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Changdong Yeo



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    P1.03 - Biology (ID 161)

    • Event: WCLC 2019
    • Type: Poster Viewing in the Exhibit Hall
    • Track: Biology
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/08/2019, 09:45 - 18:00, Exhibit Hall
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      P1.03-41 - Chronic Nicotine Exposure Affects PD-L1 Expression and Sensitivity to EGFR-TKI in Lung Cancer (ID 262)

      09:45 - 18:00  |  Presenting Author(s): Changdong Yeo

      • Abstract

      Background

      Smoking histories are independently associated with poor response to epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) in non-small cell lung cancer (NSCLC) patients with activating EGFR mutations. The aim of the present study was to determine the effect of nicotine exposure on programmed death-ligand 1 (PD-L1) expression in EGFR mutant lung cancer cells.

      Method

      Human lung adenocarcinoma PC9 cells were exposed to 1 μM nicotine for 3 months designated as PC9/N, and cells were stimulated with gefitinib (0, 0.1, or 1 µM) for 48 hrs. Cell viability by the MTT assay and morphological changes by immunofluorescence staining were assessed. The protein expression of EGFR, mTOR, AKT, α1-nicotine acetylcholine receptor (nAchR) and PD-L1 were measured by Western blot. Gene expression of α1-nAchR and PD-L1 were examined by RT-PCR. Intratumoral levels of PD-L1 expression were compared according to the burden of smoking dosage in EGFR mutant lung cancer patients.

      Result

      Cellular growth was inhibited by treatment with gefitinib, and PC9 cells were significantly more sensitive to gefitinib than PC9/N cells. Pleomorphic appearance with atypical nuclei and to be detached and shrunken with condensed nuclei in PC9 than PC9/N cells. The gene expression level of α1-nAchR and PD-L1 gene were higher in PC9/N cells compared to those in PC9 cells after treatment with gefitinib. Phosphorylation levels of EGFR, mTOR, AKT and PD-L1 level were decreased by gefitinib in PC9/N cells, which was to a lesser extent than that in PC9 cells. In tumors, heavy smokers (≥ 30 PY) showed 28.5% of ≥ 50% PD-L1 tumor proportion score (TPS) while light smoker and never smokers had 12.5% and 9.7% of ≥ 50% PD-L1 TPS, respectively.

      Conclusion

      Chronic nicotine exposure could increase PD-L1 expression related to intrinsic resistance to EGFR-TKI in NSCLC patients harboring activating EGFR mutation. Considering the clinical importance of inevitable EGFR resistance, further studies regarding the role of anti-PD-1/PD-L1 treatment are needed, especially in EGFR mutant smokers.

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    P2.11 - Screening and Early Detection (ID 178)

    • Event: WCLC 2019
    • Type: Poster Viewing in the Exhibit Hall
    • Track: Screening and Early Detection
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/09/2019, 10:15 - 18:15, Exhibit Hall
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      P2.11-20 - Risk Factors of Lung Cancer Development in IPF Patients (ID 676)

      10:15 - 18:15  |  Author(s): Changdong Yeo

      • Abstract

      Background

      Idiopathic pulmonary fibrosis (IPF) is known as a risk factor for lung cancer (LC) by several previous studies, and that the presence of LC shortens survival in patients with IPF. However, the risk factors for the development of LC after the diagnosis of IPF have not been fully evaluated. We investigated the predictive factors for LC by longitudinal cohort analysis.

      Method

      This was a retrospective study of a single center interstitial lung disease cohort. Study patients were consecutively enrolled to the cohort between March 2006 and December 2018 at Bucheon St. Mary’s Hospital, The Catholic University of Korea. This cohort study consists of 102 patients with IPF, and the incidence of LC and the outcomes were investigated.

      Result

      During the mean follow-up periods of 62.7 months, 27 patients (26%) developed LC. The most frequent cell type was Squamous cell carcinoma, and the proportion of male was higher in IPF-LC group (92.6% vs 70.7%, p=0.021). In univariate cox regression analysis, low forced vital capacity (FVC) <75% (p<0.001), and low diffusion capacity of the lungs for carbon monoxide (DLco) <55% (p<0.001) was associated with LC development. In Cox proportional hazards model, low FVC (hazard ratio [HR]: 5.65; 95% confidence interval [CI]: 1.78-17.84, p=0.003) and low DLco (HR: 27.5; 95% CI: 1.97-386.6, p=0.014) were independent predictive factors for LC in stepwise multivariate analysis.

      Conclusion

      Low FVC and Low DLco, which are pulmonary function parameters reflecting their severity of IPF, are suggested as independent risk factors for LC development in IPF patients.