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Yu Shyr



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    MS 01 - Clinical Development of Novel Agents (ID 523)

    • Event: WCLC 2017
    • Type: Mini Symposium
    • Track: Clinical Design, Statistics and Clinical Trials
    • Presentations: 1
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      MS 01.04 - Is "Big Data" the Solution to the Complex Therapeutic Landscape? (ID 7643)

      11:00 - 12:30  |  Presenting Author(s): Yu Shyr

      • Abstract
      • Presentation
      • Slides

      Abstract:
      The Holy Grail of precision medicine is the comprehensive integration of patient genotypic with phenotypic data to develop personalized disease prevention and treatment strategies. Single cell sequencing, single cell mass cytometry (CyTOF), microbiome, and other types of high-throughput assays have exploded in popularity in recent years. The ability to generate big data brings us one step closer to the realization of precision medicine; nevertheless, across the life cycle of such data, from experimental design to data capture, management, analysis, and utilization, many challenges remain. In this session, I will discuss the artificial intelligence in cancer research, common statistical and bioinformatic mistakes for designing, analyzing, and interpreting the Omics based biomarker research. I will also discuss potential pathways for the seamless integration of cellular and molecular data with clinical, behavioral, and environmental parameters – a critical next step in advancing the goals of precision medicine.

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    P3.03 - Chemotherapy/Targeted Therapy (ID 719)

    • Event: WCLC 2017
    • Type: Poster Session with Presenters Present
    • Track: Chemotherapy/Targeted Therapy
    • Presentations: 1
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      P3.03-007 - LCMC2: Expanded Profiling of Lung Adenocarcinomas Identifies ROS1 and RET Rearrangements and TP53 Mutations as a Negative Prognostic Factor (ID 8338)

      09:30 - 16:00  |  Author(s): Yu Shyr

      • Abstract
      • Slides

      Background:
      The Lung Cancers Mutation Consortium (LCMC) is a multi-institutional effort where 16 sites identify oncogenic drivers and pool data to assess the impact of targeted therapies in patients with lung adenocarcinomas. We now report the results of the second patient cohort (LCMC2) with an expanded multiplex molecular panel to include RET and ROS1 and tumor suppressors.

      Method:
      904 patients with centrally confirmed stage IV lung adenocarcinomas who were candidates for therapy had at least one of 14 oncogenic drivers assessed in a CLIA-compliant laboratory using genotyping, FISH, massively parallel sequencing (NGS), and immunohistochemistry (IHC) analyses.

      Result:
      Among 423 patients tested for all 14 targets, we found a driver in 65%. Mutated KRAS was found in 31%, sensitizing EGFR in 14%, MET amplification in 5%, ALK rearrangements in 4%, BRAF V600E in 3%, and HER2 in 3%. Rearrangements in RET and ROS1 were each found in 2% (CI 1 to 3%). Using IHC, PTEN loss was found in 8% (CI 6 to 11%) and MET expression in 58% (CI 55 to 61%). Use of targeted therapies in patients with EGFR, HER2, or BRAF mutations, ALK, ROS1, or RET rearrangements, and MET amplification was associated with a gain in overall survival of 1.5 years relative to those with the same drivers not receiving targeted therapy and a gain of 1 year relative to those without an actionable driver. Current and former cigarette smokers derived a survival benefit from targeted therapies similar to never smokers (p=0.975). Among 154 patients who had all drivers assessed and NGS testing in addition, any TP53 mutation was associated with poorer survival among those with EGFR, ALK, or ROS1 (p=0.014). STK11 was detected in 11%, all in patients with KRAS mutations.

      Conclusion:
      Using an expanded testing panel, LCMC2 demonstrates the survival benefit of matching targeted treatments to oncogenic drivers in patients with lung adenocarcinomas, identifies additional prognostic factors, and supports the performance of multiplex molecular testing on specimens from all individuals with lung adenocarcinomas irrespective of clinical characteristics. We detected either MET amplifications or HER2 mutations in 7%, together more than the 4% with ALK. A targeted drug is available in the United States for 35% of patients with lung adenocarcinomas. The routine use of massively parallel sequencing (NGS) detects both targetable drivers and tumor suppressor genes that have significance for therapy selection and prognosis. Supported by Free to Breathe

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