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Kentaro Tanaka



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    P3.09 - Pathology (Not CME Accredited Session) (ID 975)

    • Event: WCLC 2018
    • Type: Poster Viewing in the Exhibit Hall
    • Track:
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/26/2018, 12:00 - 13:30, Exhibit Hall
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      P3.09-15 - Genetic Profiling of Idiopathic Pulmonary Fibrosis Associated Non-Small Cell Lung Cancer by Targeted Next-Generation Sequencing (ID 13842)

      12:00 - 13:30  |  Author(s): Kentaro Tanaka

      • Abstract

      Background

      Little is known about the pathogenesis or genetic profiles of idiopathic pulmonary fibrosis (IPF) associated non-small cell lung cancer (NSCLC). This study was performed to investigate the genetic profiles of IPF associated NSCLC and to explore the possibility of defining potential therapeutic targets by using next-generation sequencing (NGS).

      a9ded1e5ce5d75814730bb4caaf49419 Method

      The Oncomine Comprehensive Assay v3 (OCAv3) from Thermo Fisher was used to detect clinically relevant single nucleotide variants (SNVs), insertions/deletions (INDELs), copy number variations (CNVs), and gene fusions from 161 unique cancer-related genes.

      4c3880bb027f159e801041b1021e88e8 Result

      Surgically resected tumor specimens from 18 patients with IPF associated NSCLC (adenocarcinoma, n=9; squamous cell carcinoma, n=9) were collected. A total of 61 gene mutations was identified by targeted NGS and a median number of mutated genes per patient was 5 (range, 2–26). No sensitizing EGFR mutation (exon 19 del, L858R, G719X, L861Q) and fusions genes (ALK, ROS1, RET) were identified. Fourteen samples had one or more mutations in oncogenes including PIK3CA (n=7, 39%), BRAF (n=5, 28%), PTEN (n=4, 22%), EGFR (n=4, 22%), MET (n=3, 17%), KRAS (n=2, 11%), HRAS (n=2, 11%), NRAS (n=1, 6%), ERBB2 (n=1, 6%) and DDR2 (n=1, 6%). In addition to these potentially druggable oncogenes, loss-of-function mutations in ARID1A (n=10, 56%) and TP53 (n=7, 39%), tumor suppressor genes regulating DNA damage checkpoint were frequently identified. Furthermore, loss-of-function deletions (P2415del) in NOTCH1 which plays a role in cell fate determination, growth, and survival was observed in six (33%) patients.

      8eea62084ca7e541d918e823422bd82e Conclusion

      This study demonstrated novel genetic profiles of IPF associated NSCLC using NGS.

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