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J.C. Lee



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    Poster Display Session (ID 63)

    • Event: ELCC 2017
    • Type: Poster Display Session
    • Track:
    • Presentations: 3
    • Moderators:
    • Coordinates: 5/07/2017, 12:30 - 13:00, Hall 1
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      103P - Re-biopsy for advanced non-small cell lung cancer after EGFR tyrosine kinase inhibitor therapy: CT characteristics of patients with T790M mutation and the use of various re-biopsy procedures (ID 385)

      12:30 - 13:00  |  Author(s): J.C. Lee

      • Abstract

      Background:
      Re-biopsy for mutation analysis of non-small cell lung cancer (NSCLC) after EGFR-tyrosine kinase inhibitor treatment is important to determine further chemotherapy regimen. There have been no studies about the radiologic characteristics of NSCLC with T790 mutation and the use of the various re-biopsy procedures.

      Methods:
      Between January and December 2016, 78 patients underwent re-biopsy for mutation analysis of NSCLC, and among them, 76 were assessed with adequate specimen. Patients’ treatment course, serial CT scans and pathologic reports were retrospectively reviewed. Re-biopsy methods are varied: EBUS or BFS-guided (n = 27), CT-guided (n = 18), fluoroscopy-guided (n = 5) biopsies, US-guided supraclavicular lymph node (n = 6) or other sites (n = 6) biopsies and pleural fluid analysis (n = 14). CT images obtained at the time of initial biopsy and re-biopsy were compared between patients with and without T790M mutation. Re-biopsy associated complications were assessed.

      Results:
      Among 76 patients, 40 (52.6%) presented T790M mutation on re-biopsy. Progression free survivals between patients with and without T790M mutation were not statistically different (322 and 389 days, respectively). On initial CT, pleural retraction (odds ratio (OR), 4.1; p = 0.03) and the presence of pleural metastasis (OR, 3.4; p = 0.03) were significant factors that related to the positive T790M mutation by multivariate logistic analysis. Pleural retraction (OR, 26.8, p = 0.03) and pleural metastasis (OR, 11.4; p = 0.004) are also shown as significant factors that related to the positive T790M mutation on CT obtained at the time of re-biopsy. Three patients developed pneumothorax, and two were managed by chest tube insertion. One patient who was negative T790M mutation on pleural fluid analysis finally diagnosed as positive T790M mutation by following CT-guided biopsy.

      Conclusions:
      Pleural retraction and pleural metastasis were significantly associated factors to positive T790M mutation in NSCLC patients who underwent re-biopsy. Negative T790M on pleural fluid analysis could not give a guarantee for true negative, and further core biopsy might be recommended.

      Clinical trial identification:


      Legal entity responsible for the study:
      None

      Funding:
      N/A

      Disclosure:
      All authors have declared no conflicts of interest.

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      107P - The real world experience of first generation Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitor (EGFR-TKI) in patients with advanced lung cancer: Explorative analysis of big data from national health insurance service of Korea (ID 437)

      12:30 - 13:00  |  Author(s): J.C. Lee

      • Abstract

      Background:
      Although the effectiveness of EGFR-TKI in patients with advanced lung cancer has been proven in previous trials, the real-world efficacy of EGFR-TKI has not been investigated. The object of this study was to evaluate the outcomes of first-generation EGFR-TKI in female patients with advanced lung cancer using big data analysis.

      Methods:
      We retrospectively reviewed the Korean health insurance service data of advanced lung cancer patients from January 2004 to December 2013. Patients older than 20 years in palliative setting were grouped into three categories: Group A received 1st-generation EGFR-TKI ≥6 months, group B given EGFR-TKI < 6 months, and group C was treated with cytotoxic chemotherapy alone. For each group, we determined progression-free survival (PFS) and overall survival (OS).

      Results:
      Of 11,045 patients enrolled in the study, 6,170 (55.8%) received EGFR-TKI at least 1 month, and 4,875 (44.2%) never treated with EGFR-TKI. 2,572 were in the group A and 3,598 were in the group B. In the group C, platinum based doublet agent or monotherapy such as docetaxel, gemcitabine and pemetrexed was administered. The median OS of patients treated with EGFR-TKI was significantly longer than that of EGFR-TKI naïve patients (19.1 months [95% confidence interval (CI) 18.5-19.7] vs 9.5 months [95% CI 9.1-9.8]; p < 0.0001). In subgroup analysis, the median OS was 30.3 months [95% CI 29.5-31.2] in the group A, compared with 12.3 months [95% CI 11.9-12.7] in the group B and 9.5 months [95% CI 9.1-9.8] in the group C (p < 0.001). Patients age < 65 years, treated with EGFR-TKI ≥ 6months, and received docetaxel, pemetrexed chemotherapy were independent predictors of longer OS (Hazard ratio (HR) 0.78 [95% CI 0.74-0.81]; p = 0.002, HR 0.41 [95% CI 0.38-0.43]; p < 0.001, HR 0.81 [95% CI 0.77-0.85]; p < 0.001, HR 0.77 [95% CI 0.74-0.81]; p < 0.001, respectively). Median PFS was 15.8 months [95% CI 15.1-16.3] in group A and 3.7 months [95% CI 3.5-3.8] in group B (p < 0.001).

      Conclusions:
      The current study demonstrated that EGFR-TKI conferred a significant PFS and OS benefit in female patient with advanced lung cancer in real-world.

      Clinical trial identification:


      Legal entity responsible for the study:
      Asan Medical Center

      Funding:
      None

      Disclosure:
      All authors have declared no conflicts of interest.

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      35P - CDK7 inhibition as a promising therapeutic strategy in lung squamous cell carcinoma with SOX2 amplification (ID 188)

      12:30 - 13:00  |  Author(s): J.C. Lee

      • Abstract

      Background:
      Molecular targeted therapy has much improved the survival of lung adenocarcinoma while few advances have been made in the treatment of lung squamous cell carcinoma (SCC). SOX2 amplification is one of the most common genetic alterations in SCC. We investigated the effects of THZ1, a potent inhibitor of cyclin-dependent kinase 7 (CDK7) which plays a key role in gene transcription, on SCC cell lines with SOX2 amplification.

      Methods:
      SOX2-amplified SCC cell lines (H520, H1703, HCC95) and SCC cell lines without SOX2 amplification (H226, SK-MES1, H1975) were used. Along with the general drug efficacy of THZ1 and the effect of SOX2 knockout by CRISPR on cell growth, the differential gene expression following THZ1 treatment was evaluated by microarray analysis.

      Results:
      Genetic inhibition of SOX2 by CRISPR resulted in the suppression of cell growth in SOX2-amplified SCC cell lines. The treatment of THZ1 led to the suppression of cell growth and apoptotic cell death only in SOX2-amplified SCC cell lines while the modest growth-inhibitory effect of cisplatin was not different according to the status of SOX2 amplification. The phosphorylation of carboxyl-terminal domain (CTD) of RNAPII and the expression of SOX2 and survivin were decreased by THZ1 in Western blotting. Accordingly, the expression of transcription-associated genes including SOX2 was down-regulated by THZ1 in SOX2-amplified SCC cell lines.

      Conclusions:
      THZ1 could effectively control the proliferation and survival of SOX2-amplified SCC cells with the decrease of global transcriptional activity. It suggests that CDK7 inhibition leading to suppression of transcription may be considered as one of promising therapeutic options in lung SCC with SOX2 amplification.

      Clinical trial identification:


      Legal entity responsible for the study:
      Jae Cheol Lee

      Funding:
      Asan Medical Center

      Disclosure:
      All authors have declared no conflicts of interest.