EPHA2, LTK, ROS1 and SLK. In animal studies, CNS concentration of ensartinib in mice given at the therapeutic dose was 4 times higher than the IC50 for growth inhibition of ALK+ cells in vitro. Ensartinib was significantly more effective than crizotinib (C) at inhibiting the intracranial (IC) growth of the SH-SY5Y neuroblastoma model harboring the F1174L mutation. We subsequently evaluated the CNS activity of ensartinib in pts with ALK+ NSCLC.

      Methods:
      In this multicenter phase I/II study, pts with ALK+ NSCLC were enrolled and given ensartinib orally on a continuous 28-day schedule. 225 mg QD was selected for further evaluation. Pts enrolled with asymptomatic CNS metastases (with or without systemic disease) who were ALK TKI naïve or had received prior C or a 2nd generation ALK TKI were allowed to enroll. Overall and systemic response was assessed using RECIST 1.1. CNS response was assessed using modified RANO criteria. Pts with only CNS disease had to have at least 1 measurable target lesion ≥ 3 mm in diameter.

      Results:
      26 pts with ALK+ NSCLC and baseline CNS metastases were treated at ≥ 200 mg. Of the 26 pts, 13 pts had baseline target lesions, and 13 pts had only non-target lesions. CNS responses were observed in ALK TKI naïve pts and pts that received prior C or a 2[nd] generation ALK TKI. In the 13 pts with baseline target CNS lesions, IC response rate (RR) was 69%, including 1 CR, and 31% had SD, a 100% disease control rate. In the 13 pts with only non-target baseline lesions, 1 CR was achieved and 8 pts had SD. The IC RR in the 3 ALK TKI naïve pts with baseline target lesions was 100%, and 62% in 8 pts that received prior C only. Of 2 pts with baseline target lesions who received a prior 2[nd] generation ALK TKI, 1 had a PR and 1 SD. Median duration of IC response in the 10 pts who responded (9 with target lesions, 1 with non-target lesions only) is 5.8+ months, with the longest duration being 24 months.

      Conclusions:
      Our clinical findings support the preclinical results that the use of ensartinib may result in favorable therapeutic outcomes in pts with ALK+ NSCLC with CNS metastases. The ongoing phase III eXalt3 study will assess CNS RR and time to CNS progression in pts receiving 1st-line ensartinib vs C.

      Clinical trial identification:
      NCT02767804 and NCT01625234

      Legal entity responsible for the study:
      Xcovery Holding Company

      Funding:
      Xcovery Holding Company

      Disclosure:
      K. L. Reckamp: Xcovery Holding Company research funds to institution Ariad consultant and research funds to institution. H. A. Wakelee: Peregrin: Consultant/Independent contractor and honorarium recipient. Novartis: Grants/research support, consultant, honorarium recipient. ACEA: Consultant and honorarium recipient. Pfizer: Grants/research support, consultant, honorarium recipient. BMS: Grants/research support. Xcovery: Grants/research support. Celgene: Grants/research support. Roche/Genentech: Grants/research support. Medimmune: Grants/research support. Lilly: Grants/research support. S. Patel: Research funding from: Bristol-Myers Squibb, Eli Lilly, MedImmune, Pfizer, Roche/Genentech, Xcovery. Speaking fees from: Boehringer Ingelheim, Merck. G. Blumenschein: Grants/Research Support Recipient, Consultant- BMS, Bayer, Merck, Celgene Consultant- Clovis, AbbVie Grants/Research Support Recipient- Novartis, Xcovery, Astrazeneca. J. W. Neal: Consulting or Advisory role: Clovis Oncology, CARET/Physicians Resource Management, Nektar, Boehringer Ingelheim Research Funding- Genentech/Roche, Merck, ArQule, Novartis, Exelixis, Boehringer Ingelheim, Nektar. B. Gitlitz: Speakers Bureau for Lilly Speakers Bureau for Genentech. F. Tan: Manager- Xcovery Holding Company Chief Medical Officer- Betta Pharmaceuticals. K. Harrow: Xcovery Holding Company- Full-time Employee. L. Horn: Consulting for Xcovery Holding Company, BMS, BI, abbvie, Genentech, Merck. All other authors have declared no conflicts of interest.

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      Invited Discussant 3O, 87O and 88O (ID 536)

      16:45 - 18:15  |  Author(s): S. Popat

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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    The implications of TNM staging on clinical practice (in NSCLC) (ID 3)

    • Event: ELCC 2017
    • Type: Educational session
    • Track:
    • Presentations: 4
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      The impact on bronchoscopic staging (ID 7)

      14:30 - 16:00  |  Author(s): D. Gompelmann

      • Abstract
      • Slides

      Abstract not provided

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      Surgical implications (ID 8)

      14:30 - 16:00  |  Author(s): T. Mitsudomi

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      M1b: Will it be useful to establish a new paradigm of oligometastatic disease? (ID 9)

      14:30 - 16:00  |  Author(s): W.E.E. Eberhardt

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      Combination of molecular markers and TNM staging to refine prognosis and therapy (ID 10)

      14:30 - 16:00  |  Author(s): M.S. Tsao

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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    The role of the pathologist in guiding therapy (ID 12)

    • Event: ELCC 2017
    • Type: Specialty Session
    • Track:
    • Presentations: 4
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      Conventional therapy for lung cancer (ID 47)

      11:00 - 12:30  |  Author(s): M.S. Tsao

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      Targeted therapy for lung cancer (ID 48)

      11:00 - 12:30  |  Author(s): S. Lantuejoul

      • Abstract
      • Slides

      Abstract not provided

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      Immunomodulatory therapy for lung cancer (ID 49)

      11:00 - 12:30  |  Author(s): F.R. Hirsch

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      Therapy for mesothelioma and other thoracic malignancies (ID 50)

      11:00 - 12:30  |  Author(s): A.G. Nicholson

      • Abstract
      • Slides

      Abstract not provided

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    What should non-surgeons expect from surgeons? (ID 24)

    • Event: ELCC 2017
    • Type: Educational session
    • Track:
    • Presentations: 4
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      Minimal requirements for surgical participation in CT screening programmes (ID 98)

      11:00 - 12:30  |  Author(s): G. Veronesi

      • Abstract
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      Surgeon-led randomised trials: The case of mesothelioma (ID 99)

      11:00 - 12:30  |  Author(s): J. Edwards

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      The approach of surgeons towards N2 NSCLC (ID 100)

      11:00 - 12:30  |  Author(s): G. Massard

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      The impact of international surgical registries on multidisciplinary decisions: The case of thymic tumours and NET (ID 101)

      11:00 - 12:30  |  Author(s): P.L. Filosso

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    T790M: Liquid biopsy or histological samples? (ID 17)

    • Event: ELCC 2018
    • Type: Controversy session
    • Track:
    • Presentations: 4
    • +

      Introduction and first vote (ID 69)

      15:00 - 16:00  |  Presenting Author(s): M. Denis, F. Blackhall

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      Liquid biopsy (ID 70)

      15:00 - 16:00  |  Presenting Author(s): N. Reguart

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      Histological samples (ID 71)

      15:00 - 16:00  |  Presenting Author(s): E. Rouleau

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      Second vote and conclusions (ID 72)

      15:00 - 16:00  |  Presenting Author(s): M. Denis, F. Blackhall

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    Uncommon driver alterations: Should we use off-label targeted agents? (ID 10)

    • Event: ELCC 2018
    • Type: Controversy session
    • Track:
    • Presentations: 4
    • +

      Introduction and first vote (ID 39)

      09:15 - 10:15  |  Presenting Author(s): E. Smit, F. Cappuzzo

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      Follow guidelines of non-oncogene addicted NSCLC (ID 40)

      09:15 - 10:15  |  Presenting Author(s): F. Ciardiello

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      Give an off-label prescription based on the best knowledge (ID 41)

      09:15 - 10:15  |  Presenting Author(s): J. Mazieres

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      Second vote and conclusions (ID 42)

      09:15 - 10:15  |  Presenting Author(s): E. Smit, F. Cappuzzo

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