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Hongjun Gao



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    P2.01 - Advanced NSCLC (Not CME Accredited Session) (ID 950)

    • Event: WCLC 2018
    • Type: Poster Viewing in the Exhibit Hall
    • Track:
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/25/2018, 16:45 - 18:00, Exhibit Hall
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      P2.01-101 - Dynamic Monitoring of Gene Alterations with ctDNA by NGS for EGFR Mutated Lung Adenocarcinoma Treated with Gefitinib in BENEFIT Study (CTONG 1405) (ID 14347)

      16:45 - 18:00  |  Author(s): Hongjun Gao

      • Abstract

      Background

      Blood-based cell-free tumor DNA (ctDNA) could be dynamically monitored to provide gene alterations during EGFR-TKI treatment, which might offer critical clue for prognosis and clinical treatment decision. Here we reported the dynamic gene alterations monitoring using next generation sequencing (NGS) in BENEFIT study to explore the mechanisms of different responses and resistances to EGFR-TKI in EGFR-sensitizing-mutated lung-adenocarcinoma (LADC) patients.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      Patients with systemic treatment-naïve, stage IV LADC and EGFR-sensitizing-mutation in ctDNA were enrolled to receive gefitinib. Blood samples were dynamically obtained at baseline, every 8 weeks and at disease progression (PD). The dynamic analysis of quantity of ctDNA, multiple driver genes and tumor suppressors were investigated with NGS (Nextseq500 sequencer, consisting of critical exons/introns of 168 genes), and were correlated with efficacy and resistance.

      4c3880bb027f159e801041b1021e88e8 Result

      Totally 181 LADC patients with EGFR-sensitizing-mutation (exon-19-deletion and exon-21-L858R-point-mutation) provided sufficient blood samples for NGS analysis at baseline, of which 143 patients obtained at least four timepoints of dynamic blood sample collection until PD (baseline, 8 weeks, 8 weeks before PD and PD). At baseline, 180 of patients (99.4%) were confirmed as EGFR-sensitizing-mutation with NGS (92 EGFR-19-deletion and 88 EGFR-L858R-point-mutation) including 44 (24.3%) EGFR-amplification, 116 (64%) TP53-mutation, or other known oncogenic drivers including MET (N=5, 2.8%), ERBB2 (N=7,3.9%), KRAS (N=6, 3.3%), BRAF (N=2, 1.2%), RET (N=1, 0.6%), ROS1 (N=1, 0.6%), or EGFR-T790M (N=4, 2.2%), which was correlated with poor efficacy compared with those with only EGFR-sensitizing-mutation (PFS 4.7 months [m] vs. 13.2m , p=0.002). Additionally, tumor suppressor genes exhibiting cumulative effect to poor prognosis: PFS for 164 patients with TP53&RB1&PTEN-mutation≤1 was 11.1m, while for 16 patients with TP53&RB1&PTEN-mutation>1,PFS was 4.7 m, p<0.0001. To cut-off date, 117 patients had PD, among them, 63 (54%) patients acquired EGFR-T790M-mutation presented as dominant resistance mechanism besides MET-amplification/ERBB2-amplification/ERBB2-S310F (N=16, 14%), RET fusion/splice (N=2, 1.7%), ROS1-C2336F-mutation (N=1, 0.9%), RB1-nonsense-mutation (N=2, 1.7%), TP53-Y205S-mutation (N=1, 0.9%) and TP53-Y205S-mutation accompanied with FGFR1-amplification (N=1, 0.9%). The remaining resistance mechanisms (31%) were unknown. Patients with only T790M-mutation had a significantly longer PFS (11.5m) compared with patients obtaining other acquired resistant mechanisms (3.0m). Interestingly, seventy-five (53.2%) patients had molecular progression before radiographic progression, and the median time difference was 8.7 weeks.

      8eea62084ca7e541d918e823422bd82e Conclusion

      Dynamic alterations of multi-drivers and suppressors together with EGFR-sensitizing-mutation and T790M-mutation could separate LADC into different subgroups with distinguished molecular features, which may play a vital role during EGFR-TKI treatment for resistance-predicting, and initial/subsequent treatment decision-making.

      6f8b794f3246b0c1e1780bb4d4d5dc53

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    P2.12 - Small Cell Lung Cancer/NET (Not CME Accredited Session) (ID 961)

    • Event: WCLC 2018
    • Type: Poster Viewing in the Exhibit Hall
    • Track:
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/25/2018, 16:45 - 18:00, Exhibit Hall
    • +

      P2.12-06 - The Efficacy of Apatinib Plus Topotecan as Laterline Therapy for Advanced Small Cell Lung Cancer (ID 13099)

      16:45 - 18:00  |  Author(s): Hongjun Gao

      • Abstract
      • Slides

      Background

      Small cell lung cancer(SCLC) is a malignant, aggressive and rapidly progressing cancer. There is no standard treatment strategy for patients with advanced SCLC who experienced progression with first line of chemotherapy. Apatinib, an oral tyrosine kinaese inhibitor targeting vascular endothelial growth receptor 2 (VEGFR 2), has shown well anti-tumor activity and manageable toxicities in SCLC. Some previous cases showed that apatinib plus topotecan for laterline therapy for advanced SCLC patients is safe and effective, but there is no similar studies at home and abroad.Small cell lung cancer(SCLC) is a malignant, aggressive and rapidly progressing cancer. There is no standard treatment strategy for patients with advanced SCLC who experienced progression with first line of chemotherapy. Apatinib, an oral tyrosine kinaese inhibitor targeting vascular endothelial growth receptor 2 (VEGFR 2), has shown well anti-tumor activity and manageable toxicities in SCLC. Some previous cases showed that apatinib plus topotecan for laterline therapy for advanced SCLC patients is safe and effective, but there is no similar studies at home and abroad.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      Our study retrospectively assessed the efficacy and safety of apatinib plus topotecan in patients with advanced SCLC after the first line of chemotherapy. The primary endpoint was progression free survival (PFS). The study was expected to enroll 25 patients who received apatinib (250mg QD) plus topotecan (2mg QD; day1-5, every four weeks). Treatment was continued until disease progression and the tumor response was determined according to the Response Evaluation Criteria in Solid Tumors (RECIST) Version 1.1.

      4c3880bb027f159e801041b1021e88e8 Result

      The main results are showed as follows.

      秦海峰-wclc.png

      8eea62084ca7e541d918e823422bd82e Conclusion

      Apatinib plus topotecan exhibits superior activity and generally manageable toxicities for the pretreated patients with advanced small cell lung cancer. It may provide a new therapy strategy for them, but large sample and additional clinical trials are also needed.

      6f8b794f3246b0c1e1780bb4d4d5dc53

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