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T.S.K. Mok

Moderator of

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    First line for oncogene addicted lung cancer (ID 2)

    • Event: ELCC 2018
    • Type: Educational session
    • Track:
    • Presentations: 4
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      First vs second vs third generation EGFR TKI (ID 3)

      14:30 - 16:00  |  Presenting Author(s): J. Wolf

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      Is PFS still a relevant endpoint for first-line TKIs? (ID 2)

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

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      Key factors that determine the selection of first-line ALK inhibtiors (ID 4)

      14:30 - 16:00  |  Presenting Author(s): F. Blackhall

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      The role of first-line combination therapy for oncogene addicted lung cancer (ID 5)

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

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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    Resistance to TKIs (ID 23)

    • Event: ELCC 2018
    • Type: Educational session
    • Track:
    • Presentations: 4
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      Focus on local treatment options (ID 96)

      11:00 - 12:30  |  Presenting Author(s): F. McDonald

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      General mechanisms of resistance (ID 93)

      11:00 - 12:30  |  Presenting Author(s): T. Mitsudomi

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      Therapeutic strategies to overcome ALK and ROS1 (ID 95)

      11:00 - 12:30  |  Presenting Author(s): S. Ortiz-Cuaran

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      Therapeutic strategies to overcome EGFR (ID 94)

      11:00 - 12:30  |  Presenting Author(s): T.S.K. Mok

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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Author of

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    Poster Display session (Friday) (ID 65)

    • Event: ELCC 2018
    • Type: Poster Display session
    • Track:
    • Presentations: 2
    • Moderators:
    • Coordinates: 4/13/2018, 12:30 - 13:00, Hall 1
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      194TiP - eXalt3: Phase 3 randomized study comparing ensartinib to crizotinib in anaplastic lymphoma kinase (ALK) positive non-small cell lung cancer (NSCLC) patients (ID 644)

      12:30 - 13:00  |  Author(s): T.S.K. Mok

      • Abstract

      Background:
      Ensartinib (X-396) is a novel, potent ALK small molecule tyrosine kinase inhibitor (TKI) with additional activity against MET, ABL, Axl, EPHA2, LTK, ROS1 and SLK. Ensartinib is well-tolerated and has shown promising activity in NSCLC patients in a phase 1/2 study in patients that were both ALK TKI naïve and patients that received prior crizotinib, as well as those with CNS metastases. The safety profile of ensartinib appears to be different than other ALK TKIs.

      Trial design:
      In this global, phase 3, open-label, randomized study, approximately 270 patients with ALK+ NSCLC who have received no prior ALK TKI and up to one prior chemotherapy regimen will be randomized with stratification by prior chemotherapy (0/1), performance status (0 − 1/2), brain metastases at screening (absence/presence), and geographic region (Asia/other), to receive oral ensartinib (225 mg, once daily) or crizotinib (250 mg, twice daily) until disease progression or intolerable toxicity.Eligibility also includes patients ≥ 18 years of age, stage IIIB or IV ALK+ NSCLC. Patients are required to have measurable disease per RECIST 1.1, adequate organ function, and an ECOG PS of ≤ 2. Adequate tumor tissue (archival or fresh biopsy) must be available for central testing. The primary endpoint is progression-free survival assessed by independent radiology review based on RECIST v. 1.1 criteria. Secondary efficacy endpoints include overall survival, response rates (overall and central nervous system [CNS]), PFS by investigator assessment, time to response, duration of response, and time to CNS progression. The study has > 80% power to detect a superior effect of ensartinib over crizotinib in PFS at a 2-sided alpha level of 0.05.Phase 3 recruitment began in June, 2016 and currently has 98 active sites in 20 countries. The duration of recruitment will be approximately 24 months.

      Clinical trial identification:
      NCT02767804

      Legal entity responsible for the study:
      Xcovery Holding Corporation

      Funding:
      Betta Pharmaceuticals

      Disclosure:
      L. Horn: Consulting for Xcovery Holding Company, BMS, BI, Abbvie, Genentech, Merck. Y-L. Wu: Speaker fees from AstraZeneca, Roche, Eli Lily. M. Reck: Honoraria for lectures and consultancy: Hoffman-La Roche, Lily, BMS, MSD, AstraZeneca, Merck, Celgene, Boehringer-Ingelheim, Pfizer, Novartis. C. Liang, K. Harrow, V. Oertel, G. Dukart: Full-Time Employee: Xcovery Holding Corporation, F. Tan: Manager: Xcovery Holding Company Chief Medical Officer: Betta Pharmaceuticals. T.S.K. Mok: Grant/Research Support from AstraZeneca, BI, Pfizer, Novartis, SFJ, Roche, MSD, Clovis Oncology, BMS, Eisai, Taiho; Speaker's fees with: AstraZeneca, Roche/Genentech, Pfizer, Eli Lilly, BI, MSD, Novartis, BMS, Taiho; Major Stock Shareholder in: Sanomics Ltd.; Advisory Board for: AstraZeneca, Roche/Genentech, Pfizer, Eli Lilly, BI, Clovis Oncology, Merck Serono, MSD, Novartis, SFJ Pharmaceutical, ACEA Biosciences, Inc., Vertex Pharmaceuticals, BMS, geneDecode Co., Ltd., OncoGenex Technologies Inc., Celgene, Ignyta, Inc.; Board of Directors: IASLC, Chinese Lung Cancer Research Foundation Ltd., Chinese Society of Clinical Oncology (CSCO), Hong Kong Cancer Therapy Society (HKCTS).

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      8P - Noncanonical Wnt11, a tumor suppressive gene by antagonizing canonical Wnt signaling, represents a putative molecularly therapeutic target in lung cancer (ID 502)

      12:30 - 13:00  |  Author(s): T.S.K. Mok

      • Abstract

      Background:
      Most studies focused on the role of canonical Wnt signaling pathway, an increasing field of research, however, is concerning about the noncanonical Wnt pathways. The role of Wnt11, a noncanonical Wnt family member, has not been established in lung cancer. Epigenetic inactivation of tumor suppressive genes through promoter CpG methylation is a fundamental regulatory process during tumorigenesis.

      Methods:
      The expression levels of Wnt11 were assessed in human normal tissues and lung cancer cell lines panel by semi-quantitative reverse transcription-PCR(RT-PCR). The promoter CpG methylation of Wnt11 were tested in bisulfite treated DNA by methylation-specific PCR (MSP). Western blots assay, colony formation assay, cell proliferation assay, wound-healing assay, dual-luciferase reporter assay and apoptosis assay were used to characterize the changes induced by overexpression of Wnt11.

      Results:
      In our study, analysis of Wnt11 expression revealed it was broadly expressed in human normal adult and fetal tissues, while it's frequently downregulated or silenced in multiple lung cancer cell lines. By performing methylation-specific PCR (MSP), promoter CpG methylation of Wnt11 were frequently detected in multiple lung cancer cell lines. Functional assays show that ectopic expression of Wnt11 could suppress tumor cell growth, possibly through inducing apoptosis. Moreover, Wnt11 represses canonical Wnt/β-catenin signaling and AKT signaling pathway. Wnt11 overexpression also reversed EMT and downregulated stem cell markers.

      Conclusions:
      Together our data suggest that in lung cancer, Wnt11 is lost by methylation and represents a tumor suppressor by antagonizing canonical Wnt/β-catenin signaling and AKT signaling pathway. Restoration of Wnt11 expression through demethylation could be an important therapeutic approach in the treatment of lung cancer.

      Legal entity responsible for the study:
      The Chinese University of Hong Kong

      Funding:
      RGC (TBRS #T12-401/13R), China Natural Science Foundation (NSFC #81572327), Johns Hopkins Singapore, and VC special research fund from The Chinese University of Hong Kong

      Disclosure:
      The author has declared no conflicts of interest.

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    Resistance to TKIs (ID 23)

    • Event: ELCC 2018
    • Type: Educational session
    • Track:
    • Presentations: 1
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      Therapeutic strategies to overcome EGFR (ID 94)

      11:00 - 12:30  |  Presenting Author(s): T.S.K. Mok

      • Abstract
      • Presentation
      • Slides

      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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