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S. Ekman

Moderator of

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    Management of brain metastases (ID 2)

    • Event: ELCC 2017
    • Type: Educational session
    • Track:
    • Presentations: 4
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      Local management of brain metastases: The surgeon’s perspective (ID 4)

      14:30 - 16:00  |  Author(s): M. De Praeter

      • Abstract
      • Presentation
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      Abstract not provided

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      Molecular characteristics of brain metastases: Are they different? (ID 2)

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

      • Abstract
      • Presentation
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      Abstract not provided

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      Radiation therapy of brain metastases (ID 5)

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

      • Abstract
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      Abstract not provided

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      Systemic treatment of brain metastases (ID 3)

      14:30 - 16:00  |  Author(s): J.C. Yang

      • Abstract
      • Presentation
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      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.

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      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.

  • +

    Targeted therapies and management of brain metastasis (ID 40)

    • Event: ELCC 2017
    • Type: Proffered Paper session
    • Track:
    • Presentations: 7
    • +

      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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      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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      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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      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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    • +

      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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    • +

      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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Author of

  • +

    Management of brain metastases (ID 2)

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

      Molecular characteristics of brain metastases: Are they different? (ID 2)

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

      • 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 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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