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F. Cappuzzo
Moderator of
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Optimizing targeted therapy in lung cancer (ID 56)
- Event: ELCC 2018
- Type: Poster Discussion session
- Track:
- Presentations: 7
- Moderators:F. Cappuzzo, N. Peled
- Coordinates: 4/12/2018, 16:45 - 17:45, Room W
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Invited Discussant 3PD, 51PD and 132PD (ID 678)
16:45 - 17:45 | Presenting Author(s): F. Cappuzzo
- Abstract
- Presentation
Abstract not provided
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Invited Discussant 52PD and 133PD (ID 679)
16:45 - 17:45 | Presenting Author(s): N. Peled
- Abstract
- Presentation
Abstract not provided
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132PD - Plasma concentrations of pemetrexed to predict clinical outcomes in patients with advanced NSCLC (ID 614)
16:45 - 17:45 | Presenting Author(s): S. Visser | Author(s): S. Koolen, P. de Bruijn, R. Mathijssen, B. Stricker, J. Aerts
- Abstract
Background:
Currently, there are no clinically useful predictors of efficacy and toxicity to pemetrexed (PMX) in advanced non-small-cell lung cancer (NSCLC). Using population pharmacokinetic (pop-PK) modelling, we explored whether total exposure to PMX predicts for progression-free and overall survival (PFS/OS) and occurrence of (severe) chemotherapy (CTx)-related adverse events (AEs).
Methods:
In a prospective observational multi-center study, patients with stage IIIB/IV NSCLC receiving first- or second-line PMX(/platinum) were enrolled. PMX (500 mg/m[2]) was administered as a 10-min intravenous infusion every 21 days. Prior to and weekly after each PMX administration, plasma sampling was performed (cycle PK). In a subgroup, blood samples were also collected at 10, 30 minutes and 1, 2, 4, 8, 24 hours after start of PMX infusion (24h PK). With pop-PK modelling total exposure (AUC) to PMX per patient was estimated. The relation between AUC during cycle 1 (AUC~1~) and OS/PFS in treatment-naïve patients was examined using Cox regression analyses and in all patients we compared the difference in mean AUC~1~ between patients with and without grade ≥3 CTx-related AEs (CTCAE 4.03) during total treatment of 4 cycles.
Results:
For 106 of the 165 patients, concentrations of PMX were quantified (24h PK, n = 15; cycle PK, n = 106). Median estimated AUC~1~ was 201 mg·h/L (interquartile range: 179–224). In treatment-naive patients (n = 95), AUC~1~ did neither univariably predict for OS/PFS, nor multivariably when adjusted for prognostic factors sex, disease stage and WHO performance score (OS, HR = 1.05, 95%CI: 1.00–1.11; PFS, HR = 1.03, 95%CI:0.98–1.08). Compared to patients without ≥ grade 3 CTx-related AEs (n = 51), patients with ≥ grade 3 CTx-related AEs (n = 55) had significantly higher AUC~1~ values (220 vs 191, p < 0.001). When seperating ≥ grade 3 CTx-related AEs into clinical and laboratory AEs, identical results were found.
Conclusions:
Total systemic exposure to PMX does not predict for PFS/OS, but is significantly associated with more frequent occurrence of severe CTx-related AEs. Although the impact of peak concentrations on efficacy remains unclear, our findings suggest that lower dosage might prevent severe toxicity with preservation of efficacy.
Clinical trial identification:
Legal entity responsible for the study:
Erasmus MC
Funding:
ZonMw
Disclosure:
J. Aerts: Member of Scientific Committee ELCC 2018; consultant/advisory role with Eli Lilly and Company. All other authors have declared no conflicts of interest.
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133PD - Adjuvant epidermal growth factor receptor tyrosine kinase inhibitors (EGFR TKIs) for non-small cell lung cancer (NSCLC): A systematic review and meta-analysis (ID 256)
16:45 - 17:45 | Presenting Author(s): J. Raphael | Author(s): M. Vincent, G. Boldt, P. Shah, G. Rodrigues, P. Blanchette
- Abstract
Background:
The role of adjuvant EGFR-TKIs in NSCLC is not well defined. Recently 2 randomized trials showed a significant disease free survival (DFS) benefit with the use of adjuvant TKIs compared to platinum-based chemotherapy in EGFR-mutant patients. Yet, older trials conducted on patients with any EGFR status did not demonstrate the same benefit. Herein, we conduct a systematic review and meta-analysis to assess the efficacy and safety of adjuvant TKIs in NSCLC patients.
Methods:
The electronic databases Medline (PubMed) and EMBASE were searched for relevant randomized trials between January 2000 and October 2017. Pooled hazard ratios (HR) for DFS and overall survival (OS), and pooled risk ratios (RR) and odds ratios (OR) for 2-year DFS and toxicity were extracted using the generic inverse variance and the Mantel-Haenszel and Peto method to perform a meta-analysis. To account for between-studies heterogeneity, random-effect models were used. Subgroup analyses assessed patients with a sensitizing EGFR mutation.
Results:
Six studies met the inclusion criteria and were included. In patients with any EGFR status, adjuvant TKIs marginally improved the DFS (5 trials, 1,860 participants, HR = 0.65, 95%CI 0.43–1.00) but not OS (4 trials, 662 participants, HR = 0.8, 95%CI 0.48–1.33). The risk of developing grade 3 or higher skin toxicity (6 trials, 1,831 participants, OR = 6.07, 95%CI 4.34–8.51) and diarrhea (6 trials, 1, 831 participants, OR = 4.05, 95%CI 2.44–6.74) was increased compared to chemotherapy, placebo or no treatment. In EGFR-mutant patients, adjuvant TKIs decreased the risk of disease recurrence by 48% (5 trials, 560 participants, HR = 0.52, 95%CI 0.35–0.78), improved the 2-year DFS (6 trials, 599 participants, HR = 0.53, 95%CI 0.43–0.66) but had no effect on OS (4 trials, 662 participants, HR = 0.64, 95%CI 0.22–1.89).
Conclusions:
Adjuvant TKIs significantly decrease the risk of recurrence in EGFR-mutant NSCLC patients but do not improve OS. Yet, OS data are still immature and longer follow up is needed for a definitive assessment of this outcome measure. Further results from ongoing well-designed trials will define the role of adjuvant TKI in NSCLC and provide stronger conclusions.
Clinical trial identification:
N/A
Legal entity responsible for the study:
Jacques Raphael
Funding:
Has not received any funding
Disclosure:
All authors have declared no conflicts of interest.
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3PD - Co-targeting PIM1 or Src to overcome the limits of single MET inhibition (ID 333)
16:45 - 17:45 | Presenting Author(s): I. Attili | Author(s): N. Karachaliou, J. Bracht, J. Berenguer, C. Codony-Servat, M. Ito, M. Rugge, P.F. Conte, L. Bonanno, R. Rosell
- Abstract
Background:
Single MET inhibition has controversial effects in MET addicted tumors. Proviral integration site for Moloney murine leukemia virus-1 (PIM1) is activated upon MET inhibition in MET addicted cells. PIM1 drives the expression of receptor tyrosine kinases (RTKs). SHP2, a non-receptor protein tyrosine phosphatase, is central in RTKs signaling and in Src activation. We have shown that the overexpression of RTKs like AXL and the transmembrane protein CUB domain-containing protein-1 (CDCP1) as well as Src activation, are mechanisms of intrinsic resistance to EGFR inhibition in EGFR mutant lung cancer. We are now testing whether RTKs, SHP2 or CDCP1 expression and activation are driven by PIM1 or Src and cause resistance to MET inhibitors in MET addicted tumors.
Methods:
We studied the inhibitory effect of the class I MET inhibitors tepotinib and savolitinib, the pan-PIM inhibitor AZD1208, and the Src inhibitor dasatinib in five MET addicted cell lines: 2 MET amplified lung cancer cells (EBC1 and H1993), 2 MET exon 14 mutant cells (Hs746T and H596) and a glioma cell line that carries the still not well recognized MET exon 7–8 splicing variant (E98). We assessed the effect of combined MET and PIM or MET and Src inhibition in cell viability and protein immunoblotting.
Results:
All the cell lines were sensitive to single MET inhibition (except H596) and resistant to single AZD1208 or dasatinib. The combination of savolitinib or tepotinib with AZD1208 was synergistic in the EBC1 cell line and slightly synergistic or additive in the H1993, Hs746T and E98 cell lines. The combination of savolitinib or tepotinib with dasatinib was highly synergistic in all four cell lines. The treatment of EBC1 cells with tepotinib monotherapy was not able to inhibit AXL activation while it induced the activation of SHP2 and CDCP1. AXL, CDCP1 and SHP2 expression or activation were downregulated when tepotinib was combined with dasatinib.
Conclusions:
Co-targeting PIM or Src with MET can be more effective than MET inhibition alone in MET addicted cell lines. Overexpression and activation of RTKs, CDCP1 and SHP2 can be mechanisms of resistance to single MET inhibition. The investigation of combinatorial strategies in MET addicted tumors, merits further investigation.
Clinical trial identification:
Legal entity responsible for the study:
IGTP – Germans Trias i Pujol Research Institute, Badalona, Barcelona, Spain
Funding:
Fundació Obra Social “La Caixa”
Disclosure:
All authors have declared no conflicts of interest.
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51PD - Effect of MEK inhibition on PDL1 and and on cytokinesproduction profilein NSCLC cell lines and in human lymphocites (ID 535)
16:45 - 17:45 | Presenting Author(s): F. Morgillo | Author(s): C.M. Della Corte, G. Viscardi, R. Di Liello, F. Papaccio, F. Ciardiello
- Abstract
Background:
Preclinical models suggest that MAPK pathway is implicated in the immune-resistance of tumors and MEK-inhibition can increase the CD8+ T-cell infiltration and the efficacy of PD-1/PD-L1 blockade.
Methods:
First, we evaluated PD-L1 mRNA expression by Real Time qPCR and its protein production, togheter with MAPK proteins in a panel of non-small cell lung cancer (NSCLC) cell lines. Then, we studied the changes in PD-L1 and major histocompatibility complex class-I (MHC-I) expression and cytokines’ production, after inhibition with selumetinib or stimulation of MAPK signalling by phorbol 12-myristate 13-acetate (PMA). In addition, we explored the effect of MEK inhibition on T-cell function by using Peripheral blood mononuclear cells (PBMC) from healthy volunteers.
Results:
A consistent correlation between PD-L1 mRNA and protein expression across cell lines suggested that expression mainly depends on trascriptional regulation, and it is regulated by MAPK signal, through the bindng of p65 to the PD-L1 promoter. Moreover, MEK inhibition resulted in an increased expression of MHC-I on cancer cells and increased mRNA expression levels of IFN gamma, IL-6, IL-1B, and TNFalpha, all molecules involved in the activation and differentiation of TCD8+ cytotoxic lymphocytes (CTL) subset. In this scenario, we also tested the effect of MEK inhibitor on activated T-lymphocytes from PBMC of healthy volunteers. After five days of treatment, RT-qPCR analysis revealed a significant increase of mRNA expression of some typical CD8+ T cell pro-inflammatory cytokines, like IL-12, TNFalpha and IFNgamma.
Conclusions:
These results further support the idea that MEK inhibitor reduces PD-L1 expression and this allows the establishment of a pro inflammatory microenvironment. On the other side, pheripheral T cells, treated with selumetinib, produce pro inflammatory cytokines typical of CTL subset, that seems more involved in immune response against cancer. In this context, MEK inhibition may represent a potential mechanism to convert otherwise resistant cancers and suggest new potential treatment combination strategies of MEK-inhibitors with anti-PD-L1 antibodies in NSCLC.
Clinical trial identification:
Legal entity responsible for the study:
University of Campania “L. Vanvitelli”
Funding:
Has not received any funding
Disclosure:
All authors have declared no conflicts of interest.
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- Abstract
Background:
TKI has significantly improved survival time of NSCLC pts with sensitive mutation. However, pts present different outcome while receiving TKI treatment. We conduct a prospective multicenter clinical trial to determine whether clonality of sensitive mutation is related to the efficacy of TKI. We also evaluate the consistency of TMB between tissue and blood in this cohort.
Methods:
Paired tumor and plasma samples at diagnosis were obtained from systemic treatment naïve pts with advanced NSCLC. DNA was sequenced by target-capture deep sequencing of 1021 previously annotated genes related to solid tumors. Clonal EGFR mutation was defined if EGFR mutation was in the cluster with the highest mean variated allele frequency with PyClone, and otherwise subclonal EGFR mutation. TMB of tissue (tTMB) and blood (bTMB) analysis interrogated single nucleotide variants, small insertion and deletion, with VAF ≥3% and ≥0.5%, respectively. TMB-high pts were identified with ≥9 mut/MB (upper quartile of data from geneplus).
Results:
During February to November 2017, 80 advanced NSCLC pts were enrolled from 9 centers. A total of 371 somatic variations were detected in tissues. Mutations occurred most frequently in TP53 (52%), EGFR (47%), ALK (13%), KRAS (11%). In matched plasma, 258 (70%) tumor-derived mutations were detected by pan-caner panel sequencing. A total of 41 EGFR mutations were detected in 37 pts, most of which occurred in tyrosine kinase domain (Ex19del, 42%; L858R, 37%). Most EGFR mutation were clonal in tissue and plasma, with a consistence of 85% in paired samples. In addition, bTMB was significantly correlated to tTMB (Pearson r = 0.75, p-value = 2.3e-12), with a consistence of 90%. Interestingly, high TMB was observed in a small fraction of patients (6%) with driver mutations, such as mutations in EGFR, ALK fusion, ERBB2 and PIK3CA.
Conclusions:
Deep sequencing with the pan-cancer panel can effectively detect mutations and evaluate TMB in both tissue and blood with high consistence. EGFR mutations can be clonal or subclonal in both tissue and blood. Prospective multicenter study is ongoing to determine the EGFR clonality as a predictive factor for the TKI efficacy in NSCLC (TRACELib-NSCLC).
Clinical trial identification:
NCT03059641
Legal entity responsible for the study:
Shanghai Chest Hospital
Funding:
Geneplus-Beijing Institute
Disclosure:
All authors have declared no conflicts of interest.
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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
- Moderators:E. Smit, F. Cappuzzo
- Coordinates: 4/12/2018, 09:15 - 10:15, Room A
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Follow guidelines of non-oncogene addicted NSCLC (ID 40)
09:15 - 10:15 | Presenting Author(s): F. Ciardiello
- Abstract
- Presentation
Abstract not provided
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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
- Abstract
- Presentation
Abstract not provided
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Introduction and first vote (ID 39)
09:15 - 10:15 | Presenting Author(s): E. Smit, F. Cappuzzo
- Abstract
- Presentation
Abstract not provided
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Second vote and conclusions (ID 42)
09:15 - 10:15 | Presenting Author(s): E. Smit, F. Cappuzzo
- Abstract
- Presentation
Abstract not provided
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Author of
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Immunotherapy and next-generation TKIs: From second to frontline treatment (ID 55)
- Event: ELCC 2018
- Type: Poster Discussion session
- Track:
- Presentations: 1
- Moderators:P. Garrido Lopez, S. Ekman, S. Ortiz-Cuaran, E. Wauters
- Coordinates: 4/12/2018, 07:45 - 09:00, Room A
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134PD - Primary PFS and safety analyses of a randomized phase III study of carboplatin + paclitaxel +/− bevacizumab, with or without atezolizumab in 1L non-squamous metastatic NSCLC (IMpower150) (ID 469)
07:45 - 09:00 | Author(s): F. Cappuzzo
- Abstract
Background:
Atezolizumab (atezo; anti–PD-L1) inhibits PD-L1 binding to PD-1 and B7.1, restoring anti-cancer immunity. Bevacizumab (bev) may further enhance atezo efficacy by inhibiting VEGF immunosuppression and promoting T-cell tumour infiltration. IMpower150 evaluates the addition of atezo to carboplatin (C) + paclitaxel (P) ± bev in chemo-naive patients (pts) with non-squamous (NSQ) mNSCLC.
Methods:
1202 pts received atezo 1200 mg + C AUC 6 + P 200 mg/m[2] (Arm A) or atezo + bev 15 mg/kg + C + P (Arm B) vs bev + C + P (Arm C) IV q3w for 4 or 6 cycles per investigator (INV) discretion, then maintenance atezo, atezo + bev or bev, respectively. Co-primary endpoints assessed at this data cutoff (15 Sep 2017; minimum follow up, 9.5 mo) were INV-assessed PFS in the ITT-WT (EGFR or ALK negative) population and in WT pts with expression of a tumour T-effector gene signature (Teff-WT; centrally assessed), and OS in the ITT-WT population, for the Arm B vs Arm C comparison. Due to pre-specified statistical testing hierarchy, Arm A vs Arm C has not been formally tested yet.
Results:
356 pts in Arm B and 336 pts in Arm C were enrolled in the ITT-WT. Median age was 63 y; 60% were previous smokers (both arms). 61% and 62% were male, and 39% and 43% had ECOG PS 0 in Arms B and C, respectively. The HRs for INV-assessed PFS in Arm B vs C were 0.62 (95% CI: 0.52, 0.74; P < 0.0001) in the ITT-WT and 0.51 (0.38, 0.68; P < 0.0001) in the Teff-WT populations. Median PFS in Arm B vs C was 8.3 mo vs 6.8 mo and 11.3 mo vs 6.8 mo in the ITT-WT and Teff-WT populations, respectively. PFS benefit was seen regardless of PD-L1 IHC status, including PD-L1–negative pts (TC0/IC0; HR, 0.77 [95% CI: 0.61, 0.99]). Landmark PFS and ORR are shown (Table). Arm B had a comparable safety profile to Arm C; treatment-related serious AEs were 25% vs 19%, respectively.Table:IMpower150 Primary PFS Analysis, Landmark PFS and ORR
HR, hazard ratio; ORR, objective response rate; PFS, progression-free survival; Teff, T-effector; WT, wild-type.aWT populations exclude patients with EGFR or ALK driver mutations.bUnconfirmed ORR.cn = 353 in Arm B and n = 331 in Arm C.dn = 153 in Arm B and n = 127 in Arm C.Arm C (bev + C + P; N = 400) Arm B (atezo + bev + C + P; N = 400) ITT-WT population[a] n = 336 n = 356 Median PFS (95% CI), mo 6.8 (6.0, 7.1) 8.3 (7.7, 9.8) HR (95% CI; P value) 0.62 (0.52, 0.74; P < 0.0001) ITT-WT landmark PFS (95% CI), % 6-month 56% (51, 62) 67% (62, 72) 12-month 18% (13, 23) 37% (31, 42) ORR[b,c] (95% CI), % 48% (43, 54) 64% (58, 68) Teff-WT population[a] n = 129 n = 155 Median PFS (95% CI), mo 6.8 (5.9, 7.4) 11.3 (9.1, 13.0) HR (95% CI; P value) 0.51 (0.38, 0.68; P < 0.0001) Teff-WT landmark PFS (95% CI), % 6-month 57% (48, 66) 72% (65, 79) 12-month 18% (10, 25) 46% (38, 54) ORR[b,d] (95% CI), % 54% (44, 62) 69% (61, 76)
Conclusions:
IMpower150 is the first Phase III study to show a statistically significant and clinically meaningful PFS benefit with atezo + bev + chemo vs bev + chemo in pts with 1L NSQ mNSCLC. Acknowledgement of contribution: G. Finley (Allegheny Cancer Center, Pittsburgh, PA, USA), R. Jotte (Rocky Mountain Cancer Centers, Denver, CO, USA), C. Kelsch, A. Lee, S. Coleman, Y. Shen, M. Kowanetz, A. Lopez-Chavez, A. Sandler (Genentech, Inc., South San Francisco, CA, USA).
Clinical trial identification:
NCT02366143
Legal entity responsible for the study:
F. Hoffmann-La Roche Ltd/Genentech, Inc
Funding:
F. Hoffmann-La Roche Ltd/Genentech, Inc
Disclosure:
M. Reck: Consulting or Advisory Role: Lilly, F.Hoffmann‐La Roche, BI, BMS, MSD, AstraZeneca, Merck, Novartis, Pfizer, Celgene. Speakers’ Bureau: F. Hoffmann‐La Roche, Lilly, Pfizer, BI, AstraZeneca, MSD, BMS, Merck, Novartis, Pfizer, Celgene. M. A. Socinski: Honoraria: Genentech, Speakers Bureau: Genentech, Research Funding: Genentech. F. Cappuzzo: Participation in advisory boards for Roche, AZ, BMS, Takeda, MSD, Lilly, Pfizer. F. Orlandi: Research grants from Astrazeneca, MSD, Genetech-Roche, Advisory tasks for AstraZeneca, Roche, Boehringer Ingelheim, Pfizer. N. Nogami: Honoraria: Meiji Seika Pharma Co., Ltd., AstraZeneca, Pfizer Inc., Bristol‐Myers Squibb, ONO Pharmaceutical CO., LTD., Kyowa Hakko Kirin, Taiho Phamaceutical Co., Ltd., Chugai Pharmaceutical Co., Ltd, Eli Lilly Japan, Boehringer Ingelheim. D. Rodríguez-Abreu: Honoraria for lectures and Advisory Board from Bristol-Myers-Squibb, Merck Sharp & Dohme and Hoffmann-La Roche. D. Moro-Sibilot: Advisory boards for Roche, MSD, Pfizer, Novartis, BMS, Astra Zeneca, Lilly. F. Barlesi: Honarium from Genentech & Roche. G. Finley: Promotional speaking on behalf of Bristol Meyers, Boehringer Ingleheim, and Astellas Medivation, and Merck. C. Kelsch: Genentech Employee with Roche Stock. A. Lee: Genentech Employee with Roche Stock. S. Coleman: Genentech Employee with Roche Stock. Y. Shen: Genentech Employee with Roche Stock. M. Kowanetz: Genentech Employee with Roche Stock. A. Lopez-Chavez: Genentech Employee with Roche Stock. A. Sandler: Genentech Employee with Roche Stock. All other authors have declared no conflicts of interest.
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Optimizing targeted therapy in lung cancer (ID 56)
- Event: ELCC 2018
- Type: Poster Discussion session
- Track:
- Presentations: 1
- Moderators:F. Cappuzzo, N. Peled
- Coordinates: 4/12/2018, 16:45 - 17:45, Room W
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Invited Discussant 3PD, 51PD and 132PD (ID 678)
16:45 - 17:45 | Presenting Author(s): F. Cappuzzo
- 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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Uncommon driver alterations: Should we use off-label targeted agents? (ID 10)
- Event: ELCC 2018
- Type: Controversy session
- Track:
- Presentations: 2
- Moderators:E. Smit, F. Cappuzzo
- Coordinates: 4/12/2018, 09:15 - 10:15, Room A
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Introduction and first vote (ID 39)
09:15 - 10:15 | Presenting Author(s): F. Cappuzzo
- Abstract
- Presentation
Abstract not provided
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Second vote and conclusions (ID 42)
09:15 - 10:15 | Presenting Author(s): F. Cappuzzo
- Abstract
- Presentation
Abstract not provided
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