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G. Lou



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    JCES01 - Joint IASLC - Chinese Society for Clinical Oncology - Chinese Alliance Against Lung Cancer Session (ID 413)

    • Event: WCLC 2016
    • Type: Joint Chinese / English Session
    • Track:
    • Presentations: 2
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      JCES01.14 - Mutational Profiling of Non-Small-Cell Lung Cancer Patients Resistant to First-Generation EGFR Tyrosine Kinase Inhibitors Using next Generation Sequencing (ID 7056)

      G. Lou

      • Abstract
      • Slides

      Background:
      Patients with advanced non-small-cell lung cancer (NSCLC) harboring sensitive epithelial growth factor receptor (EGFR) mutations invariably develop acquired resistance to EGFR tyrosine kinase inhibitors (TKIs). Although previous research have identified several mechanisms of resistance, the systematic evaluation using next generation sequencing (NGS) to establish the genomic mutation profiles at the time of acquired resistance has not been conducted.

      Methods:
      In our single center, we performed NGS of a pre-defined set of 416 cancer-related genes in a cohort of 97 patients with NSCLC harboring TKI-sensitive EGFR mutations at the time of acquired resistance to first-generation EGFR-TKIs between January 2015 to December 2015.

      Results:
      In 97 samples we found total 345 gene alterations (mean 3.6 mutations per patient, range 1-10). Fifty-six patients (57.7%) still exhibit EGFR-sensitive mutations as pretreatment, 93 patients (95.9%) exhibit at least one mutation except for previous existed EGFR-sensitive mutations. In all the 97 patients, most frequently mutated genes were TP53 (59.8%), T790M (28.9%), TET2 (11.3%), EGFR amplification (10.3%), PIK3CA (8.2%), BIM (8.2%), KRAS (7.2%), APC (7.2%), RB1 (7.2%), HER2 (6.2%), DNMT3A (6.2%) and MET (5.2%).

      Conclusion:
      NGS in this study uncovered many new genetic alterations potentially associated with EGFR TKI resistance and provided information for the further study of drug resistance and corresponding relevant tactics against the challenge of disease progression.

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      JCES01.21 - Molecular Profiling and Survival of Primary Pulmonary Neuroendocrine Carcinoma with Completely Resection (ID 7063)

      G. Lou

      • Abstract
      • Slides

      Background:
      According to the 2015 World Health Organization classification of lung tumors, pulmonary Large cell neuroendocrine carcinoma (PLCNC) is grouped with the small cell lung cancer (SCLC) and carcinoid as pulmonary neuroendocrine carcinoma(PNC) for the common features of neuroendocrine characteristics . Molecular profiles and prognosis of primary pulmonary neuroendocrine carcinoma(PNC) are not well investigated currently. We conducted present study to evaluate genomic abnormality and survivals in patients with primary PNC.

      Methods:
      Tumor samples of PNC after completely resection from Zhejiang Cancer Hospital were collected from 2008 to 2015. Nine driver genes including six mutation (EGFR, KRAS, NRAS, PIK3CA, BRAF, HER2) and three fusions (ALK, ROS1, RET) were evaluated by RT-PCR. Survival analysis was evaluated using the Kaplan-Meier method.

      Results:
      Totally, 108 patients with pathologic confirmed PNC were enrolled. Samples included 52 PLCNC, 44 small cell lung cancer (SCLC) and 12 carcinoid. Twelve patients were found to harbor genomic aberrations (11.1%). The most frequent gene abnormality was PIK3CA (n=5,4.6%),followed with EGFR (n=3,2.8%), KRAS (n=2,n=1.9%), ALK (n=1,0.9%), RET (n=1,0.9%). No ROS1,BRAF,NRAS and HER2 mutations were observed. The frequencies of gene aberrations in PLCNC, SCLC and carcinoid were 15.4%,6.8% and 8.3%,respectively. Sixty-seven patients were with recurrence or metastasis after surgery, including 32 PLCNC, 33 of SCLC, and two of carcinoid (both were atypical carcinoid). Among the 32 patients with PLCNC,none received molecular targeted treatment,28 received first-line chemotherapy,including 18 of etoposide/platinum regimen and 10 of other platinum-based treatment. The progression free survival in patients with etoposide/platinum regimen was longer than patients with non-etoposide/platinum treatment (4.8 vs.3.4 months,P=0.019) . Survival difference was observed among the PLCNC,SCLC and carcinoid group (37.0 vs. 34.0 vs.not reached, P=0.035), but no difference existed between the PLCNC and SCLC group (P=0.606).

      Conclusion:
      Common genomic abnormality is rare in PNC patients and most frequently observed in PLCNC. Patients with carcinoid had a superior survival than PLCNC and SCLC.

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    P3.02b - Poster Session with Presenters Present (ID 494)

    • Event: WCLC 2016
    • Type: Poster Presenters Present
    • Track: Advanced NSCLC
    • Presentations: 1
    • Now Available
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      P3.02b-105 - Mutational profiling of non-small-cell lung cancer patients resistant to first-generation EGFR tyrosine kinase inhibitors using next generation sequencing (Now Available) (ID 3801)

      G. Lou

      • Abstract
      • Slides

      Background:
      Patients with advanced non-small-cell lung cancer (NSCLC) harboring sensitive epithelial growth factor receptor (EGFR) mutations invariably develop acquired resistance to EGFR tyrosine kinase inhibitors (TKIs). Although previous research have identified several mechanisms of resistance, the systematic evaluation using next generation sequencing (NGS) to establish the genomic mutation profiles at the time of acquired resistance has not been conducted.

      Methods:
      In our single center, we performed NGS of a pre-defined set of 416 cancer-related genes in a cohort of 97 patients with NSCLC harboring TKI-sensitive EGFR mutations at the time of acquired resistance to first-generation EGFR-TKIs between January 2015 to December 2015.

      Results:
      In 97 samples we found total 345 gene alterations (mean 3.6 mutations per patient, range 1-10). Fifty-six patients (57.7%) still exhibit EGFR-sensitive mutations as pretreatment, 93 patients (95.9%) exhibit at least one mutation except for previous existed EGFR-sensitive mutations. In all the 97 patients, most frequently mutated genes were TP53 (59.8%), T790M (28.9%), TET2 (11.3%), EGFR amplification (10.3%), PIK3CA (8.2%), BIM (8.2%), KRAS (7.2%), APC (7.2%), RB1 (7.2%), HER2 (6.2%), DNMT3A (6.2%) and MET (5.2%).

      Conclusion:
      NGS in this study uncovered many new genetic alterations potentially associated with EGFR TKI resistance and provided information for the further study of drug resistance and corresponding relevant tactics against the challenge of disease progression.

      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.