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J. Si



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    P1.05 - Poster Session with Presenters Present (ID 457)

    • Event: WCLC 2016
    • Type: Poster Presenters Present
    • Track: Early Stage NSCLC
    • Presentations: 1
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      P1.05-023 - Induction of Patient-Derived Xenograft Formation and Clinical Significance for PD-L1 in Lung Cancer Patients (ID 4668)

      14:30 - 14:30  |  Author(s): J. Si

      • Abstract
      • Slides

      Background:
      The relevance of programmed cell death ligand 1 (PD-L1) to patient-derived xenograft (PDX) formation and clinicopathological characteristics in early stage lung cancer was studied

      Methods:
      Cell counting kit-8 and flow cytometry were carried out to examine proliferation and apoptosis in PC9 and H520 cells transfected with siRNAs. Nod-scid mice were used to establish PDX. Immunohistochemistry was done to investigate PD-L1 expression in tumor tissues.

      Results:
      Proliferation was reduced and apoptosis was induced when PD-L1 was inhibited in the cells. Higher PD-L1 expression rate was observed in the primary tumors with PDX formation than in the tumors without PDX formation. Moreover, PD-L1 was found to be related to smoking, histological types, stages and overall survival in 209 of lung cancer patients.

      Conclusion:
      This study suggests that PD-L1 promotes PDX formation ability and is an independent prognostic marker for the early stage lung cancer patients.

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    P2.03a - Poster Session with Presenters Present (ID 464)

    • Event: WCLC 2016
    • Type: Poster Presenters Present
    • Track: Advanced NSCLC
    • Presentations: 1
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      P2.03a-051 - CMTM1_v17 Promotes Chemotherapy Resistance and is Associated with Poor Prognosis in Non-Small Cell Lung Cancer (ID 4371)

      14:30 - 14:30  |  Author(s): J. Si

      • Abstract
      • Slides

      Background:
      Despite a consistent rate of initial responses, chemotherapy treatment often results in the development of chemoresistance, leading to therapeutic failure in non-small cell lung cancer (NSCLC). CMTM1_v17 is highly expressed in human testis tissues and solid tumor tissues but relatively low expression was obtained in the corresponding normal tissues. This study aims to investigate the significance of CMTM1_v17 in NSCLC and its association with cisplatin-based neo-adjuvant chemotherapy (NAC) response

      Methods:
      31 pairs of tumor tissues before and after NAC and 78 resected tumor tissues after NAC were utilized for immunohistochemistry (IHC) staining of CMTM1_v17 protein. Flow cytometry was used to detect the change of CMTM1_v17 expression in NSCLC patient-derived xenografts (PDX models) with cisplatin treatment.

      Results:
      CMTM1_v17 expression was found to be significantly related to treatment effect and outcome in the tumor tissues after NAC but not in the tissues before NAC from the 31 cases of NSCLC. We identified that high CMTM1_v17 expression was associated with low objective remission rate (ORR) (p=0.008) and poor prognosis (the median OS: 35.1 months vs 65.6 months,p=0.0045;the median DFS: 17.27 months vs 35.54 months,p=0.0207) in the 31 patients. Next, we detected CMTM1_v17 expression to confirm correlation between this protein status and clinical characteristics in 78 NSCLC patients with NAC. The up-regulation of CMTM1_v17 had a higher SD rate (p=0.007) and worse outcome ( the median OS: 41.0 months vs 80.6 months, p=0.0028;the median DFS: 33.4 months vs 64.8 months,p=0.0032). COX multivariate analysis indicated that CMTM1_v17 is an independent prognostic risk factor on patients who received NAC (OS:HR=3.642,p=0.002;DFS:HR=2.867,p=0.003). Then, we tested CMTM1_v17 expression in the lung cancer PDX mice with different treatment, showing that this protein was up-regulated in the tumor tissues received cisplatin treatment, compared to the tumor tissues with saline stimulation of control group.

      Conclusion:
      CMTM_v17 expression was significantly associated with chemoresistance and poor prognosis of the early stage NSCLC patients who received NAC. Cisplatin could induce the expression of CMTM1_v17 in lung cancer cells from PDX model.

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