Virtual Library

Start Your Search

W. Wang



Author of

  • +

    Poster Display session (Friday) (ID 65)

    • Event: ELCC 2018
    • Type: Poster Display session
    • Track:
    • Presentations: 4
    • Moderators:
    • Coordinates: 4/13/2018, 12:30 - 13:00, Hall 1
    • +

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

      12:30 - 13:00  |  Author(s): W. Wang

      • 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.

      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.

    • +

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

      12:30 - 13:00  |  Author(s): W. Wang

      • 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.

    • +

      28P - The study of ALK rearrangement in advanced primary non-small cell lung cancer and associated metastatic lesions (ID 201)

      12:30 - 13:00  |  Author(s): W. Wang

      • Abstract
      • Slides

      Background:
      ALK rearrangement in non-small cell lung cancer (NSCLC) patients has recently been identified as a driver gene and benefited from crizotinib treatment. However, no data are available for ALK rearrangement NSCLC about the relationship between primary and metastatic patients. The aim of this study was to examine the positive rate of ALK rearrangement in primary and metastatic NSCLC, and to investigate their relationships.

      Methods:
      From January 2013 to May 2015, 384 cases of primary NSCLC, 246 cases of matched metastatic tumors, and 47 cases of normal lung specimens, as the control group, were collected in our multicenter. The positive rate of ALK rearrangement among the NSCLC population was established, and thus the consistency of ALK rearrangement in advanced primary NSCLC and associated metastases and the relationship between ALK rearrangement and clinical data was analyzed.

      Results:
      The positive rate of ALK rearrangement on primary tumor was 11.46% (44/384). For those 246 paired cases, the positive rate on primary tumor was 10.98% (27/246), with that of metastases 7.32% (18/246). Among the 246 cases, there were two cases whose metastases were positive but primary tumors were negative and 11 case whose primary tumors were positive but metastases were negative. Positive rate of ALK rearrangement was higher in the primary lesions than in metastases. It was of statistical significance between the two groups (χ[2] = 112.208, P < 0.001). The positive rate of primary tumors could be predicted by metastases (κ = 0.683, P < 0.001). The sensitivity was 59.26% (16/27) and the specificity was 99.09% (217/219).

      Conclusions:
      The metastases of NSCLC can predict ALK rearrangement of the primary lesions. It can be used as an alternative means for metastases to detect ALK rearrangement which are not readily available.

      Clinical trial identification:


      Legal entity responsible for the study:
      Chunwei Xu

      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.

    • +

      31P - Analysis of ROS1 rearrangement non-small cell lung cancer cell blocks from pleural effusion (ID 202)

      12:30 - 13:00  |  Presenting Author(s): W. Wang

      • Abstract
      • Slides

      Background:
      ROS1 rearrangement in non-small cell lung cancer (NSCLC) patients has recently been identified as a driver gene event and patients benefi from crizotinib treatment. The aim of this study was to investigate the clinical value of ROS1 rearrangement non-small cell lung cancer (NSCLC) cell blocks from pleural effusion.

      Methods:
      Two hundred and fifteen cases of ROS1 rearrangement non-small cell lung cancer (NSCLC) blocks cell from pleural effusion, and 404 cases of tissues were analysed by the reverse transcription polymerase chain reaction (RT-PCR) method. The consistency of ROS1 rearrangement was examined in 74 cases of patients with tissues and cell blocks.

      Results:
      ROS1 rearrangement was found in 7 of 215 cell blocks (positive detection rate of 3.26%). ROS1 rearrangement was detected in 8 of 404 tissue blocks (positive detection rate of 1.98%). There were 71 cases of the 74 (95.95%) cases that had the same consistency as tissue block. ROS1 rearrangement was detected in 2 of 74 (2.70%) cell blocks, and 5 of 74 (6.76%) tissue blocks.

      Conclusions:
      The rate of ROS1 rearrangement in cell blocks of NSCLC is higher than in matched tissue blocks. The patients with malignant pleural effusion are likely to tend to ROS1 rearrangement.

      Clinical trial identification:


      Legal entity responsible for the study:
      Wenxian Wang

      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.