Virtual Library

Start Your Search

Masaaki Yanai



Author of

  • +

    P2.14 - Targeted Therapy (ID 183)

    • Event: WCLC 2019
    • Type: Poster Viewing in the Exhibit Hall
    • Track: Targeted Therapy
    • Presentations: 2
    • Now Available
    • Moderators:
    • Coordinates: 9/09/2019, 10:15 - 18:15, Exhibit Hall
    • +

      P2.14-04 - Clinical Validation of Large NGS Gene Panel Using Residual Specimen (Now Available) (ID 391)

      10:15 - 18:15  |  Author(s): Masaaki Yanai

      • Abstract
      • Slides

      Background

      Precision medicine based on driver oncogenes is now developed for non-small cell lung cancer (NSCLC). A large number of next-generation sequencing (NGS) gene panels with various characteristics have been developed, and it is important to use properly according to the purpose. TruSight Oncology (TSO) 500 is an NGS tumor profiling assay that targets over 500 genes to analyze cancer-related biomarkers including SNVs, indels, fusions, splice variants, tumor mutation burden (TMB) and microsatellite instability (MSI).

      Method

      Of the cases diagnosed with advanced NSCLC at Tottori University Hospital, 30 cases with consent to this observational study were enrolled. TSO500 was performed at the CLIA-certified laboratory (RIKEN GENESIS CO., LTD.) using DNA and RNA extracted from archived formalin-fixed paraffin-embedded (FFPE) lung cancer specimens. These were compared with gene alterations measured in the clinical practice.

      Result

      Specimens were collected by bronchoscopy in 21 cases (70%), percutaneous biopsy in 3 cases (10%), surgery in 3 cases (10%), cell block of pleural effusion in 2 cases (7%) and thoracoscopy in 1 case (3%). The success rates of DNA analyses, including TMB and MSI analysis, and RNA analyses were 83% (25/30 cases) and 97% (29/30 cases), respectively. In the 30 cases analyzed, a total of 25 actionable gene alterations (13 EGFR mut, 4 ALK fus, 2 KRAS mut, 2 BRAF mut, 2 MET ex14 skipping, 1 RET fus, 1 PIK3CA mut) were detected in 24 cases (80%). Of the 21 cases that actionable gene alterations were identified in the clinical practice, TSO500 detected similar gene alterations in 20 cases (95%) except for one case that RNA analysis was failed. In addition, TSO500 detected BRAF V600E mutation in one case that had not been tested for BRAF mutation. TMB analysis succeeded in 26/30 cases (87%) and 9/26 cases (35%) were TMB-high when 10 mutations per mega base was set as the threshold.

      Conclusion

      Despite analyzing small biopsy specimens with a large NSG panel, TSO500 could detect not only gene alterations for clinical use but also exploratory gene alterations.

      Only Active 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 or select "Add to Cart" and proceed to checkout.

    • +

      P2.14-44 - Tumor Mutation Burden and Efficacy of Molecular Targeted Therapy in Lung Cancer (ID 1584)

      10:15 - 18:15  |  Author(s): Masaaki Yanai

      • Abstract

      Background

      Precision medicine based on driver oncogenes is now developed for non-small cell lung cancer (NSCLC). Recently, next-generation sequencing (NGS) has made it possible to analyze Tumor mutation burden (TMB), and it was revealed that TMB is an effective biomarker of immune checkpoint inhibitors. However, the impact of TMB on the effects of targeted therapy for driver alterations is still unclear.

      Method

      Of the cases diagnosed with advanced NSCLC at Tottori University Hospital, 30 cases with consent to this observational study were enrolled. TruSight Oncology (TSO) 500 was performed at the CLIA-certified laboratory (RIKEN GENESIS CO., LTD.) using DNA and RNA extracted from archived formalin-fixed paraffin-embedded (FFPE) lung cancer specimens.

      Result

      Specimens were collected by bronchoscopy in 21 cases (70%), percutaneous biopsy in 3 cases (10%), surgery in 3 cases (10%), cell block of pleural effusion in 2 cases (7%) and thoracoscopy in 1 case (3%). The success rate of TMB analysis was 83% (25/30 cases). In the 25 cases, a total of 23 actionable gene alterations (11 EGFR mut, 4 ALK fus, 2 KRAS mut, 2 BRAF mut, 2 MET ex14 skipping, 1 RET fus, 1 PIK3CA mut) were detected in 22 cases (88%). The median TMB was 7.84 (1.56-21.11) mutations/Mb. 7 of 25 (28%) patients showed high TMB, and the others showed low TMB when 10 mutations per mega base was set as the threshold. 5 of 7 (71%) patients with high TMB had one of the common driver mutations (2 EGFR mut, 2 BRAF mut and 1 PIC3CA mut) and 17 of 18 (94%) patients with low TMB had one of the driver mutations (9 EGFR mut, 4 ALK fus, 2 KRAS, 2 MET ex14 skipping and 1 RET fus). Additionally, no ALK fusion was identified in patients with high TMB. 12 of 15 patients (80%) received targeted therapy with low TMB achieved clinical response, while no patient (0/2 pts, 0%) received targeted therapy with high TMB achieved clinical response.

      Conclusion

      TMB might have the impact for the presence of driver alterations and the effects of targeted therapies.