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C. Hu



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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: 1
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      JCES01.15 - Analysis of Genomic Alterations and Heterogeneity in Pulmonary Adenoid Cystic Carcinoma by Next-Generation Sequencing (ID 7057)

      C. Hu

      • Abstract
      • Slides

      Background:
      Pulmonary adenoid cystic carcinoma (PACC) is one of the rare malignancies, that primary from glandular tissues of lung. Currently, the treatment of PACC relies on surgery and local radiotherapy. However the therapy for advanced PACC patients is limited. A larger number of studies demonstrated that advanced PACC patients obtained little benefit from chemotherapy. Moreover, only a few case reports revealed PACC patients were appropriate for target therapy. Using high-flux and high-resolution techniques to detect the genomic alterations of PACC could provide theoretical foundation for the precision therapy of PACC.

      Methods:
      8 PACC patients who received surgical resection between January 2013 to December 2015 were enrolled. The tumor tissues from different locations and blood samples were collected. The oncoscreen[TM] panel by Illumina platform, which utilizing probe hybridization to gathering 287 exon regions and 22 intron regions, were used to detect the gene mutation status of PACC. And the embryonal system mutations were filtered by contrasting the gene mutation status of the leukocytes. The tumor heterogeneity was revealed by comparing the gene mutation status in different areas of the same PACC, and the phylogenetic relationships were analyzed to disclose the evolving and developing progression of PACC.

      Results:
      There were 69 gene mutations together among 8 patients including 29 samples. Each patient has 8.6 mutations averagely. The high-frequency mutations were PAK3-D219E, FBXW7-D112E, TET2-T418I, KAT6A-E796A, and MET-R1005Q. However, the common mutations in other NSCLC, like EGFR, KRAS, ALK, etc., weren’t happened in this group of PACC. In this study, the spatial heterogeneity was discovered in PACC, not only in the mutation site, but also in the mutant abundance. Moreover, the phylogenetic relationships revealed that the clonal evolution and development existed in PACC.

      Conclusion:
      The status of genomic alterations in PACC was different from the other non-small cell lung cancer (NSCLC). PACC showed obvious spatial heterogeneity and clonal evolution.

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    P2.03b - Poster Session with Presenters Present (ID 465)

    • Event: WCLC 2016
    • Type: Poster Presenters Present
    • Track: Advanced NSCLC
    • Presentations: 1
    • Now Available
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      P2.03b-029 - Analysis of Genomic Alterations and Heterogeneity in Pulmonary Adenoid Cystic Carcinoma by Next-Generation Sequencing (Now Available) (ID 3831)

      C. Hu

      • Abstract
      • Slides

      Background:
      Pulmonary adenoid cystic carcinoma (PACC) is one of the rare malignancies, that primary from glandular tissues of lung. Currently, the treatment of PACC relies on surgery and local radiotherapy. However the therapy for advanced PACC patients is limited. A larger number of studies demonstrated that advanced PACC patients obtained little benefit from chemotherapy. Moreover, only a few case reports revealed PACC patients were appropriate for target therapy. Using high-flux and high-resolution techniques to detect the genomic alterations of PACC could provide theoretical foundation for the precision therapy of PACC.

      Methods:
      8 PACC patients who received surgical resection between January 2013 to December 2015 were enrolled. The tumor tissues from different locations and blood samples were collected. The oncoscreen[TM] panel by Illumina platform, which utilizing probe hybridization to gathering 287 exon regions and 22 intron regions, were used to detect the gene mutation status of PACC. And the embryonal system mutations were filtered by contrasting the gene mutation status of the leukocytes. The tumor heterogeneity was revealed by comparing the gene mutation status in different areas of the same PACC, and the phylogenetic relationships were analyzed to disclose the evolving and developing progression of PACC.

      Results:
      There were 69 gene mutations together among 8 patients including 29 samples. Each patient has 8.6 mutations averagely. The high-frequency mutations were PAK3-D219E, FBXW7-D112E, TET2-T418I, KAT6A-E796A, and MET-R1005Q. However, the common mutations in other NSCLC, like EGFR, KRAS, ALK, etc., weren’t happened in this group of PACC. In this study, the spatial heterogeneity was discovered in PACC, not only in the mutation site, but also in the mutant abundance. Moreover, the phylogenetic relationships revealed that the clonal evolution and development existed in PACC.

      Conclusion:
      The status of genomic alterations in PACC was different from the other non-small cell lung cancer (NSCLC). PACC showed obvious spatial heterogeneity and clonal evolution.

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    PL03 - Presidential Symposium (ID 428)

    • Event: WCLC 2016
    • Type: Plenary
    • Track:
    • Presentations: 1
    • Now Available
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      PL03.05 - BRAIN: A Phase Ⅲ Trial Comparing WBI and Chemotherapy with Icotinib in NSCLC with Brain Metastases Harboring EGFR Mutations (CTONG 1201) (Abstract under Embargo until December 6, 7:00 CET) (Now Available) (ID 4570)

      C. Hu

      • Abstract
      • Presentation
      • Slides

      Background:
      Non-small cell lung cancer (NSCLC) with brain metastases (M) had a poor prognosis. Whole brain irradiation (WBI) is a standard of care for this critical medical condition. The median survival is only 4-6 months. Small molecule inhibitors of epidermal growth factor receptor (EGFR) including icotinib achieved very successful results in advanced NSCLC with EGFR mutations. There were no prospective randomized clinical trials to explore the efficacy of EGFR tyrosine kinase inhibitors (TKIs) on brain M.

      Methods:
      Advanced NSCLC with EGFR sensitive mutations and brain M were randomized to WBI plus chemotherapy (chemo) or icotinib. Patients in WBI arm received radiotherapy with 30Gy/3Gy/10 fractions plus concurrent or sequential doublet chemo of 4-6 cycles. Patients in EGFR TKI arm received icotinib 125mg orally tid until disease progression. Icotinib could be continued beyond progression if clinical benefit was observed by the investigator. Crossover to icotinib from WBI could be permitted. Key inclusion criteria were EGFR mutations and radiologically confirmed brain M with at least 3 lesions. The primary endpoint was intracranial progression-free survival (iPFS) by investigator assessments according to RECIST v1.1. The secondary endpoints included objective response rate (ORR), PFS and overall survival (OS). Safety and tolerability were assessed by measuring adverse events (AEs) (CTCAE v4).

      Results:
      From Dec. 2012 to June 2015, 176 patients from 17 sites were randomized to WBI+Chemo arm (N=91) or icotinib arm (N=85). The baseline clinicopathologic factors were balanced between the two groups. Median age was 58, PS 1 was 87.2%, non-smoker 70.9%, adenocarcinoma 96.8%, symptomatic brain M were 16.5%. Icotinib significantly improved median iPFS compared with WBI+chemo: hazard ratio [HR] 0.56; 95% CI: 0.36-0.90; p=0.014 (10.0 vs 4.8 months). Median PFS was 6.8 vs 3.4 months, (HR 0.44, 95% CI 0.31-0.63, P<0.001). Median OS had no significant difference between the arms (18.0 vs 20.5 months, HR 0.93, 95%CI 0.60-1.44, P=0.734). Intracranial ORR was significantly improved with icotinib than WBI+Chemo (67.1% vs 40.9%; p<0.001); Overall ORR was 55.0% vs 11.1% (P<0.001). Grade ≥3 AEs assessed by the investigators were reported in 8.2% (N=7) of patients treated with icotinib and 26.2% (N=28) treated with WBI+Chemo. Most common causally related AEs in the icotinib arm were increased liver transaminase & rash; in the WBI+Chemo arm were hematologic toxicity.

      Conclusion:
      Icotinib demonstrated superior iPFS, PFS and ORR over WBI+Chemo in EGFR mutant advanced NSCLC with brain M, and well-tolerated safety profile. Icotinib would be a treatment option for EGFR mutant patients with brain M (NCT01724801).

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