Scientific Program

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    JCSE 01 - Joint IASLC/CSCO/CAALC Session: Immunotherapy for Management of Lung Cancer: Ongoing Research from East and West

    • Type: Joint Session IASLC/CSCO/CAALC
    • Track: Immunology and Immunotherapy
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      JCSE 01.01 - Breakfast and Poster Viewing

      07:30 - 11:30

      • Abstract

      Abstract not provided

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      JCSE 01.02 - Welcome and Introduction

      07:30 - 11:30

      • Abstract

      Abstract not provided

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      JCSE 01.03 - The Science of Immunotherapy

      07:30 - 11:30  |  Presenting Author(s): Roy S. Herbst

      • Abstract

      Abstract not provided

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      JCSE 01.05 - PD-1+CD8+ T and iNKT Cell Based Immunotherapy on Lung Cancer

      07:30 - 11:30  |  Presenting Author(s): Jianqing Xu

      • Abstract

      Abstract not provided

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      JCSE 01.06 - ctDNA Based Tumor Mutation Burden Evaluation for Predicting Immunotherapy Effect

      07:30 - 11:30  |  Presenting Author(s): Jie Hu

      • Abstract

      Abstract not provided

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      JCSE 01.07 - Ongoing Trials in China on Checkpoint Inhibitors and Other Immunotherapies

      07:30 - 11:30  |  Presenting Author(s): Qing Zhou

      • Abstract

      Abstract:
      Immunotherapy gets the breakthrough after almost 100 years of silence. PD1/PD-L1 inhibitors as the representative has been extensively studied in various human malignant tumors and get promising long term response with relatively fewer adverse event. The first PD1 inhibitor indication was approved for melanoma in Japan on July 2014. By the end of December 2016, the US Food and Drug Administration had approved several PD-1 pathway blockade treatments including nivolumab, pembrolizumab and atezolizumab using in first line and second line of NSCLC. But In China, no PD-1 or PD-L1 inhibitors have received marketing approval from the Chinese Food and Drug Administration (CFDA) until July 2017. One sides, IO arena faces intense in-class competition from both MNC (Multi-National Corporation) and domestic pharmaceutical company in China. Now there are 20 IO antibodies from 7 MNCs and 10 pharmaceutical companies in China. But all the antibodies only confined to PD1/PD-L1 and CTLA4, no other hot IO drugs such as IDO or Lag3 et al. In the field of innovation, China is several years behind research in other areas of the world. The other sides various clinical trials are actively investigating MNC and domestic drugs in China. Between January 1, 2013 and April 6, 2017, Clinical Trials.-gov registered 270 international clinical trials using PD-1/PD-L1 therapies for NSCLC (e.g.nivolumab,pembrolizumab,atezolizumab,and durvalumab). These 270 trials included 61 studies that involved East Asian sites and 14studies that involved Chinese sites (12 multinational trials and 2 trials that only evaluated Chinese patients). These trials cover from second line and first line to adjuvant therapy in NSCLC. Most of the ongoing MNC NSCLC clinical trials joined in global study design that may accelerate the patient access to PD1/PD-L1. But Chinese population has relatively high rates of hepatitis B virus infection and much higher proportion of EGFR mutation. The delightful changing recently is some studies emerging to consider the characteristics of the Chinese or Asian populations. Domestic company clinical trials focus on GI (Gastrointestinal) and only 1 NSCLC study in China. Chinese clinical trials using IO remain in their early stages, and further efforts are needed to improve the design of future clinical trials. Meanwhile, the other hot IO drug phase I study need speed up in China.

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      JCSE 01.08 - Coffee Break and Poster Viewing

      07:30 - 11:30

      • Abstract

      Abstract not provided

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      JCSE 01.09 - Therapeutic Practices in Europe for Immunotherapy, including Biomarkers

      07:30 - 11:30  |  Presenting Author(s): Solange Peters

      • Abstract

      Abstract not provided

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      JCSE 01.10 - The Main Treatment Failure Pattern for Completely Resected Stage II–IIIA (N1–N2) EGFR-Mutation Positive Lung Cancer

      07:30 - 11:30  |  Presenting Author(s): Songtao Xu  |  Author(s): W. Zhong, Y. Zhang, W. Mao, L. Wu, Y. Shen, Y. Liu, C. Chen, Ying Cheng, L. Xu, J. Wang, K. Fei, X. Li, J. Li, C. Huang, Z. Liu, S. Xu, K. Chen, S. Xu, L. Liu, P. Yu, B. Wang, H. Ma, H. Yan, X. Yang, Yi-Long Wu, Q. Wang

      • Abstract

      Background:
      ADJUVANT (CTONG 1104) is the first randomized trial shows significantly prolonged disease-free survival (DFS) in completely resected stage II-IIIA (N1-N2) epidermal growth factor receptor (EGFR)-mutation positive non-small-cell lung cancer (NSCLC) through adjuvant gefitinib compare with vinorelbine plus cisplatin (VP). Further we aim to analyze the treatment failure pattern in ADJUVANT study.

      Method:
      In the ADJUVANT trial, a total of 222 patients with completely resected stage N1–N2 EGFR-mutation positive NSCLC were randomized 1:1 into gefitinib group (250mg, QD, 24 months ) or vinorelbine (25mg/m[2] Day 1/Day 8) plus cisplatin (75mg/m[2] Day 1) group (every 3 weeks for 4 cycles) respectively. Any recurrence or metastases occurred during the follow-up period was defined as treatment failure. Recurrent pattern in both group were analyzed with follow-up data (until Mar 9[th] 2017) integrated.

      Result:
      At the Data cut-off date for the primary analysis of DFS, 124 progression events (55.9% maturity overall) had occurred; 114 patients had disease recurrence,10 patients died before disease recurrence. Analysed recurrent pattern include lung, brain, liver, bone adrenal gland, pleura, pericardium, spleen and regional lymph nodes metastasis. Even no significant differences were found, highest proportion of patients in both group(18.9% for VP and 26.1% for gefitinib, p=0.199) surfer brain metastasis with lung metastases being the second common recurrent site. Time to brain metastases showed no significantly difference between the two groups (not reach vs 40.8m, p>0.05). Among the 29 brain metastases patients with gefitinib, the brain metastases occurred in 17 patients during the gefitinib treament, and 12 patients relapse after the gefitnib termination. Figure 1



      Conclusion:
      Compared with other site metastases, lung, brain and regional lymph nodes metastases account for major proportion of recurrence in ADJUVANT study. (NCT01405079)

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      JCSE 01.11 - A Multicenter, Non-Interventional Study on Real World EGFR Testing and in Patients with IIIB/IV NSCLC in Northern China

      07:30 - 11:30  |  Presenting Author(s): Ying Cheng  |  Author(s): Y. Wang, J. Zhao, Y. Liu, H. Gao, K. Ma, S. Zhang, H. Xin, J. Liu, H. Chengbo, Z. Zhu, Y. Wang, J. Chen, F. Wen, J. Li, Z. Jie, Z. Zheng, Z. Dai, H. Piao, X. Li, Y. Li, M. Zhong, R. Ma, Y. Zhuang, Y. Xu, Z. Qu, H. Yang, C. Pan, F. Yang, D. Zhang, B. Li

      • Abstract

      Background:
      EGFR mutation plays a dominant role in the precise treatment of non-small cell lung cancer (NSCLC), and EGFR-TKIs has been recommended for patients with positive EGFR-sensitive mutation as a standard regimen in clinical practice. In China, application of EGFR-TKIs without knowing EGFR mutation status has been a common phenomenon due to various reasons including the vast territory, uneven distribution of medical resources, differences level of testing technology and others. Therefore, we prospectively conducted a real-world investigation to understand the actual situation of EGFR testing in Northern China, and identify the underlying causes affecting EGFR detection, in order to provide references to improve the standardized treatment (NCT02620657).

      Method:
      The patients with IIIB/IV NSCLC who were firstly diagnosed or postoperative recurrence between 2014-1-1 and 2014-12-31 in 28 research centers of Northern China were analyzed. The primary endpoint was testing rate,the secondary endpoints were factors affecting EGFR testing, EGFR mutation status, detection methods and the survival outcomes of patients.

      Result:
      Among 2809 patients, 2250 (90.78%) were adenocarcinoma, 208 (7.40%) were squamous carcinoma, 51 (1.82%) were other pathologic types. Testing rate was 42.54% (1195/2809) and was significantly related to city level (first-tier cities vs. new first-tier cities vs. second-tier cities vs. third-tier and above cities : 69.04% vs. 38.08% vs. 34.05% vs. 14.11%, P < 0.001, smoking status (never smoking vs. ever smoking vs. smoking: 45.42% vs. 51.10% vs. 33.37%, P<0.001, ECOG PS (0 vs.1vs.2vs.≥3:47.93%vs. 44.48vs.34.89%vs.20.37%, P=0.011), pathological type (adenocarcinoma vs. squamous carcinoma: 44.94% vs.19.23%, P=0.003 and medical insurance situation (social basic medical insurance vs. new rural cooperative medical insurance vs. own expense: 44.98% vs. 36.49% vs. 29.55%, P=0.001. EGFR sensitive mutation rate was 46.44%, the most common subtype was 19Del (42.16%), followed by L858R(40.00%), Exon 20 insertions (1.62%) and other subtypes (16.20%). The most common methodology is ARMS (63.77%), the second common one is DNA sequencing (5.36%). The 1-year and 2-year survival rate in patients receiving EGFR testing was 73.6% and 51.9%, compared with 64.3% and 43.7% respectively in patients without EGFR testing.

      Conclusion:
      There were regional differences in EGFR testing rates among IIIB/IV NSCLC patients in Northern China. The intention of doctors and patients, medical insurance coverage and differences technical level are major factors affecting the testing rate of EGFR. Approaches should be taken to improve the situation, such as strengthening the training, expanding the coverage of medical insurance, and relying on commercial gene detection companies, and further standardize the molecularly pathological diagnosis and treatment of NSCLC.

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      JCSE 01.12 - A Phase II Study of Fruquintinib in Combination with Gefitinib in Stage IIIb/IV NSCLC Patients Harboring EGFR Activating Mutations

      07:30 - 11:30  |  Presenting Author(s): Shun Lu  |  Author(s): J. Zhou, X. Niu, M. Chen, Y. Hua, W. Su

      • Abstract

      Background:
      Seveal studies have demonstrated targeting EGFR mutations and tumor angiogenesis simultaneously has synergistic effect in the 1[st] line setting in EGFR mutant NSCLC. However, in JO25567 trial, the ≥grade 3 hypertension incidence with combination therapy was much higher (60%) when compared to historic incidence of hypertension with bevacizumab (10-15%). Considering relatively shorter half-lives for small molecule tyrosine kinase inhibitors, it might be a better choice to combine EGFR TKI and VEGFR TKI when it comes to hypertension management. Fruquintinib is a potent and highly selective oral kinase inhibitor targeting VEGFR and it has demonstrated favorable benefit-to-risk profile in third line treatment in NSCLC patients.Thus it is important to assess safety, tolerability and efficacy of this new combination in the 1[st] line setting in EGFR mutant NSCLC patients. NCT02976116

      Method:
      This is a single arm, open-label, multi-center study. All patients will receive gefitinib continuously at 250 mg qd. Fruquintinib will be given at 4 mg as starting dose for 3 weeks followed by 1 week off in the first 4-week cycle. Fruquintinib dose can be escalated to 5 mg with the same 4-week cycle if no ≥grade 3 adverse event (AE) or ≥grades 2 liver dysfunction occurs in the first cycle. Treatment continues until disease progression, unacceptable toxicity, or patient withdrawal. The primary objective is to assess the safety and tolerability of this combination. Key eligibility criteria include: histologically or cytologically confirmed NSCLC, ECOG PS 0-1, no prior systematic treatment, no brain metastasis. Key exclusion criteria include: known T790M mutation and bleeding history within 1 month before enrollment.

      Result:
      As of Jun 20, 2017, 9 patients have been enrolled and received at least one dose of fruquintinib and gefitinib. Six patients had L858R mutations, and three patients had exon 19 deletions. All patients reported AEs, but only one patient (11.1%) had grade 3 proteinuria. No SAE was reported. The most common AEs were increased ALT (3 [33.3%] patients), increased AST (3 [33.3%] patients), increased TBIL (3 [33.3%] patients), proteinuria (3 [33.3%] patients) and rash (3 [33.3%] patients). Fruquintinib dose reduction occurred in 3 patients due to grade 3 proteinuria, grade 2 increased ALT and grade 2 hemoptysis, respectively.

      Conclusion:
      The study is ongoing. As of the cut-off date, no unexpected toxicities were identified. The combination of fruquintinib and gefitinib showed an expected and manageable preliminary safety profile. Additional patients and follow-up data are required to further confirm the full potential of this combination treatment.

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      JCSE 01.13 - Discussant Oral Abstracts - JCSE 01.10, JCSE 01.11, JCSE 01.12

      07:30 - 11:30  |  Presenting Author(s): Joel W. Neal

      • Abstract

      Abstract not provided

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      JCSE 01.14 - Discussant Poster Abstracts

      07:30 - 11:30  |  Presenting Author(s): Bob T. Li, Jonathan W Riess

      • Abstract

      Abstract not provided

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      JCSE 01.15 - Next Generation Sequencing of Large-Cell Neuroendocrine Carcinoma Reveals an Association of PIK3CA Mutations with Brain Metastases

      07:30 - 11:30  |  Presenting Author(s): Mian Xie  |  Author(s): X. Wu, Y. Gu

      • Abstract

      Background:
      Large-scale genomic characterization of large-cell neuroendocrine carcinoma (LCNEC) has revealed several putative oncogenic drivers. There are, however, little data to suggest that these alterations have clinical relevance.

      Method:
      We performed comprehensive genomic profiling of 68 stage IV LCNECs of the lung (including next-generation sequencing) and analyzed differences in the clinical characteristics of two major LCNECs subtypes: KRAS mutation and PIK3CA mutation. In order to better understand the divergence that might exist between brain metastases and their lung primaries, we performed whole-exome sequencing of paired lung primaries and brain metastases from four lung LCNEC patients.

      Result:
      Patients with PIK3CA mutation tumors had aggressive disease marked by worse survival (median OS 7.9 vs. 18.6 mo, P = 0.002), higher metastatic burden (> 3 organs 15.2% vs. 4.7%, P = 0.029), and greater incidence of brain metastases (19.0% vs.2.3% in others, P = 0.001). Whole-exome and RNA sequencing on paired brain metastases and primary LCNECs of the lung revealed that LCNEC primaries that gave rise to brain metastases harbored PIK3CA mutation. Significant tumor growth inhibition with GDC0941 was observed exclusively in the LCNEC patient-derived xenograft model that harbored PIK3CA mutation.

      Conclusion:
      PIK3CA mutation defines a distinct disease phenotype characterized by brain metastasis in LCNEC of the lung. The result may be relevant for targeted therapy and prophylaxis of NSCLC brain metastases.

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      JCSE 01.17 - The Correlation of DLL3 Expression with High-Grade Pulmonary Neuroendocrine Carcinoma Clinicopathologic Features and Prognose

      07:30 - 11:30  |  Presenting Author(s): Li-Xu Yan  |  Author(s): Y. Liu, J. He, D. Luo

      • Abstract

      Background:
      Rovalpituzumab tesirine is a promising first-in-class DLL3-targeted antibody-drug conjugate for the treatment of HGNECs. In clinical practice, biopsies are often rendered for diagnoses of HGNECs before treatment. We tested DLL3 in paired biopsy and surgical specimens, aiming to assess the reliability of the scoring system in biopsy specimens and the correlation with HGNEC clinical characteristics and prognoses.

      Method:
      A total of 378 patients with de novo HGNECs, including 43 LCNECs and 335 SCLCs, were recruited between 2006 and 2015. All 43 LCNECs and 42 of 335 SCLCs had paired biopsy and surgical excision specimens, and the remaining 293 SCLCs had only biopsies. Immunohistochemical evaluation of DLL3 expression was performed using anti-DLL3 antibody (Abcam, ab103102) and was determined using immunohistochemical H score (HS).

      Result:
      No significant differences of DLL3 expression levels were observed in paired biopsy and excision specimens of LCNECs and SCLCs (Figure B-C). Discordant DLL3 results (high, HS > 150 vs low, HS ≤ 150) in paired specimens were observed in none of LCNECs and 2 of 42 SCLCs. DLL3 levels were significantly higher (p = 0.015) in all SCLCs (n = 335, median HS 200, IQR 100-300) than in LCNECs (n = 43, HS 160, IQR 100-200; Figure D). SCLCs with high DLL3 levels were more frequently male (p = 0.037), smokers (p = 0.019), and TTF-1 positive (p = 0.005) than SCLCs with low DLL3. SCLCs with low DLL3 experienced a superior overall survival compared with SCLCs with high DLL3, with the difference, however, not reaching statistical significance (p = 0.077; Figure F). Figure 1



      Conclusion:
      Biopsy specimen is a reliable material for evaluating DLL3 expression, which is equivalent to surgical specimen in a large percentage of HGNECs. High DLL3 level in SCLCs demonstrate a correlation with smoking history, TTF1 (neuroendocrine differentiation) and a trend of poor survival.

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      JCSE 01.18 - Uncommon Mutation Types of EGFR and Response to EGFR Tyrosine Kinase Inhibitors in Chinese Non-Small Cell Lung Cancer Patients

      07:30 - 11:30  |  Presenting Author(s): Yun Fan  |  Author(s): K. Chen, X. Yu, H. Wang, Z. Huang, Y. Xu, L. Gong

      • Abstract

      Background:
      Epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) is the standard therapy for advanced lung adenocarcinomas with common EGFR mutations. However, the efficacy of EGFR-TKIs in patients with these uncommon EGFR mutations (other than exon 19 deletions or exon 21 L858R mutation) remains undetermined.

      Method:
      Seven hundred and fifty-five non-small cell lung cancer (NSCLC) patients with EGFR mutation analyses for TKI therapy were identified between October 2010 and December 2015 in East of China. And 66 patients bearing uncommon EGFR mutations were included to collect data from TKI response and prognosis.

      Result:
      Rare sensitive mutations (G719X, L861Q, S768I), primary resistant mutation (Ex20 ins), and complex mutations (G719X + L861Q, G719X+S768I, 19 del+T790M, 19 del+L858R, L858R+S768I, and L858R+T790M) of EGFR were identified in 37 (56.1%), 9 (13.6%), and 20 (33.3%) patients, respectively. TKI treatment in patients harboring uncommon EGFR mutations exhibited a tumor response rate of 28.8% and a median progression-free survival (PFS) of 4.8 months. Importantly, patients with complex EGFR mutations had significantly longer PFS when compared with the remaining sensitizing rare mutations or Ex20 ins (8.6 versus 4.1 versus 3.1 months; p=0.041). Furthermore, complex EGFR mutations were independent predictors of increased overall survival in NSCLC patients (Hazard Ratios=0.31; 95% confidence intervals: 0.11-0.90; p=0.031). Among them, patients harboring Del-19 compound L858R mutations showed a tendency to have higher response rate and improved median PFS than those regarding patients with other complex mutations patterns (66.7% verse14.3%, p=0.021; 10.1 verse 8.6 months, p=0.232).

      Conclusion:
      Personalized treatment should be evolving in different types of uncommon EGFR mutations. And complex mutations of EGFR may benefit more from EGFR-TKIs than other uncommon mutations in Chinese NSCLC patients.

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      JCSE 01.20 - Primary Tumor Resection versus Maintenance Therapy for Patients with Oligometastatic Non-Small Cell Lung Cancer

      07:30 - 11:30  |  Presenting Author(s): Xiaozheng Kang  |  Author(s): H. Zhou, W. Yan, L. Dai, Y. Yang, H. Yang, H. Fu, M. Fan, Y. Lin, Z. Liang, H. Xiong, K. Chen

      • Abstract

      Background:
      To evaluate (1) the potential effect of primary tumor resection, an aggressive local consolidative therapy, for patients with oligometastatic NSCLC on 3 year overall survival; (2) the surgical outcomes in the treatment of patients with oligometastatic NSCLC; (3) the potential clinical factors predicting survival in order to better select patients for surgery.

      Method:
      According to the extent of pulmonary resection, the patients were divided into two subgroups. A. intent to cure (ITC: removal of total or primary pulmonary lesions); B. intent to biopsy (ITB: preservation of major lesions, only diagnostic biopsy via minimally invasive approach). M stage classified based on 8th UICC/AJCC TNM M categories.

      Result:
      From Jan 2002 through Dec 2015, a total of 115 consecutive metastatic NSCLC patients were enrolled from Peking University Cancer Hospital. The 3-year overall survival (OS) of ITC and ITB were 64.3% and 34.9% (log-rank p = 0.0009), respectively. Multivariate cox proportional regression analysis identified multiple station lymph nodes (LN) and bone involvement may be prognostic indicators. Figure 1Figure 2





      Conclusion:
      The current findings suggest that aggressive surgical therapy can extend the survival in selected stage IV NSCLC patients, and should be further explored in phase 3 trials as a standard treatment option in this clinical scenario.

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      JCSE 01.21 - Combination of Biomarker and Clinicopathologic Characters May Circle out Beneficiaries through Second-Line Immunotherapy: A Meta Analyse

      07:30 - 11:30  |  Presenting Author(s): Si-Yang Liu  |  Author(s): Z. Dong, C. Zhang, W. Zhong, Yi-Long Wu

      • Abstract

      Background:
      Programmed cell death ligand 1 (PD-L1) expression had been proposed as predictive biomarker to immune-checkpoint inhibitors. Yet treatment responses are not always consistent with this single agent in the second-line therapy of NSCLC. Whether combination of PD-L1 and clinicopathologic characters could circle out optimal beneficiaries are still unknown.

      Method:
      We performed a meta-analysis of randomized control trials that compared immune-checkpoint inhibitors against chemotherapy in second-line therapy. Data including smoking status, EGFR status, KRAS status and histology were extracted as subgroup analyse to estimate the potential predictor of efficacy for anti PD-1/L1.

      Result:
      Five clinical trials that compared immune-checkpoint inhibitors against chemotherapy for second-line therapy were included. Both PD-L1 positive (HR=0.64, 95%CI=0.56-0.73, P<0.00001) and PD-L1 negative (HR=0.88, 95%CI=0.78-1.00, P=0.05) favored anti PD-1/L1. Subgroup analyse indicated that adenocarcinoma (ADC) as well as squamous cell carcinoma (SCC) preferred anti PD-1/L1. Never smokers may not benefit from anti PD-1/L1 but current/ever smokers did (HR=0.70, 95%CI=0.63-0.79, P<0.00001). Patients with EGFR mutation could not gain benefit from anti PD-1/L1 while the EGFR wild type could (HR=0.67, 95%CI=0.60-0.76, P<0.00001). Both KRAS mutation (HR=0.60, 95%CI=0.39-0.92, P=0.02) and wild type/unknown (HR=0.81, 95%CI=0.67-0.97, P=0.02) were apt to anti PD-1/L1. Figure 1



      Conclusion:
      Regardless of PD-L1 status, immune-checkpoint inhibitors could achieve better efficacy than chemotherapy in second-line therapy. Current/ever smokers without EGFR mutations may benefit more from anti PD-1/L1. Combination of PD-L1 and strongly relevant clinicopathologic characters should be considered to tailor optimal patients for anti PD-1/L1.

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      JCSE 01.23 - The Feasibility of Osimertinib Treatment on Brain Metastases in NSCLC Patients After 1st Generation EGFR-TKI Resistance: A Preliminary Study

      07:30 - 11:30  |  Presenting Author(s): Lucheng Zhu  |  Author(s): S. Zhang, B. Xia, X. Chen, S. Ma

      • Abstract

      Background:
      NSCLC patients with activating EGFR mutations benefit from 1[st] generation EGFR-TKIs. It eventually develops acquire resistance after 10-12 months during of response. Of note, approximately one-third of those patients develop brain metastases, which deteriorate their quality of life and survival. Few effective therapeutic options are currently available for BM patients. Several case studies have showed the well response with osimertinib in BM patients. BM model also found the high penetration rate of Osimertinib into blood-brain barrier. This study evaluated the feasibility of osimertinib treatment on BM patients after 1st generation EGFR-TKI resistance.

      Method:
      Patients with advanced or recurrent NSCLC who had progressed during EGFR-TKIs treatment were collected from our previous clinical trial (NCT02418234) from March 2015 to March 2016. Blood samples were drawn within two weeks from PD occurred. T790M mutations were evaluated by droplet digital PCR. We undertook follow-up every 3 months by phone until April 2017. The median follow-up time was 11 months (range, 2 to 22 months).

      Result:
      Fifty NSCLC patients with BM after EGFR-TKI resistance were collected from our previous trials. After TKI resistance, ten patients received subsequent osimertinib treatment. Finally, ten patients included three males and seven females were included in the study. The median age was 66.5 (56 to 73). Seven were detected acquired T790M mutation. The median survival was 15.3 months (95% CI, 10.1 to 20.6 mo), 15.3 mo for T790M negative and 12.9 mo for T790M positive patients.

      Conclusion:
      Our preliminary study showed the well efficacy of osimertinib on NSCLC patients with BM. It provides well survival benefit. Randomized control trials should be required before it is widely used.

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      JCSE 01.24 - Detection of EGFR, ALK and Other Driver Oncogenes from Plasma cfDNA by Single Molecule Amplification and Re-sequencing Technology (cSMART)

      07:30 - 11:30  |  Presenting Author(s): Tony SK Mok  |  Author(s): Shun Lu, Ying Cheng, Jie Wang, Y. Wang, T. Wang, T. Yung, X. Su, F. Sun, F. Sun, L.T. Wang, Yi-Long Wu

      • Abstract

      Background:
      All patients with advanced stage NSCLC should have their EGFR and ALK mutation status known prior to initiation of first line therapy. Multiple plasma-based technologies such as ARMS and ddPCR are available for rapid detection of EGFR mutation, while only the more laborious Next Generation Sequencing (NGS) may cover EGFR, ALK and other uncommon mutations in a single blood test. cSMART is a novel NGS-based technology with rapid turnaround time that can detect EGFR, ALK and KRAS mutations plus others less common lung cancer specific driver oncogenes (BRAF, ROS-1, HER-2, PIK3CA, RET, MET14skipping).

      Method:
      Objectives of this study is to investigate the clinical application of cSMART on patients with advanced NSCLC. In cSMART assay, each cfDNA single allelic molecule is uniquely barcoded and universally amplified to make duplications. The amplified products are circularized and re-amplified with target-specific back-to-back primers. These DNA are then ligated with sequencing adapters and pair-end sequenced (>40,000x) with illumine sequencers. The original cfDNA molecules are reconstituted by multi-step bioinformatics pipeline for censor and correction. The final products are quantified for calculation of allele frequencies

      Result:
      Out of the 1664 samples tested, total of 1469 were of advanced stage NSCLC. We detected EGFR mutations in 758 (51.6%), ALK translocation in 34 (2.3%) and KRAS mutation in 78 (5.8%) patients. Among the patients with activating EGFR mutations, 301(39.7%) have exon 19 deletion and 279 (36.8%) have exon 21 point-mutation. Total of 6 (0.8%) patients with EGFR mutation have concurrent presence of ALK translocation. Incidence and mean allele frequency of the less common target mutation is summarized in Table. Median sample turnaround time is 7 days.

      Incidence (%) Median Mutation Allele frequency (%)
      BRAF 29 (1.97%) 0.08%
      ROS1 2 (0.14%) 0.77%
      HER-2 19 (1.29%) 0.20%
      PIK3CA 70 (4.77%) 0.17%
      RET 14 (0.95%) 0.57%
      MET14skipping 63 (4.29%) 0.08%


      Conclusion:
      cSMART is a novel plasma cfDNA-based technology that can detect the actionable target oncogenes for patients with advanced NSCLC. This is a sensitive method with capacity of detecting the uncommon targets at relatively low allele frequency.

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      JCSE 01.25 - Detection of EGFR T790M Mutations by Four Testing Platforms in ctDNA from Chinese Patients with Advanced NSCLC

      07:30 - 11:30  |  Presenting Author(s): Xu-Chao Zhang  |  Author(s): Z. Liang, Y. Chen, H. Zhang, W. Gang, Y. Lu, Z. Liang, Ying Cheng, Y. Hu, Jie Wang, J. Ying, W. Liu, Yi-Long Wu

      • Abstract

      Background:
      Osimertinib is used to treat patients with locally advanced or metastatic epidermal growth factor receptor (EGFR) T790M mutation-positive non-small cell lung cancer (NSCLC). Detection of the T790M mutation in tissue samples may not be possible in some patients due to unfeasible or unsuccessful rebiopsies; detection in circulating cell-free tumor DNA (ctDNA) may represent a promising alternative. Here we evaluated four platforms to detect T790M using ctDNA in plasma from Chinese patients as part of the ADELOS study.

      Method:
      ADELOS is being conducted in China in 256 patients with advanced NSCLC, sensitizing mutations and progression on previous tyrosine kinase inhibitor. T790M was detected in plasma ctDNA by cobas® real-time polymerase chain reaction (PCR), super amplification refractory mutation system (Super-ARMS) PCR, QuantStudio3D digital PCR, and next-generation sequencing (NGS). T790M positive patients by any of the four platforms received osimertinib 80 mg/day orally. The relationship between T790M detection by each platform and objective response rate (ORR) was investigated. Concordance, sensitivity and specificity, and positive/negative predictive value between platforms were assessed. T790M mutation level in ctDNA was dynamically monitored every 6 weeks using digital PCR and NGS during osimertinib treatment, and its correlation with clinical outcome was evaluated. NGS also provided information about the heterogeneity of other genetic alterations in patients before osimertinib treatment.

      Result:
      Section will be completed in late-breaking abstract submission

      Conclusion:
      Section will be completed in late-breaking abstract submission

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      JCSE 01.26 - Circulating Cell-Free DNA of Cerebrospinal Fluid May Function as Liquid Biopsy for Leptomeningeal Metastases of ALK Rearrangement NSCLC

      07:30 - 11:30  |  Presenting Author(s): Yangsi Li  |  Author(s): B. Jiang, Jin -Ji Yang, X. Zhang, Z. Zhang, Qing Zhou, H. Tu, Z. Wang, H. Chen, C. Xu, B. Wang, Yi-Long Wu

      • Abstract

      Background:
      Leptomeningeal metastases (LM) are more frequent in non-small cell lung cancer (NSCLC) patients with oncogenic drivers. Resistance mechanisms of LM with ALK rearrangement remained unclear due to limited access to leptomeningeal lesions.

      Method:
      Primary tumor, cerebrospinal fluid (CSF) and plasma in patients with suspected LM of NSCLC were tested by Next-Generation Sequencing.

      Result:
      In patents with ALK rearrangement, driver genes were detected in 66.7%, 50.0% and 28.6% patients of CSF cfDNA, CSF precipitates and plasma, respectively; and all of them had much higher allele fractions in CSF cfDNA than the other two media. The diagnosis criteria of LM were positive in brain MRI or CSF cytology, and driver genes were identified in CSF cfDNA of all patients with positive CSF cytology while in those CSF cytology negative all genes were negative. Resistance mutations including gatekeeper genes ALK G1202R and ALK G1269A were identified in CSF cfDNA but they were absent in their plasma. Moreover, tailor therapy based on CSF cfDNA obtained surprising outcomes, and genetic profiles of CSF cfDNA showed dynamic changes, suggesting the potential role of CSF for follow-up studies. Figure 1



      Conclusion:
      CSF cfDNA could reveal the driver and resistant genes of LM, and it may function as the media of liquid biopsy for LM in NSCLC with ALK rearrangement.

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      JCSE 01.27 - Patients with ALK IHC-Positive/FISH-Negative NSCLC Benefit from ALK TKI Treatment: Response Data from the Global ALEX Trial

      07:30 - 11:30  |  Presenting Author(s): Tony SK Mok  |  Author(s): Solange Peters, D. Ross Camidge, Shirish M Gadgeel, S.I. Ou, D. Kim, Rafal Dziadziuszko, F. De Marinis, R. Sangha, A. Zeaiter, J. Noe, E. Nueesch, T. Liu, I. Loftin, C. Williams, Alice Shaw

      • Abstract

      Background:
      Patients with ALK-positive NSCLC have seen significant advances and increased options in ALK targeted therapies recently, and therefore rely on high quality, robust ALK status testing. Fluorescence in-situ hybridization (FISH) and immunohistochemistry (IHC) are the most common methods to determine ALK status for ALK tyrosine kinase inhibitor (TKI) treatment. However, availability of clinical outcome data from randomized trials linked directly to specific methods is limited. The ALEX trial (BO28984, NCT02075840) provides a unique dataset to assess ALK IHC- and FISH-based assays regarding clinical outcome for alectinib and crizotinib, particularly for the subset of patients with IHC-positive/FISH-negative NSCLC.

      Method:
      The VENTANA ALK (D5F3) CDx Assay (ALK IHC) performed in central laboratories was used as an enrollment assay for the selection of patients with ALK-positive NSCLC for inclusion in the ALEX trial. Additional samples from these patients were retrospectively tested in central laboratories with the Vysis ALK Break Apart FISH Probe Kit (ALK FISH).

      Result:
      Overall, 303 patients all with ALK IHC-positive NSCLC were randomized in the ALEX trial, of those 242 patients also had a valid ALK FISH result, with 203 patients having ALK FISH-positive disease and 39 patients having ALK FISH-negative disease (alectinib, n=21; crizotinib, n=18). For 61 of 303 (20.1%) patients with an ALK IHC-positive result, a valid ALK FISH result could not be obtained due to the test leading to an uninformative FISH result (10.9%), or not having adequate/no tissue available (9.2%). Ventana IHC staining success rates were higher than for Vysis FISH testing for the ALEX samples. Exploratory analysis of investigator-assessed progression-free survival (PFS) in patients with a FISH-positive result (HR 0.40, 95% CI 0.27–0.61; p<0.0001; median not reached [alectinib] versus 12.7 months [crizotinib]) was consistent with the primary endpoint analysis in the Ventana ALK IHC-positive population. Patient outcome data show that 28% of central ALK IHC-positive/ALK FISH-negative samples were from patients who responded to ALK TKI treatment (complete response or partial response) and 33% had stable disease according to investigator assessment.

      Conclusion:
      This analysis shows that ALK IHC is a robust testing approach, which may identify more patients with a valid ALK testing result who benefit from ALK TKI treatment than ALK FISH testing. While PFS of patients with ALK FISH-positive NSCLC was similar to that of patients with ALK IHC-positive NSCLC, the analysis also revealed that the majority of patients with ALK IHC-positive/ALK FISH-negative NSCLC may derive clinical benefit from ALK TKI treatment.

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      JCSE 01.28 - NGS Sequencing Based Liquid / Tissue Biopsy Identified Coexistence of HER2 Amplification and Mutation in Advanced NSCLC Patients

      07:30 - 11:30  |  Presenting Author(s): Rongrong Chen  |  Author(s): J. Zhao, G. Lin, L. Liu, L. Chen, X. Hu, X. Ai, Z. Fan, C. Xu, W. Wang, W. Zhuang, M. Fang, Y. Zhu, G. Chen, Y. Guan, L. Yang, X. Xia, X. Yi

      • Abstract

      Background:
      Human epidermal growth factor 2 (HER2, ERBB2) mutations / amplifications have been identified as oncogenic drivers in 2-5% of lung cancers. It has been reported that hybridization capture-based next-generation sequencing (NGS) could reliably detect HER2 amplification in qualified breast and gastroesophageal tumor tissue samples. However, there is little data in lung cancer, especially for advance NSCLC with only ctDNA samples available.

      Method:
      We reviewed 2000 consecutive samples from advanced NSCLC patients sequenced in our institute between 2015 and 2016. Tumor biopsy and/or ctDNA samples were analyzed using hybridization capture-based NGS ER-Seq method, which enables simultaneously assess single-nucleotide variants, insertions/deletions, rearrangements, and somatic copy-number alterations at least 59 genes (range 59 – 1021 genes).

      Result:
      We identified 54 samples from 48 patients with HER2-mutation or amplification in the cohort (54/2000=2.7%). The 54 samples included 14 tissue biopsy samples, 37 ctDNA samples, and 3 pleural effusion samples. Thirty-six samples carried HER2 mutations, and 23 samples carried HER2 amplification with 5 samples have concurrent HER2 mutation and amplification. A 9-base pair (bp) in-frame insertion in exon 20 (Y772_A775dup) was detected in 18 samples (18/36=50%). In addition, there were 5 other insertions in exon 20; eight single bp substitutions (S310F) in exon 8; three exon 17 V659E mutations (from the sample patient with 3 ctDNA samples submitted at different time); one exon 19 D769H mutation; and one exon 21 V842I mutation. Amplification were identified in 23 samples, with copy number range from 3.8 to 19.6 in tissue samples (n=7, medium 11.6); from 4.3 to 51.8 in ctDNA samples (n=16, medium 7.3); 3.2 and 6 in the 2 pleural effusion samples. Interestingly, the allele frequency (AF) of HER2 mutation was the maximal in 4 of the 5 patients with concurrent HER2 mutation and amplification. Two patients were EGFR-TKI resistant with EGFR L858R mutation remaining and HER2 mutation and amplification might be the major reason for the resistance.

      Conclusion:
      HER2 mutations might coexist with HER2 amplification in advanced NSCLC patients, and it could be detected simultaneously with hybridization capture-based NGS sequencing both in tissue and liquid biopsy samples. Further quantative analysis of HER2 amplification / mutation and anti-HER2 therapeutic effects are underway.

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      JCSE 01.29 - Closing Remarks

      07:30 - 11:30

      • Abstract

      Abstract not provided

  • +

    YI 01 - Young Investigator and First Time Attendee Session

    • Type: Young Investigator
    • Track: Education/Publication/Career Development
    • +

      YI 01.01 - Introduction to IASLC: What It Can Do For You

      08:00 - 11:30  |  Presenting Author(s): Silvia Novello

      • Abstract

      Abstract not provided

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      YI 01.02 - Planning an Academic Career in Lung Cancer

      08:00 - 11:30  |  Presenting Author(s): Navneet Singh

      • Abstract

      Abstract:
      Decision making in life is not always easy. This is applicable not just for patient care but also for matters related to our own-self and is particularly true in the context of career options in medicine. Over the past few decades, the level of expertise provided by health-care providers has enhanced considerably from having comprehensive ‘all-in-one’ doctors to specialists to super-specialists and currently focused super-specialists. This has been associated with the practice of medicine having changed from ‘evidence-based-medicine’ to ‘personalized medicine’ and currently of ‘precision medicine’ and ‘tailor-made’ therapies. This has largely been based on an increase in the quantity and quality of research being conducted worldwide. A majority of this research occurs in academic medical centers/university hospitals wherein faculty/attending consultants are not just involved in patient care but have to devote a substantial percentage of their time in planning and conducting research as well as teaching undergraduate/postgraduate residents and fellows. So the natural questions that crop up for someone in training are: 1) ‘How do I decide whether I am inclined to be working in an academic institute?’ [Will I be able to ‘gel-in’ or be a complete misfit?] ‘2) What is the time-point during my training/post-training period when I need to take the decision of pursuing an academic career?’ 3) ‘What are the essential and desirable qualities/traits that are conducive to working in an academic set-up?’ There are no straightforward answers to any of these. However, generally during the final year of fellowship, most individuals are able to decide whether they would like to continue working in an academic centre or not. This is often possible with guidance from course faculty. The chief-guide under whom the individual has been pursuing research (thesis/dissertation) may be able to identify if the latter has an ‘academic bent of mind’ and provide mentorship and help the transition from ‘fellow’ (in-training) to full-time faculty [‘attending’ consultant]. It is important for anyone intending to pursue an academic career to realize that conducting and participating in research is an integral part as opposed to working in non-academic centers where patient care is the primary focus. Inclination towards research may sometimes manifest as being able to identify ‘grey’ areas in practice of medicine (clinical situations for which there are no clear-cut answers). The best researchers are and often have been those who are able to identify these areas of uncertainty related to diagnosis and treatment of a particular condition or disease and carry out research directed to answer the queries that they had in their minds when picking up these uncertainties. Keeping abreast of the latest developments in one's focus area (by regularly accessing and reading the latest publications in peer reviewed journals) as well as publishing one's own experience/research in such journals is thus part and parcel of one's job profile while working in an academic center. For lung cancer – a disease that carries the highest cancer-related mortality amongst both gender combined and the commonest cancer in males, there have been very encouraging developments in the last couple of decades and especially the last five years. We now have five pillars for treatment – targeted therapy and more lately immunotherapy coming in as very useful additions to traditional modalities (surgery, chemotherapy and radiotherapy). And these are truly exciting times for carrying out research in lung cancer in several ways: 1) Number of investigational molecules (targeted therapy and immunotherapy) being developed/tested in preclinical/clinical trials is increasing at an unparalleled rate 2) Conventional pathway followed for testing [preclinical, phase-1, phase-2, phase-3 clinical trials] is being modified to reduce time to clinical approval for successful drugs by having combined phase 1/2 or phase 2/3 trials. 3) Intense efforts are being made to expand indications for already approved/available drugs e.g. assessing utility of targeted agents in early stage/resectable NSCLC and of combination regimens (EGFR-TKIs/ALK inhibitors+ chemotherapy, PD-1/PD-L1 immune check-point inhibitors+ chemotherapy). Several unaddressed issues exist in lung cancer currently which require concerted efforts and inputs from researchers worldwide including: 1) Improving the screening algorithm for early detection such that false positive results and need for/number of invasive procedures required is reduced. Development of blood, sputum or exhaled-breath based screening tests could find greater acceptability and applicability worldwide. 2) Improving the genomic understanding of SCLC – a histological subtype without significant advances in the past leading treatment to be essentially with two modalities (chemotherapy and radiation). Identifying ‘targetable’ molecular aberrations can revolutionize management of this aggressive histological type while ongoing efforts to establish the role of immune check-point inhibitors continue. 3) Detection of EGFR sensitizing mutations and acquired T790M resistance-conferring mutation (for initiating 1[st]/2[nd] generation EGFR-TKIs and osimertinib respectively) in circulating tumor DNA (ctDNA; sometimes called circulating free tumor DNA - cfDNA) is already applicable in clinical practice and potentially can be used for monitoring treatment responses also. Next-generation-sequencing(NGS) platforms appear promising in detecting both somatic point-mutations and rearrangements/fusions with minimal tissue and/or ctDNA. Development and validation of methods for non-invasive biological monitoring of responses to chemotherapy, radiation, immunotherapy and non-EGFR targeted therapies in the complete spectrum of histological types (SCLC, squamous and non-squamous NSCLC) and disease stage distribution (neoadjuvant treatment preceding surgery, post surgery – adjuvant setting, locally advanced NSCLC following induction concurrent chemo-radiation and metastatic setting) will make it more convenient for patients and treating oncologists alike. The advantages of working in an academic setup in lung cancer are apparent both for the clinician and his/her colleagues in other clinical departments/basic sciences. Current research and clinical practice requires collaboration of different disciplines [pulmonology, diagnostic and interventional radiology (including nuclear imaging), pathology (histopathology, cytopathology, molecular pathology), thoracic surgery/surgical oncology, radiation oncology and medical oncology]. Based upon the academic institute’s geographical location, the number/work profile of departments that exist for a given discipline may vary considerably. These variations notwithstanding, the bottom-line is that reaching out to and working together with colleagues from other departments and disciplines [multidisciplinary team approach] is mandatory for attempting conduct of high-quality research and delivery of high-quality patient care in thoracic oncology. This potential advantage and benefit also comes with several challenges. One is required to carefully balance and utilize working hours for patient care, research and training while attempting to do the best in all three fields. This invariably, if not mandatorily, leads to spill-over of work into ‘off-work’ hours and impinges on ‘family-hours’ or ‘personal-time.’ The support of one's spouse, parents and children in such settings cannot be undermined or understated. One needs to keep a balance between ‘All-work-and-no-play makes Jack a frustrated man’ versus ‘Jack-of-all-trades and master-of-none’. Neither is desirable and the ultimate aim is to have a satisfying career in thoracic oncology while working in an academic setting wherein one is able to: 1) provide patients (often under-privileged and belonging to poor socio-economic strata) the best diagnostic and treatment facilities (despite presence of resource constraints) – Patient Care 2) be involved in clinically relevant basic and translational research that has the potential to improve patient care in one’s own geographical location – Research 3) share one’s experience with residents/fellows and colleagues within the institute and outside – Medical Education Navneet Singh MD DM Email: [The author is a thoracic medical oncologist-cum-pulmonologist currently working as an Associate Professor of Pulmonary Medicine at the Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India. He is a member of IASLC’s Staging & Prognostic Factors Committee; Publications Committee and is IASLC’s Regent for the Indian Subcontinent. Additionally, he is Chair-Elect of the American Society of Clinical Oncology’s (ASCO) International Development and Education Award (IDEA) Working Group and a member of its Multidisciplinary Cancer Management Course Working Group and Thoracic Cancer Guideline Advisory Group. His detailed profile is accessible at http://www.linkedin.com/in/navneet-singh-160012.]

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      YI 01.03 - Community versus Academic Oncology

      08:00 - 11:30  |  Presenting Author(s): Philip Bonomi

      • Abstract

      Abstract:
      Relatively little information is available for hematology oncology fellows to inform their choice for an academic oncology(AO) vs a community oncology(CO) career. In 2006, Desch and Blayney(1) described practical differences between AO and CO careers which are still pertinent today. A more recent report from Vanderbilt(2) describes factors which appear to influence oncology fellows’ career decisions. Once a career path has been selected, does this choice affect career and work-life balance satisfaction? Shanafelt and his colleagues have described the impact of career choice and related factors on job satisfaction(3,4). This review will summarize the results of these reports and share a perspective regarding possible changes in oncology practices which could impact career choice. Desch and Blayney(1) describe mission, governance, patient care, financial considerations, referral bases, career flexibility, and determinants of success. The mission for community oncologists(COs) consists of delivering excellent patient care and running a successful business. In contrast, the mission for academic oncologists(AOs) encompasses patient care, research and teaching. CO governance offers more autonomy and usually consists of a doctor owned corporation with equal ownership. AOs work in a hierarchical system with multiple levels between the physician and senior leadership. There are significant differences in delivering patient care. Desch and Blayney point out that “ COs are intern, resident, fellow, and attending all rolled into one. ” COs have more weekend and night call. In addition, COs provide care for multiple types of cancer patients , while AOs’ practice is usually limited to one or two types of malignancy. Patient referrals for COs depend upon building relationships with primary care physicians and surgeons in their community. AOs also get patient referrals from primary care physicians and surgeons, but they rely heavily on institutional reputation, the reputation of disease specific experts, and a robust clinical trial program. Publishing and giving presentations at local and national meetings establishes AOs as disease specific experts which results in physician referrals and in patient initiated consultations. Revenue for COs depends upon fees for physician services, for administration of intravenous treatment , for laboratory tests, for imaging, and revenue from chemotherapy/immunotherapy treatments. For AOs, revenue comes from fees for physician services, grants, clinical trial revenue, and philanthropy. In some academic institutions, revenue may also come from the ancillary sources, similar to private practice. Starting and subsequent compensation is higher for COs who receive significant salary increases when they become full partners in the corporation, 2-5 years after joining the practice. Salary for AOs increases with increasing academic rank and may be supplemented with bonuses and honorariums for lectures and participation in advisory boards. Desch and Blayney(1) suggest that there are critical success factors for COs and AOs. . Building a reputation as a local expert and being readily available to referring MD’s and partners is essential for COs. . They also point out that it is essential for COs to invest time to understand bonuses and to show that they value and support the practice staff. AOs must focus on area of expertise, choose a good mentor, publish results of research, and apply for grants. It is not realistic to expect AOs with a large clinical practice to be the principal investigator on a grant. However, these clinicians can learn the concepts of basic science and partner with laboratory investigators in translational research grant proposals. Horn and her collegues(2) studiedfactors associated with selecting an AO or CO career. They invited program directors at 56 NCI designated and National Comprehensive Cancer Network cancer centers. Fellows at these institutions were asked to complete a questionnaire regarding their interest in AO vs CO careers. . Fellows with a high interest in AO were more likely to be women, have an additional graduate degree, and to have participated in basic research. Also fellows who were more interested in AO gave more presentations at scientific meetings and had more publications. Having an influential mentor and a desire to teach were also related to pursuing a career in AO. . Fellows who were more interested in CO were motivated by work-life balance and autonomy. This study suggest that fellows who are primarily motivated by being involved in identifying new information and teaching are more likely to pursue AO , while fellows who are motivated by favorable work-life balance and having more autonomy are more likely to pursue a CO career. How do practicing oncologists feel about their careers? Shanafelt and colleagues(3,4) have published two reports describing results of a survey which evaluated burnout, career satisfaction, life – work balance satisfaction and retirement. They(3) found that COs spent more time in clinic and saw more patients.. Younger age and more hours in clinic were associated with increased risk of burnout, which was defined as a combination of emotional exhaustion and depersonalization (loss of concern for patients),. There was a trend for higher rate of emotional exhaustion and a significantly higher rate of depersonalization in community oncologists. Although the majority of oncologists would choose a career in oncology, there was a higher number of COs who stated they would not choose an oncology career. In the second report(4), they did not compare AOs and COs. They saw that although most oncologists find meaning in their work, 52% were dissatisfied with work-life balance. “They like their work but want to do less of it.” Work-life balance was affected by more night and weekend call, while method of compensation salary +/- bonuses (most AOs) versus incentive (most COs) was not related work-life balance. For oncologists who planned to reduce work hours, the most common reason was to spend more time with family. In summary, when making a career choice, oncology fellows should identify what motivates them. I suspect that the majority of oncologists will continue to be happy with their career choice and that the current differences between AO and CO careers may decrease because more COs will be employed by hospital systems. References 1.Desch CE, Blayney DW. Making the Choice Between Academic Oncology and Community Practice: The Big Picture and Details About Each Career. Oncol Pract 2:132-138, 2006 2.Horn L, Koehler E, Gilbert J, et al. Factors Associated with the Career Choices of Hematology and Medical Oncology Fellow Trained ar Academic Insitutions in the United States. J Clin Oncol 29: 3932 - 3938, 2011 3.Shanafelt TD, Gradishar WJ, Kosty M, et al.Burnout and Career Satisfaction Among US Oncologists. J Clin Oncol 32: 678-686, 2016 4.Shanafelt TD, Raymond M, Kosty M, et al.Satisfaction with Work-Life Balance and the Career and Retirement Plans of US Oncologists.J Clin Oncol 32:1127-1135, 2014

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      YI 01.04 - Clinical Trials 101

      08:00 - 11:30  |  Presenting Author(s): Julie R Brahmer

      • Abstract

      Abstract not provided

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      YI 01.05 - Investigator Initiated Trials

      08:00 - 11:30  |  Presenting Author(s): Daniel SW Tan

      • Abstract

      Abstract not provided

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      YI 01.06 - Coffee Break

      08:00 - 11:30

      • Abstract

      Abstract not provided

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      YI 01.07 - How to Get Your Paper Published

      08:00 - 11:30  |  Presenting Author(s): Alex Adjei

      • Abstract

      Abstract not provided

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      YI 01.08 - Why Should I Publish? An Overview of the Manuscript Cycle: From Submission to Publication

      08:00 - 11:30  |  Presenting Author(s): Jim Jett

      • Abstract

      Abstract not provided

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      YI 01.09 - How to Prepare an Abstract for an International Conference and How to Prepare Your Presentation for the Conference (Tips and Tricks)

      08:00 - 11:30  |  Presenting Author(s): Michael Boyer

      • Abstract

      Abstract not provided

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      YI 01.10 - How to Write a Grant Application for Young Investigators

      08:00 - 11:30  |  Presenting Author(s): Heather A Wakelee

      • Abstract

      Abstract:


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      YI 01.11 - The Young Investigator Travel Award Experience - A Report from a Previous Award Winner

      08:00 - 11:30  |  Presenting Author(s): Takahiro Karasaki

      • Abstract

      Abstract:
      I received the WCLC 2016 Young Investigator Travel Award for my presentation entitled “Immunogram for cancer-immunity cycle towards personalized immunotherapy of lung cancer”. It was my great honor to receive the award, and I want to thank the conference committee and all the conference attendees. This was my first time to attend the WCLC, and I enjoyed the conference and my stay in Vienna. I was given the opportunity to join the Faculty Dinner held in Vienna City Hall. It was a fabulous experience, and I thoroughly enjoyed sitting at the same table as world-renowned surgeons and oncologists. During the conference, I mainly attended immunotherapy sessions where I learned about the results of the most recent clinical studies. Furthermore, while attending the biomarker session, I realized that biomarkers in this field are still inadequate and the development of useful biomarkers in immunotherapy is an urgent need. Receiving the young investigator scholarship has encouraged me to continue our efforts to unveil the tumor microenvironment in each patient using individual next-generation sequencing data in order to develop “next-generation biomarkers” and achieve optimal personalized immunotherapy. Last year, in a Perspectives article in Science, Blank et al. proposed the concept of the cancer immunogram, a framework to illustrate multiple parameters that influence the cancer-immunity interaction (1). In their article, the concept was applied theoretically to patients but not tested in practice. To accomplish this, we developed an immunogram reflecting the cancer immunity cycle using next-generation sequencing data, and applied it to real patients with lung cancer. An immunogram for the cancer immunity cycle is a radar chart that consists of eight molecular profiles relevant to the development of T-cell immunity to tumor cells. We sought to translate cumbersome omics data into easily comprehensible “report cards” for clinicians. Immunograms can be used as integrated biomarkers, and may become a valuable resource for optimal personalized immunotherapy. After the presentation at the WCLC 2016, our findings were published in the Journal of Thoracic Oncology in May (2). It was an honor that our article was chosen by the Editor to be a featured article and was introduced by an elegant review (3). We recently updated our method by normalizing the immunogram score using TCGA data. We are pleased to share the details of this improvement during the present conference. Although we are working in a challenging field and there is still a long way to go, we are encouraged by the award and will continue to struggle toward further breakthroughs.  References (1) Blank CU, Haanen JB, Ribas A, Schumacher TN. Cancer immunology. The “cancer immunogram” Science. 2016;352:658-60. (2) Karasaki T, Nagayama K, Kuwano H, et al. An Immunogram for the Cancer-Immunity Cycle: Towards Personalized Immunotherapy of Lung Cancer. J Thorac Oncol.2017;12(5):791-803. (3) Botling J, Sandelin M. Immune Biomarkers on the Radar-Comprehensive "Immunograms" for Multimodal Treatment Prediction. J Thorac Oncol.2017;12(5):770-2.

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      YI 01.12 - Making the Most of the WCLC: A Guide for First Time Attendee - From an Expert Perspective

      08:00 - 11:30  |  Presenting Author(s): Suresh Senan

      • Abstract

      Abstract not provided

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      YI 01.13 - Making the Most of the WCLC: A Guide for First Time Attendee - From a Second Time Attendee

      08:00 - 11:30  |  Presenting Author(s): Deepali Jain

      • Abstract

      Abstract:
      The IASLC (International association for the study of lung cancer) WCLC (World Conference on Lung Cancer) is world’s largest academic platform dedicated for the study of lung cancer and other thoracic malignancies which not only caters to physicians but also includes active participation from each discipline of medicine involves in patient care. In addition health advocacy groups and patients will also join WCLC to obtain and exchange the information. The focus of the meeting is on the biology, diagnosis, pathogenesis, treatment and management of lung cancer so to begin from active prevention and accurate diagnosis to advanced care. Because of advancing science of lung cancer, IASLC decided to hold WCLC every year so people will be kept abreast with the current knowledge and updates in this field. There are many academic opportunities for the young investigators or first-time attendee to pursue their career in the field of thoracic oncology. They can meet the experts during the conference, attend various educational sessions and take guidance in the field of basic, translational and clinical research. There are many awards which help in not only enhancement of academic career but also in attending conference from resource poor countries. Travel awards given to developing nation investigators so that they can attend the conference and present their latest research in addition to make collaborations and academic networking. International mentorship program of IASLC is very useful professional development and education program for early-career doctors from economically-developing countries in which you get an opportunity to spend a week time in a well established hospital or laboratory under the mentorship of an international expert in that field. This year, the Core Program Committee has organized a scientific program that includes more than 450 presentations. The conference motto is “Synergy to Conquer Lung Cancer” which will be very overwhelming at both scientific and educational fronts. The education sessions include state-of-the-art talks by experts on academically challenging and evolving topics. The scientific program includes research presentations in the form of posters and platform formats. There are many events and platforms where first time attendees can interact and do networking for future collaborations. It is certain that the 18[th] WCLC will help young investigators and first time attendees to build and shape-up their career in thoracic oncology.

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      YI 01.14 - Q&A

      08:00 - 11:30

      • Abstract

      Abstract not provided

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    SS 01 - Supporting the Clinical Management of Lung Cancer Patients through Innovation in Diagnostics - Roche

    • 08:15 - 12:00
    • 10/15/2017
    • Location: Room 315
    • Moderators:
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      SS 01.01 - Welcome & Opening

      08:15 - 12:00

      • Abstract

      Abstract not provided

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      SS 01.02 - Unmet Medical Needs and Challenges in Lung Cancer Patient Management - A Pulmonologists Perspective

      08:15 - 12:00  |  Presenting Author(s): Ramon Marrades

      • Abstract

      Abstract not provided

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      SS 01.03 - Protein-based Biomarkers as Tools to Support Clinical Decision Making with Results from the Laboratory

      08:15 - 12:00  |  Presenting Author(s): Rafael Molina

      • Abstract

      Abstract not provided

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      SS 01.04 - Panel - Q&A

      08:15 - 12:00

      • Abstract

      Abstract not provided

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      SS 01.05 - Break

      08:15 - 12:00

      • Abstract

      Abstract not provided

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      SS 01.06 - Integrated Tissue and Molecular Diagnostics for Optimal Lung Cancer Patient Care

      08:15 - 12:00  |  Presenting Author(s): Stephen P Finn

      • Abstract

      Abstract not provided

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      SS 01.07 - The Evolution of Lung Cancer Treatment - Clinical Impact of Genomic Alterations Detected in Tissue and Plasma

      08:15 - 12:00  |  Presenting Author(s): Alice Shaw

      • Abstract

      Abstract not provided

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      SS 01.08 - Clinical Utility of Liquid Biopsy in Managing NSCLC Patients - Performance and Impact on Clinical Decisions

      08:15 - 12:00  |  Presenting Author(s): Shobhit Baijal

      • Abstract

      Abstract not provided

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      SS 01.09 - Panel - Q&A

      08:15 - 12:00

      • Abstract

      Abstract not provided

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      SS 01.10 - Wrap-up & Closing

      08:15 - 12:00

      • Abstract

      Abstract not provided

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    WS 03 - ITONF Lung Cancer and Mesothelioma Workshop (Ticketed Session)

    • 12:15 - 17:55
    • 10/15/2017
    • Location: Room 313
    • Moderators:
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      WS 03.01 - ITONF Members Meeting (with Lunch)

      12:15 - 17:55

      • Abstract

      Abstract not provided

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      WS 03.02 - Local Therapies for Lung Cancer and Mesothelioma

      12:15 - 17:55  |  Presenting Author(s): Caitlin Broderick

      • Abstract

      Abstract not provided

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      WS 03.03 - Welcome Address

      12:15 - 17:55  |  Presenting Author(s): Beth Ivimey

      • Abstract

      Abstract not provided

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      WS 03.04 - The Oncology Nurse Role in the Treatment of Lung Cancer and Mesothelioma: The Recent Practice in Japan

      12:15 - 17:55

      • Abstract

      Abstract not provided

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      WS 03.05 - Explaining Radiation Treatments in Lung Cancer

      12:15 - 17:55  |  Presenting Author(s): Mary Duffy

      • Abstract

      Abstract not provided

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      WS 03.06 - Local Treatments for Lung Cancer – Blade vs Beam: A Debate

      12:15 - 17:55  |  Presenting Author(s): David L Ball, Melissa Culligan

      • Abstract

      Abstract not provided

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      WS 03.07 - Wellness and Supportive Care for Lung Cancer and Mesothelioma Patients

      12:15 - 17:55  |  Presenting Author(s): Kathleen Ann Gamblin

      • Abstract

      Abstract not provided

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      WS 03.08 - Acute Thoracic Oncology Nursing

      12:15 - 17:55

      • Abstract

      Abstract not provided

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      WS 03.09 - Living Well with Lung Cancer and Mesothelioma

      12:15 - 17:55  |  Presenting Author(s): Pippa Labuc

      • Abstract

      Abstract not provided

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      WS 03.10 - Panel Discussion

      12:15 - 17:55

      • Abstract

      Abstract not provided

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      WS 03.11 - Break

      12:15 - 17:55

      • Abstract

      Abstract not provided

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      WS 03.12 - Systemic Treatments for Lung Cancer and Mesothelioma

      12:15 - 17:55  |  Presenting Author(s): Massey Nematollahi

      • Abstract

      Abstract not provided

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      WS 03.13 - Targeted Therapies: Toxicities Management and Care

      12:15 - 17:55

      • Abstract

      Abstract not provided

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      WS 03.14 - Targeted Therapies: Case Studies and Experience from Different Regions Q&A

      12:15 - 17:55  |  Presenting Author(s): Beth Ivimey, Caitlin Broderick, Beth Eaby-Sandy, John McPhelim

      • Abstract

      Abstract not provided

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      WS 03.15 - Immuno-oncology Overview

      12:15 - 17:55  |  Presenting Author(s): Marianne Davies

      • Abstract

      Abstract not provided

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      WS 03.16 - Japan’s Challenges in Immunotherapy for Lung Cancer as a Pioneer: The Nurses View

      12:15 - 17:55

      • Abstract

      Abstract not provided

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      WS 03.17 - Latest Advances in the Treatment of Malignant Pleural Mesothelioma

      12:15 - 17:55  |  Presenting Author(s): Mary Hesdorffer

      • Abstract

      Abstract not provided

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      WS 03.18 - Mesothelioma Online Educational Programs, ITONF Nurse Education Programs & N&AH Immunotherapy Guidelines Launch

      12:15 - 17:55  |  Presenting Author(s): Melissa Culligan, Liz Darlison, Anne Fraser, Kathleen Ann Gamblin

      • Abstract

      Abstract not provided

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      WS 03.19 - Close

      12:15 - 17:55  |  Presenting Author(s): Melissa Culligan

      • Abstract

      Abstract not provided

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    WS 04 - Minimally Invasive Diagnosis and Staging of Lung Cancer – Interventional Pulmonology Hands-On Workshop (Ticketed Session)

    • Type: Workshop
    • Track: Pulmonology/Endoscopy
    • Moderators:
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      WS 04.01 - Welcome and Introduction

      13:00 - 17:00  |  Presenting Author(s): Kazuhiro Yasufuku

      • Abstract

      Abstract not provided

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      WS 04.02 - EBUS-TBNA – Role in Invasive Mediastinal Staging

      13:00 - 17:00  |  Presenting Author(s): Kazuhiro Yasufuku

      • Abstract

      Abstract not provided

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      WS 04.03 - Specimen Acquisition and Processing

      13:00 - 17:00  |  Presenting Author(s): Takahiro Nakajima

      • Abstract

      Abstract not provided

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      WS 04.04 - Radial Probe EBUS – Methods and Results

      13:00 - 17:00  |  Presenting Author(s): Y. Matsumoto

      • Abstract

      Abstract not provided

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      WS 04.05 - Navigational Bronchoscopy

      13:00 - 17:00  |  Presenting Author(s): L. Donahoe

      • Abstract

      Abstract not provided

    • +

      WS 04.06 - Hands-On Session (5 work stations)

      13:00 - 17:00

      • Abstract

      Abstract not provided

    • +

      WS 04.07 - 1. EBUS-TBNA

      13:00 - 17:00

      • Abstract

      Abstract not provided

    • +

      WS 04.08 - 2. Radial Probe EBUS

      13:00 - 17:00

      • Abstract

      Abstract not provided

    • +

      WS 04.09 - 3. Specimen Handling

      13:00 - 17:00

      • Abstract

      Abstract not provided

    • +

      WS 04.10 - 4. Navigational Bronchoscopy (Super Dimension)

      13:00 - 17:00

      • Abstract

      Abstract not provided

    • +

      WS 04.11 - 5. Navigational Bronchoscopy (BF Navi)

      13:00 - 17:00

      • Abstract

      Abstract not provided