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Z. Song



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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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      202P - The clone evolutionary landscape and genomic characteristics of osteosarcoma and lung metastasis (ID 204)

      12:30 - 13:00  |  Author(s): Z. Song

      • Abstract
      • Slides

      Background:
      Tumor metastasis is still the main cause of cancer related mortality, so it is important to identify the key molecules in each step of tumor metastasis and develop new strategies for prevention and control of tumor metastasis. Osteosarcoma (OS) is a primary malignant bone tumor that has a high potential to metastasize to lungs. Few consistent clinically actionable mutations have been reported and no further improvements have been made in the last decades regarding survival. Therefore, biomarkers prognosticating for overall survival or the development of lung metastases in patients with OS may improve personalized care. The study of our aim is to investigate harbor distinct genetic alterations beyond those observed in primary tumors.

      Methods:
      Next-generation sequencing (NGS)-based 381 genes panel assay were performed on ten patients with primary OS and matched lung metastatic tumors. A set of high confident SNV, small insertion and indel and CNV in each sample were identified.

      Results:
      There were diversified metastatic progression during lung metastasis of OS including parallel evolution (6/10) and linear evolution (4/10), and metastasis-to-metastasis spread was also found in two patients with multiple metastasis. Multiple novel significantly mutated genes were identified, including CREBBP, LRP1B, MAP3K1 and LRP1B in lung metastases, SETD2, GNAS, and H3F3A in primary tumors, and CDKN2A in both. Copy number analysis indicated recurrent CNAs, including NFKBIA gain, MCL1 gain, and MYC gain in lung metastases, AMER1 loss, CTNNB1 gain in primary tumors, and CDKN2B gene family loss in both. Furthermore, phylogenetic analyses revealed that paired primary tumors and metastases underwent parallel evolution with few ubiquitous clonal mutations, suggesting that OS metastases are likely to be derived from primary tumors at a very early stage of their evolution.

      Conclusions:
      The evolution of primary and metastatic tumors were very complex. Our findings strongly support a parallel evolution model of primary and metastatic tumors. Moreover, the much higher mutation load and significantly mutated genes that are specifically associated with lung metastases may provide immune checkpoint inhibitor and target therapeutic insight for OS.

      Clinical trial identification:


      Legal entity responsible for the study:
      Jinhuo Lai

      Funding:
      Has not received any funding

      Disclosure:
      All authors have declared no conflicts of interest.

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      23P - Genomic profiling of gene aberrations in 323 Chinese NSCLC patients (ID 203)

      12:30 - 13:00  |  Author(s): Z. Song

      • Abstract
      • Slides

      Background:
      Therapeutic approaches to non-small cell lung cancer (NSCLC) have shifted toward an emphasis on molecularly targeted therapy in genotypic subsets of patients such as EGFR, ALK, ROS1. Patients with driver mutations receiving matched target drugs could have significantly longer progression free and overall survival. In this study, we aimed to analyse the genomic alterations of NSCLC.

      Methods:
      Formalin-fixed paraffin-embedded tumor samples of 323 Chinese NSCLC patients including 193 males (59.75%) and 130 females (40.25%) with a median age of 58 were collected for next-generation sequencing (NGS)-based 59-genes panel assay. Genomic alterations including single base substitution, short and long insertions/deletions, copy number variations, and gene fusions in selected genes were assessed.

      Results:
      Different histological subtypes of adenocarcinoma (278/323, 86.07%), squamous carcinoma (32/323, 9.91%), mixed carcinoma (7/323, 2.17%) and large cell carcinoma (6/323, 1.86%) were included in the Chinese NSCLC cohort. The top ranked genomic alterations were TP53 (182/323, 56.35%), EGFR (133/323, 41.18%), MSH2(51/323, 15.79%), TSC2 (46/323, 14.24%), MSH6 (30/323, 9.29%), ALK fusions (28/323, 8.67%), MET (22/323, 6.81%), KRAS (22/323, 6.81%), BRAF (20/323, 6.19%), PIK3CA (18/323, 5.57%), HER2 (16/323, 4.95%), ROS1 fusions (9/323, 2.79%), and RET fusions (8/323, 2.48%), which makes up 90.40% of the 323 patients with at least one driver mutation. In addition to common driver mutations, rare mutation types such as HIP1-ALK, CEP72-ROS1, RAD18-ROS1 and FGFR3-TACC3 were also detected by deep sequencing assay.

      Conclusions:
      With the help of NGS, our study revealed the landscape of driver gene mutations in 323 Chinese NSCLC patients, and we also found the most target locations that might be treated by targeted therapies. Further studies may emerge whether concurrent mutations, mutation burden and the number of actionable mutation are associated with survival outcome in NSCLC.

      Clinical trial identification:


      Legal entity responsible for the study:
      Yueping Liu

      Funding:
      Has not received any funding

      Disclosure:
      All authors have declared no conflicts of interest.

      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.