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B. Solomon

Moderator of

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    ISS02 - Industry Supported Symposium: ALK and ROS1 in NSCLC: Optimising the Continuum of Care - Pfizer Oncology (ID 436)

    • Event: WCLC 2016
    • Type: Industry Supported Symposium
    • Track:
    • Presentations: 8
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      ISS02.01 - Welcome & Introduction (ID 7029)

      B. Solomon

      • Abstract

      Abstract not provided

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      ISS02.02 - The Importance of Molecular Testing in NSCLC (ID 7030)

      B. Solomon

      • Abstract

      Abstract not provided

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      ISS02.03 - ALK+ NSCLC: How Can We Maximise Clinical Outcome Today? (ID 7033)

      N. Girard

      • Abstract

      Abstract not provided

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      ISS02.04 - Clinical Consequences of Resistance to ALK Inhibitors (ID 7034)

      C. Lovly

      • Abstract

      Abstract not provided

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      ISS02.05 - Panel Discussion (ID 7032)

      B. Solomon, N. Girard, C. Lovly

      • Abstract

      Abstract not provided

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      ISS02.06 - ROS1+ NSCLC: Clinical Data and Experience (ID 7031)

      B. Solomon

      • Abstract

      Abstract not provided

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      ISS02.07 - Panel Discussion (ID 7035)

      B. Solomon, N. Girard, C. Lovly

      • Abstract

      Abstract not provided

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      ISS02.08 - Meeting Close (ID 7036)

      B. Solomon

      • Abstract

      Abstract not provided



Author of

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    ISS02 - Industry Supported Symposium: ALK and ROS1 in NSCLC: Optimising the Continuum of Care - Pfizer Oncology (ID 436)

    • Event: WCLC 2016
    • Type: Industry Supported Symposium
    • Track:
    • Presentations: 6
    • +

      ISS02.01 - Welcome & Introduction (ID 7029)

      B. Solomon

      • Abstract

      Abstract not provided

    • +

      ISS02.02 - The Importance of Molecular Testing in NSCLC (ID 7030)

      B. Solomon

      • Abstract

      Abstract not provided

    • +

      ISS02.05 - Panel Discussion (ID 7032)

      B. Solomon

      • Abstract

      Abstract not provided

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      ISS02.06 - ROS1+ NSCLC: Clinical Data and Experience (ID 7031)

      B. Solomon

      • Abstract

      Abstract not provided

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      ISS02.07 - Panel Discussion (ID 7035)

      B. Solomon

      • Abstract

      Abstract not provided

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      ISS02.08 - Meeting Close (ID 7036)

      B. Solomon

      • Abstract

      Abstract not provided

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    MA07 - ALK-ROS1 in Advanced NSCLC (ID 385)

    • Event: WCLC 2016
    • Type: Mini Oral Session
    • Track: Advanced NSCLC
    • Presentations: 1
    • Now Available
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      MA07.11 - Safety and Efficacy of Lorlatinib (PF-06463922) in Patients with Advanced ALK+ or ROS1+ Non-Small-Cell Lung Cancer (NSCLC) (Now Available) (ID 5053)

      B. Solomon

      • Abstract
      • Presentation
      • Slides

      Background:
      Patients with anaplastic lymphoma kinase (ALK) and c-ros oncogene 1 (ROS1) NSCLC often become resistant to tyrosine kinase inhibitor (TKI) therapy; central nervous system (CNS) relapse is common. Lorlatinib is a selective brain-penetrant ALK/ROS1 TKI, active against most known resistance mutations.

      Methods:
      In Ph I of the ongoing Ph I/II study NCT01970865, patients had ALK+ or ROS1+ NSCLC ± brain metastases and were treatment naïve or had disease progression after ≥1 TKIs. Patients received lorlatinib on day –7 and then once or twice daily from day 1. Primary objective was identification of MTD and recommended Ph II dose (RP2D). Other objectives were safety and efficacy by RECIST v1.1 including intracranial activity.

      Results:
      Of 54 patients treated in Ph I (cutoff Jan 15, 2016), 41 were ALK+, 12 ROS1+, and 1 had mutation status unconfirmed for ALK+ or ROS1+. Patients were heavily pretreated: 27 had received ≥2 prior TKIs and 20 had 1 prior TKI; 39 patients had CNS metastases at baseline. Patients were treated across 10 dose levels (total daily dose of 10–200 mg). Response rates were:

      N CR PR uCR uPR Overall RR (CR + PR)
      n (%)
      ORR in ALK+ and ROS1+ 53 3(6) 22(42) - 1(2) 25(47)
      ORR in ALK+ with 1 prior TKI 14 1(7) 7(50) - - 8(57)
      ORR in ALK+ with ≥2 prior TKI 26 2(8) 9(34) - 1(4) 11(42)
      IC ORR (target + non-target lesions) in ALK+ and ROS+ 39 10(26) 4(10) 1(3) 2(5) 14(36)
      IC ORR (target lesions) in ALK+ and ROS+ 23 7(30 4(17) - 2(9) 11(47)
      ORR, objective response rate; IC ORR, intracranial objective response rate; CR, complete response; PR, partial response; RR, response rate; u, unconfirmed
      Median duration of response was 10.5 months (95% CI 2.9– not reached [NR]) and 12.4 months (95% CI 6.5–NR) for ALK+ and ALK+/ROS1+ pts, respectively. 26 patients remain on treatment. The most common treatment-related adverse events (TRAEs) were hypercholesterolemia (69%) and peripheral edema (37%). Hypercholesterolemia was the most common (11%) grade ≥3 TRAE. No patient discontinued due to a TRAE. Analyses of ALK resistance mutations in archival tumor tissue and plasma circulating free DNA collected before lorlatinib treatment are ongoing.

      Conclusion:
      Lorlatinib was well tolerated and demonstrated durable responses, including intracranial responses, in ALK+ and ROS1+ NSCLC, most of whom had CNS metastases and ≥1 prior TKIs. The RP2D was identified as 100 mg once daily. Ph II is ongoing.

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    MA08 - Treatment Monitoring in Advanced NSCLC (ID 386)

    • Event: WCLC 2016
    • Type: Mini Oral Session
    • Track: Advanced NSCLC
    • Presentations: 1
    • Now Available
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      MA08.01 - A Highly Sensitive Next-Generation Sequencing Platform for Detection of NSCLC EGFR T790M Mutation in Urine and Plasma (Now Available) (ID 4637)

      B. Solomon

      • Abstract
      • Presentation
      • Slides

      Background:
      Non-invasive genotyping of NSCLC patients by circulating tumor (ct)DNA is a promising alternative to tissue biopsies. However, ctDNA EGFR analysis remains challenging in patients with intrathoracic disease, with a reported 26-57% T790M mutation detection rate in plasma (Karlovich et al., Clin Cancer Res 2016; Wakelee et al., ASCO 2016). We investigated whether a mutation enrichment NGS could improve mutation detection in plasma and urine from TIGER-X, a phase 1/2 study of rociletinib in patients with EGFR mutation-positive advanced NSCLC.

      Methods:
      The therascreen (Qiagen) or cobas (Roche) EGFR test was used for EGFR T790M analysis in tumor biopsies. Urine and plasma were analyzed by trovera mutation enrichment NGS assay (Trovagene).

      Results:
      Of 174 matched tissue, plasma and urine specimens, 145 (83.3%) were T790M+ by central tissue testing, 142 (81.6%) were T790M+ by plasma, and 139 (79.9%) were T790M+ by urine. Urine and plasma combined identified 165 cases (94.8%) as T790M+. Of 25 cases positive by ctDNA but negative/inadequate by tissue, 16 were double-positive in plasma and urine, unlikely to be false positive (Figure 1). T790M detection rate was higher for extrathoracic (n=119) vs intrathoracic (n=55) disease in plasma (87.4% vs 69.1%, p=0.006) but not urine (81.5% vs 76.4%, p=0.42). Combination of urine and plasma identified T790M in 92.7% of intrathoracic and 95.8% of extrathoracic cases (p=0.47). In T790M+ patients, objective response rate was similar whether T790M mutation was identified by tissue, plasma or urine: 37.4%, 33.1% and 36.6%, respectively. 4 of 9 patients T790M+ by urine but negative by tissue responded, and 2 of 8 patients T790M+ by plasma but negative by tissue responded.

      Conclusion:
      Mutation enrichment NGS testing by urine and plasma combined identified 94.8% of T790M+ cases. Combination of urine and plasma may be considered before tissue testing in EGFR TKI resistant NSCLC, including patients without extrathoracic metastases. Figure 1



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    MA16 - Novel Strategies in Targeted Therapy (ID 407)

    • Event: WCLC 2016
    • Type: Mini Oral Session
    • Track: Chemotherapy/Targeted Therapy/Immunotherapy
    • Presentations: 1
    • Now Available
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      MA16.09 - Antitumor Activity and Safety of Crizotinib in Patients with MET Exon 14-Altered Advanced Non-Small Cell Lung Cancer (Now Available) (ID 5162)

      B. Solomon

      • Abstract
      • Presentation
      • Slides

      Background:
      MET alterations leading to exon 14 skipping occur in ~4% of non-squamous non‑small cell lung cancer (NSCLCs) and 20–30% of sarcomatoid lung carcinomas, resulting in MET activation and sensitivity to MET inhibitors in vitro.[1–4] Crizotinib, initially developed as a MET inhibitor, is currently approved for the treatment of ALK-rearranged and ROS1-rearranged advanced NSCLC. We present crizotinib antitumor activity and safety data in patients (pts) with MET exon 14-altered advanced NSCLC.

      Methods:
      Advanced NSCLC pts positive for MET exon 14-alteration status determined locally by molecular profiling were enrolled into an expansion cohort of the ongoing phase I PROFILE 1001 study (NCT00585195) and received crizotinib at a starting dose of 250 mg BID. Objective responses were assessed using RECIST v1.0.

      Results:
      As of the data cut-off of Feb 01, 2016, 21 pts with MET exon 14-altered NSCLC received crizotinib treatment (18 response-evaluable, 3 not yet evaluable). Median age was 68 y (range: 53−87). Tumor histology was: 76% adenocarcinoma, 14% sarcomatoid adenocarcinoma, 5% adenosquamous carcinoma, and 5% squamous cell carcinoma. Sixty-two percent (62%) of pts were former-smokers, 38% never-smokers, and there were no current smokers. Duration of treatment ranged from 0.2 to 12.2 mo, with 76% of pts (16/21) still ongoing. Five pts discontinued treatment (1 due to AE, 3 due to clinical or disease progression, and 1 preferred alternative treatment formulation). PRs were observed in 8 pts, for an objective response rate of 44% (95% CI: 22–69); 9 pts had stable disease. Median time to response was 7.8 weeks (range: 7.0–16.3), which was the approximate time of the scheduled first on treatment tumor scans for patients. Median progression-free survival could not be calculated. The most common (≥25%) treatment-related AEs (TRAEs) were edema (43%) diarrhea (33%), nausea (33%), vision disorder (33%), and vomiting (29%). Most TRAEs were grade 1/2 in severity and consistent with the known safety profile of crizotinib. Four grade 3 TRAEs (edema, bradycardia, anemia, and weight increased) and no grade 4 or 5 TRAEs were reported. Enrollment of pts with MET exon 14-altered NSCLC continues, and updated data will be available at the time of presentation.

      Conclusion:
      Crizotinib has clinically meaningful antitumor activity in pts with MET exon 14-altered advanced NSCLC. The drug has a tolerable AE profile, consistent with that previously reported for pts with ALK-rearranged or ROS1-rearranged advanced NSCLC. Further study of crizotinib in this pt population is warranted.

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    SC11 - ALK, ROS1 and Rare Mutations in NSCLC (ID 335)

    • Event: WCLC 2016
    • Type: Science Session
    • Track: Chemotherapy/Targeted Therapy/Immunotherapy
    • Presentations: 1
    • Now Available
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      SC11.01 - Optimal Application & Sequence of ALK Inhibition Therapy (Now Available) (ID 6641)

      B. Solomon

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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