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  • WCLC 2018

    19th World Conference on Lung Cancer

    Access to all presentations that occur during the 19th World Conference on Lung Cancer in Toronto, ON

    Presentation Date(s):
    • Sept 23 - 26, 2018
    • Total Presentations: 2384

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    Presentations will be available 24 hours after their live presentation time

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    S01 - IASLC CT Screening Symposium: Forefront Advances in Lung Cancer Screening (Ticketed Session) (ID 853)

    • Type: Symposium
    • Track: Screening and Early Detection
    • Presentations: 7
    • Now Available
    • Moderators:
    • Coordinates: 9/23/2018, 07:00 - 12:00, Room 203 BD
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      S01.04 - Lung Cancer Screening: 1999 to Date – What Have We Learnt? (Now Available) (ID 11885)

      07:35 - 07:50  |  Presenting Author(s): David F Yankelevitz

      • Abstract
      • Presentation
      • Slides

      Abstract

      In 1999, ELCAP published their initial results from baseline screening. It found that in a cohort of 1000 participants approximately 85% of the cancers could be diagnosed as clinical Stage I, and that compared with chest radiography found many more of the cancers. In a subsequent study the expanded I-ELCAP found that the long term survival as a measure of cure rate approached 80%. The publicity associated with this initial study was quite large and led to the initiation of several other trials including the NLST. The NLST published their results in 2011 and based this, screening was endorsed by insurers in the US and now other countries are similarly following suit. However, despite the positive result of the NLST, and reimbursement from insurers, screening has had extremely limited uptake in the US, with only approximately 2% of those eligible (among a restricted population) are being screened. Thus, we face a situation where the most common cancer killer has been studied in the most expensive screening trial ever performed which had a positive result, insurers are reimbursing for it, and few people are having it done.

      With lung cancer screening being touted as a major breakthrough in the war on cancer the question naturally arises as to why it is not being performed more frequently. There have been many reasons to explain the poor uptake, ranging from merely a slow start but expected steady increase, lack of awareness by the clinician or potential screenee, obstacles such as the shard decision making requirement, too many potential harms, and lack of significant benefits.

      This lack of perceived significant benefit is perhaps the most important aspect, since without a substantial benefit, even if the harms were minimized, why would anyone get screened and why would a clinician recommend it. It seems that this is clearly influencing the decision not to be screened as many experts and even guideline organizations consider the benefits to not be sufficient enough so as to recommend the screening. Even CMS considered the balance of the risks and benefits so tenuous that they took the unique step of requiring a shared decision making process to be included as necessary for reimbursement so that a person could balance the risks and benefits.

      It is this aspect of benefit that needs to be considered more carefully when explaining it to a potential screenee. Current decision aids, which are required as part of a shared decision making process, in the US and Canada rely almost exclusively on the NLST result and attempt to convert its findings into more visual aids. However, in translating those NLST results, it needs to be understood that they were highly dependent on the design parameters of the study itself, namely 3 rounds of screening and 6.5 years of follow-up. When these parameters change so do the benefits. In the US, current recommendations for screening include annual screening over the period of eligibility for the participant (although for Canada it is restricted to 3 years). Under the circumstance of continued annual screening, the reduction in mortality begins to approach the estimated cure rate for the cancer. It is this feature of cure rate that is really what is most important to any person interested in being screened, and it is substantially higher than the mortality reduction seen in a randomized trial where by necessity the mortality reduction is diluted by the time interval after screening has stopped and cancers are still being followed, and also by not including those cancers that are relatively slow growing and cured as a result of early treatment but not counted towards the mortality reduction because the trial has concluded before their counterpart in the control arm has died. Based on these considerations, it is possible to have a cancer that is 100% curable when screen detected, yet the trial may only show a 20% (or even lower) mortality reduction. Thus, there is inherently no incompatibility between the 80% cure rate seen in the I-ELCAP compared with the 20% mortality reduction seen in the NLST. The simple conversion of the 20% mortality reduction found in NLST into a cure rate as is so commonly done when explaining the benefit to a person interested in screening is highly misleading. The cure rate, which is the clinically relevant feature, is higher. This coupled with the way in which harms are currently expressed, based again almost solely on those NLST results has the effect of amplifying harms at the same time the benefits are being underestimated and surely affect the perception of overall value of CT screening both for physicians as well as people who might be interested.

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      S01.07 - The U19 Plans for Integration of Biomarkers into Future Lung Cancer Screening (Now Available) (ID 11888)

      08:00 - 08:50  |  Presenting Author(s): Rayjean J. Hung, Paul Brennan, Christopher Ian Amos

      • Abstract
      • Presentation
      • Slides

      Abstract

      We are performing a series of three integrated research projects with the unifying goal of reducing mortality from LC by applying targeted approaches to its prevention or early detection. These projects study (1) genetic susceptibility to nicotine dependence and lung cancer, (2) biomarkers for early detection, and (3) application of the results for LC screening. This proposal leverages an extensive collaborative framework and wealth of data from the International Lung Cancer Consortium (ILCCO), the Transdisciplinary Research in Cancer of the Lung (TRICL) Consortium and the Lung Cancer Cohort Consortium (LC3). Epidemiological data from 60 LC studies have been harmonized within ILCCO including 71,000 cases and more than 1 million cohort individuals.

      Aims and Results

      Project 1: Genomic Predictors of Smoking and Lung Cancer Risk. This project extends and augments genomic analyses that have been completed on 16,000 LC cases and 50,000 controls and extensively characterizes the contribution that genetic variation makes to LC susceptibility. The four aims are. Aim 1: To precisely characterize the contribution of common genetic variation to LC etiology. We will analyze a GWAS of LC of 47,506 genotyped LC cases and 63,687 controls. Aim 2: To investigate uncommon genetic variants using imputation approaches. Aim 3: To identify genetic effects on smoking behavior. Aim 4: To characterize joint effects of environmental and genetic interactions on LC risk. For this aim we will take advantage of novel statistical approaches (Mendelian Randomization, Mediation analysis, gene by environment interactions and pathway based analyses) developed by our team to provide a comprehensive approach to evaluating the impact of environmental factors according to genetic background. Recent findings from project 1 include identification of 10 new loci influencing lung cancer risk, the identification of 3 novel gene-smoking interactions contributing to lung cancer risk, identification and validation of two rare variants that convey an over four fold higher risk for lung cancer among carriers, and Mendelian randomization studies that show excess BMI and shorter telomere lengths increase lung cancer risk in a histology-dependent fashion.

      Project 2: Biomarkers of Lung Cancer Risk. Multiple preliminary studies have implicated a wide range of circulating biomarkers in risk prediction for lung cancer. In Project 2, we hypothesize that a comprehensive and extensively validated risk prediction model that incorporates such risk biomarkers has the potential to substantially improve the selection of subjects at a high risk of developing LC and that these individuals are most likely to benefit from CT screening. This project involves three aims. Aim 1: To organize the LC3, including identifying the study population of 2,300 former and current smoking LC cases that were diagnosed within 5 years of donating their blood sample along with one smoking-matched control per case; and organize sample shipments and database preparation. Aim 2: To replicate a comprehensive panel of promising risk biomarkers and identify those that may be useful for risk prediction. This will involve assaying pre-diagnostic plasma samples for immune biomarkers, protein biomarkers such as pro-surfactant protein B, micro RNAs, methylation markers, and 34 additional promising biomarkers implicated in lung cancer. We will base this initial analysis on 800 case-control pairs from three LC3 cohorts, and define a panel of replicated risk biomarkers that provide non-redundant information on disease risk. Aim 3: To extensively evaluate all replicated risk biomarkers from Aim 2, identifying a minimum set of validated risk biomarkers, and ultimately evaluate the extent to which they improve risk prediction models. This will involve performing additional assays for 1,500 additional case-control pairs selected from 16 separate LC3 cohorts. The final outcome of this work will be risk prediction models incorporating a distinct set of biomarkers that provide meaningful information on disease risk, and these biomarkers will finally be evaluated in CT screening studies in collaboration with Project 3. This project recently completed analysis of a set of 4 biomarkers that improve the classification accuracy in prediction of lung cancer risk by 14% compared with a model that only included demographic and smoking information.

      Project 3: Translating Molecular and Clinical Data to Population Lung Cancer Risk Assessment will evaluate radiographic models using data from the National Lung Screening Trial (NLST), lung cancer CT screening programs in British Columbia Cancer Agency (BCCA), Early Detection of Lung Cancer – a Pan-Canadian Study (PanCan), and the International Early Lung Cancer Action Program- Toronto (IELCAP-Toronto) along with the UK Lung Screen Trial (UKLS), and the Dutch Belgian randomized Lung Cancer Screening trial (NELSON) trial. Data from Projects 1-2 will be used to improve the risk prediction model and the nodule probability models. There are 2 specific aims. Aim 1 will establish an integrated risk prediction model to identify individuals at high risk of lung cancer, initially analyzing epidemiological and smoking related phenotypes and then integrating targeted biomarker, genomic profile, and lung function data applied to LC CT screening populations. We will study 950 CT-detected LC patients with biosamples from 46,057 screening individuals. Specific Aim 2 will establish a comprehensive LC probability models for individuals with LDCT-detected non-calcified pulmonary nodules. In this aim we will (a) first establish the 2D diameter-based probability model in N. American CT programs based on 36,481 participants, and then validate it based on 9,576 participants in the European LDCT programs; (b) establish the volume 3D and radiomics-based probability model in European CT programs based on 9,576 participants in European CT programs, and then validate it in the North American CT screening populations; and (c) assess the added predictive value and clinical usefulness of targeted genomic and molecular profiles in both the 2D diameter- and 3D and radiomics volume-based LC probability models based on risk stratification table analysis and decision curve analysis. Finally we will (d) compare the model performance with the existing classification system such as Lung-RADS. This project has developed and evaluated a polygenic risk score using data from project 1 which highly significantly improves risk prediction for lung cancer risk, but has a limited impact on prediction accuracy.

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      S01.10 - EU Position Statement on Lung Cancer Screening (Now Available) (ID 11891)

      09:00 - 09:20  |  Presenting Author(s): Matthijs Oudkerk

      • Abstract
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      Abstract not provided

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      S01.14 - Coordination of the Lung Cancer CT Screening Experience (Now Available) (ID 11895)

      09:50 - 10:05  |  Presenting Author(s): Joelle Thirsk Fathi

      • Abstract
      • Presentation
      • Slides

      Abstract

      Coordination of the Lung Cancer CT Screening Experience

      Tobacco use, including cigarette smoking is the most preventable cause of cancer in the entire world, contributing to one third of all cancers. While 80-90% of all lung cancers are directly correlated with cigarette smoking, tobacco is also identified as playing a direct role in a multitude of other malignancies and chronic diseases, and resides in the top ten contributors to human suffering, disability and death (U.S. Department of Health & Human Services, 2014). Tobacco will shorten the lives of 50% of its users, resulting in approximately 17,000 people dying every day in the world (Cahn, 2018)

      Since the National Lung Screening Trial data demonstrated that lung cancer screening provides a reduction in mortality in high-risk patients, (National Lung Screening Trial Research Team et al., 2011) interest and momentum in the adoption of lung cancer screening in the U.S. and abroad has been on a slow but upward trajectory. Yet only 2-4% of eligible people are getting screened (Jemal & Fedewa, 2017).

      Lung cancer screening patients, by having met high-risk criteria, are a defined and select population of people who could greatly benefit from a sophisticated and well-orchestrated lung cancer screening experience. Coordination of successful, high quality, and comprehensive care of patients in the screening environment is challenging, but screening represents an enormous opportunity to reduce disability and death from tobacco use. It is critical that transformation and refinement of screening practices occurs, to adapt a comprehensive model which encompasses a broader scope of diagnoses, treatments, and patient education.

      Uptake of lung cancer screening has been slow in the U.S., and education around screening needs to be continually promoted. Additionally, we need to continue to develop and refine the roles and responsibilities of all involved in the screening process, including the patient. Current diagnostic and health information technology allows for more precise, easier, faster, and safer care. In the setting of lung cancer screening, low dose computed tomography of the lung can often provide a snapshot into a patient’s overall health and has the potential to alert the healthcare team and the patient to additional potential disease states, to which we are obligated to address.

      Additionally, lung cancer screening is a unique and ideal opportunity to address tobacco cessation with patients. Technology is critical, but can’t replace coordination of care, patient engagement, and education with this invaluable opportunity for detection of tobacco related diseases and tobacco cessation efforts. Screening requirements and the high incidence of abnormal findings on screening scans represents the need for interprofessional collaboration, and a concert of sequential events and highly coordinated care potentially involving many members of different healthcare teams.

      In the setting of healthcare today, with an emphasis on collaboration and coordination of care, screening should be viewed and treated as a long-term commitment by all parties, and engagement and partnership with patients and fellow referring providers is critical in redefining the patient experience and delivery of care. It is not just about the chest CT; in fact, this is minor compared to the potential to intervene, and even halt disease progression and reduce risk with health behavior modification, while realizing earlier diagnosis and intervention, and saving money and lives.

      Cahn, Z., Drope, J., Hamill, S., Gomeshtapeh, F., Liber, Al, Nargis, N., Stoklosa, M.,. (2018). Health Effects. In J. Drope, Schluger, N., (Ed.), The tobacco atlas (pp. 24-25). Atlanta, Georgia: American Cancer Society.

      Jemal, A., & Fedewa, S. A. (2017). Lung Cancer Screening With Low-Dose Computed Tomography in the United States-2010 to 2015. JAMA Oncol, 3(9), 1278-1281. doi:10.1001/jamaoncol.2016.6416

      National Lung Screening Trial Research Team, Aberle, D. R., Adams, A. M., Berg, C. D., Black, W. C., Clapp, J. D., . . . Sicks, J. D. (2011). Reduced lung-cancer mortality with low-dose computed tomographic screening. N Engl J Med, 365(5), 395-409. doi:10.1056/NEJMoa1102873

      U.S. Department of Health & Human Services. (2014). The health consequences of smoking—50 years of progress: A report of the Surgeon General 2014, executive summary. Retrieved from http://www.surgeongeneral.gov/library/reports/50-years-of-progress/

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      S01.15 - Integration of Smoking Cessation into Lung Cancer Screening (Now Available) (ID 11896)

      10:05 - 10:20  |  Presenting Author(s): Kate Brain

      • Abstract
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      • Slides

      Abstract

      Cigarette smoking is the largest preventable risk factor for lung cancer, disproportionately affecting people from socioeconomically disadvantaged communities. Low dose computed tomography (CT) screening for high risk smokers is now the standard of care in the United States, with implementation pending in Europe. The potential health gains from combined CT lung screening and smoking cessation are considerable. Recent evidence disputes the notion that CT screening offers a “license to smoke” and reveals that engaging with lung screening can give smokers an opportunity to access smoking cessation support at a time when they are likely to be receptive to offers of help. However, considerable challenges remain in identifying methods of engaging high risk smokers in lung screening, and little evidence exists on the optimal design and delivery of effective smoking cessation interventions in this setting. Findings from studies including the United Kingdom Lung Screening trial (UKLS1) will be presented to highlight patient barriers and facilitators to successful integration of smoking cessation within the lung screening pathway, including beliefs and attitudes towards lung screening among high risk smokers, and the impact of abnormal lung scan results. Using the UK-wide Lung Symptom Awareness and Health (LUSH) study example, reflections will also be made on contextual barriers to engaging smokers with comorbid lung conditions living in areas of socioeconomic deprivation. Emerging issues and trends will be presented in methods of recruiting high risk smokers using community-based strategies, and developing personalised materials to support smoking cessation. Novel methods of designing, delivering and testing smoking cessation interventions embedded in the lung screening context will be considered. This presentation will be relevant to clinicians and scientists who are interested in the contribution of behavioural science to optimising lung cancer screening protocols as a teachable moment for smoking cessation, designing evidence-based clinical services to deliver the maximum health benefits for current and future generations.

      1 Brain K, Carter B, Lifford KJ, Burkes O, Devaraj A, Baldwin D, Duffy S, Field JK. Impact of low-dose CT screening on smoking cessation among high-risk participants in the UK Lung Cancer Screening trial. Thorax 2017 72:912–918. http://dx.doi.org/10.1136/thoraxjnl-2016-209690.

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      S01.17 - Session V: Panel Discussion: Next Steps for Lung Screening? (Now Available) (ID 11898)

      10:30 - 11:30  |  Presenting Author(s): Claudia I Henschke, Kwun M Fong, Motoyasu Sagawa, Matthew Eric Callister, Nasser Altorki, Bruce Pyenson, Andrea Katalin Borondy Kitts

      • Abstract
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      Abstract not provided

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      S01.18 - IASLC Leads the International Collaboration on Data Sharing (IASLC- ELIC-CCTRR) (Now Available) (ID 11899)

      11:30 - 11:50  |  Presenting Author(s): John Kirkpatrick Field, James L Mulshine

      • Abstract
      • Presentation
      • Slides

      Abstract

      The IASLC ELIC-CCTR vision is to create a globally-accessible, privacy-secured environment to enable the analysis and study of extremely large collections of quality-controlled internationally assembled CT lung cancer images and associated biomedical data for research and healthcare delivery. This initiative will rapidly accelerate improvements to the multi-disciplinary management of early curable, lung cancer and other major thoracic diseases. This new research environment will be deployed and used to conduct global studies within the first two years of this project and is designed to one day scale to enabling coherent analysis across millions of cases.

      The current problem is that the implementation and advancement of lung cancer low dose CT screening (LDCT) screening requires large and high-quality collections of data obtained from global populations with currently deployed scanning equipment 1-5. Furthermore, there are new opportunities to develop deep learning methods for lung cancer imaging, which requires large quality-controlled datasets. As a community we have to very aware of the privacy challenges around data sharing. Lack of high quality data has been a barrier to LDCT screening progress.

      The way forward has been developed at the recent IASLC Confederation of CT Screened Patients Registry & Resource (CCTRR) Roundtable Workshop, as outlined in figure 1.

      figure 1.jpg

      IASLC will develop and run a new international collaborative (the ELIC framework) building on the processes established in the successful TNM Staging project. An internationally-federated Hub and Spoke system will be deployed to permit analysis of CT images and associated data in a secure environment, without any requirement to reveal data itself (i.e. privacy-protecting). No identifiable data ever leaves sources under local governance (PI) control. Existing imaging collections remain in the geographic regions where they were collected, so the resulting environment remains consistent with local regulations without privacy or data disclosure risk. In addition to connecting the world’s largest lung cancer screening registries, which is necessary for exploiting advanced computing capabilities with trustworthy security, enabling the rapid ramp up and participation of new global screening groups.

      The structure will provide the ability to interrogate large, high-quality, and internationally sourced image data sets will allow the lung cancer screening community to identify key insights, publish studies, and make lung cancer recommendations based on potentially millions of screening participants. By validating and distributing common data standards for CT imaging as well as for additional clinical follow-up information, the framework can be applied to the collaborative study of related intrathoracic disease processes.

      1. Henschke CI, McCauley DI, Yankelevitz DF, et al. Early Lung Cancer Action Project: overall design and findings from baseline screening. Lancet 1999; 354(9173): 99-105.

      2. National Lung Screening Trial Research T, Aberle DR, Adams AM, et al. Reduced lung-cancer mortality with low-dose computed tomographic screening. N Engl J Med 2011; 365(5): 395-409.

      3. van Klaveren RJ, Oudkerk M, Prokop M, et al. Management of lung nodules detected by volume CT scanning. N Engl J Med 2009; 361(23): 2221-9.

      4. Tammemagi MC, Schmidt H, Martel S, et al. Participant selection for lung cancer screening by risk modelling (the Pan-Canadian Early Detection of Lung Cancer [PanCan] study): a single-arm, prospective study. Lancet Oncol 2017; 18(11): 1523-31.

      5. Field JK, Duffy SW, Baldwin DR, et al. The UK Lung Cancer Screening Trial: a pilot randomised controlled trial of low-dose computed tomography screening for the early detection of lung cancer. Health Technol Assess 2016; 20(40): 1-146.

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    JCSE01 - Perspectives for Lung Cancer Early Detection (ID 779)

    • Type: Joint IASLC/CSCO/CAALC Session
    • Track: Screening and Early Detection
    • Presentations: 10
    • Now Available
    • Moderators:
    • Coordinates: 9/23/2018, 07:30 - 11:15, Room 202 BD
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      JCSE01.02 - Necessity for Early Detection in Lung Cancer and Initial Attempts for Early Detection (Now Available) (ID 11395)

      08:00 - 08:20  |  Presenting Author(s): Annette Maree McWilliams

      • Abstract
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      Abstract not provided

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      JCSE01.03 - CT Screening for Early Detection (NLST, UKLS, NELSON, ITALUNG, DANTE, Others) (Now Available) (ID 11396)

      08:20 - 08:40  |  Presenting Author(s): Matthijs Oudkerk

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      Abstract not provided

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      JCSE01.04 - Risk Modeling for the Early Detection of Tin Miner Lung Cancer in China (Now Available) (ID 11397)

      08:40 - 09:00  |  Presenting Author(s): You-lin 13910410711 Qiao

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      • Presentation
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      Abstract

      Result of National Lung Cancer Screening Program has demonstrated a 20% reduced lung cancer mortality with low-dose computed tomography among current or former smokers with a smoking history of 30 or more pack-years[1]. Selecting high risk population for LDCT screening is a key issue for lung cancer screening. Many studies have suggested that lung cancer risk model which incorporating these factors can be more accurate to identify high risk individuals suitable for LDCT screening than the NLST criteria[2]. Thus, more precise evaluation of association between these factors are warranted to developing lung cancer risk models.

      In this study, we developed and internal validated a lung cancer risk model with data of a occupational screening cohort in Yunnan, China with the aim to exploring potential improvement of yield of lung cancer screening with Chest X-ray and Sputum cytology due to the improved risk stratification. This study was a prospective occupational cohort study among tin miners from Yunnan Tin Corporation (YTC) initiated in 1992[3]. Participants were tin miners aged 40 or over and had at least 10 years of underground work or smelting history. Participants also had received annual lung screening from 1992 to 1999, and were annually followed up through December 31, 2001. Previous studies suggested that age, education level, smoking, occupational radon and arsenic exposure, prior chronic bronchitis were risk factors of lung cancer risk in this cohort[4-6]. During the study period, a total of 443 lung cancer deaths were confirmed among 9295 participants. To reduce the potential information bias, 69 lung cancer death with 1 year since enrollment were not included into the analysis.

      To stratified those with higher lung cancer risk, we increased the age criteria from 40 to 50 years old(model 0), then further developed three risk prediction models with multivariate logistic regression respectively, and the predicted probability of lung cancer death for each participants were also calculated based on logistic regression model respectively(table1). The goodness of fit, discrimination and calibration ability of the model performance were evaluated with -2log likelihood, area under the receiver operator characteristic curve (AUC) (C-index) and Hosmer-Lemeshow test. We found that the model incorporated age, gender, smoking, educational prior chronic bronchitis, occupational radon and arsenic had the best discrimination performance with area under ROC as of 0.821(95%CI:0.805-0.836) (figure1a). The calibration performance of this model was also good(Hosmer–Lemeshow type χ2=5.413,p=0.773)(figure1b). The areas under ROC curve of model 2 and model 3 were significantly better than those of model1 and model 0(all p<0.001), however, no difference was found between model 2 and model 3. Besides, Bootstrapping techniques were used for internal validation of the model 3 to Correct for this overfit or optimism, and discrimination C-statistic from C-statics was the same to the original data.

      We stratified the participants into 4 quintiles for the predicted risk of death from lung cancer. The cumulative lung cancer death rate from quintile 1 with lowest risk to quintile 4 having the highest risk increased from 11.51, 47.66, 625.41 to 1732.37 per 105 person-years, while only 2.5% of all lung cancer deaths were in quintile 1 and 2. Similarly, in 210 screen-detected lung cancer deaths, the proportion in quintile 1 and 2 was only 2.4%.

      In conclusion, we have developed and internal validated a lung cancer risk model based on personal and occupation covariates in this occupational population, and this model showed good accuracy for the identification of lung cancer and might assist in identifying individuals at high risk of developing lung cancer in lung cancer screening in this occupational cohort.

      [1] Aberle DR, Adams AM, Berg CD, et al. Reduced lung-cancer mortality with low-dose computed tomographic screening. N Engl J Med. 2011. 365(5): 395-409.

      [2] Tammemägi MC. Application of risk prediction models to lung cancer screening: a review. J Thorac Imaging. 2015. 30(2): 88-100.

      [3] Qiao YL, Taylor PR, Yao SX, et al. Risk factors and early detection of lung cancer in a cohort of Chinese tin miners. Ann Epidemiol. 1997. 7(8): 533-41.

      [4] Lubin JH, Qiao YL, Taylor PR, et al. Quantitative evaluation of the radon and lung cancer association in a case control study of Chinese tin miners. Cancer Res. 1990. 50(1): 174-80.

      [5] Fan YG, Jiang Y, Chang RS, et al. Prior lung disease and lung cancer risk in an occupational-based cohort in Yunnan, China. Lung Cancer. 2011. 72(2): 258-63.

      [6] Yao SX, Lubin JH, Qiao YL, et al. Exposure to radon progeny, tobacco use and lung cancer in a case-control study in southern China. Radiat Res. 1994. 138(3): 326-36.

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      JCSE01.05 - Biomarkers and Liquid Biopsy for Early Detection of Lung Cancer (Now Available) (ID 11398)

      09:00 - 09:20  |  Presenting Author(s): K.C. Allen Chan

      • Abstract
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      • Slides

      Abstract

      The analysis of circulating DNA released by tumor cells, frequently known as liquid biopsy, provides a convenient and noninvasive way for the assessment of cancers. The most common application of liquid biopsy is to guide the choice of treatment in lung cancers. The detection of EGFR mutations in the plasma of patients with advanced lung cancers is useful for predicting the response to EGFR TKI treatment. Because of its noninvasive nature and quick turn-around time, liquid biopsy has been proposed to be a first line investigation for the assessment of EGFR mutational status. Another potential application of liquid biopsy is for the screening of early cancers. However, there is a lack of information regarding the biological feasibility of this approach as it is unclear if a small tumor would release sufficiently large amount of DNA into the circulation to allow early detection of the cancer. In this regard, we used nasopharyngeal cancer (NPC) as a model to address this biological question. As NPC is closely related to Epstein-Barr virus infection, we developed plasma EBV DNA as a marker for NPC. From 2013 to 2016, we screened over 20,000 asymptomatic men for NPC using a sensitive plasma EBV DNA assay. Subjects with positive test results were further investigated with nasal endoscopy and MRI. Through this arrangement, we identified 34 cases of NPC and almost half of them had stage I disease. Compared with historical cohorts, patients identified by screening had much improved progression-free survivial with a hazard ratio of 0.1. This study clearly demonstrates that a small early cancer can release sufficiently large amount of DNA into the circulation to allow sensitive detection by liquid biopsy. To apply these results to non-viral-associated cancers, we developed a generic cancer test based on copy number aberrations and altered methylation in plasma DNA. This test successfully detect various types of cancers, including lung cancer.

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      JCSE01.06 - Incorporating Artificial Intelligence for Early Detection of Lung Cancer (Now Available) (ID 11399)

      09:20 - 09:40  |  Presenting Author(s): Jie Hu

      • Abstract
      • Presentation
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      Abstract not provided

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      JCSE01.09 - Cluster Trial: Ph2 Biomarker-Integrated Study of Single Agent Alpelisib, Capmatinib, Ceritinib and Binimetinib in advNSCLC (Now Available) (ID 11678)

      10:15 - 10:25  |  Presenting Author(s): Qing Zhou  |  Author(s): Yi-Long Wu, Xu-Chao Zhang, Hai-Yan Tu, Bin Gan, Bin-Chao Wang, Chong-Rui Xu, Hua-Jun Chen, Ming-ying Zheng, Zhen Wang, Xiao-Yan Bai, Yue-Li Sun, Andrea Myers, Xueting Lv, Yajnaseni Chakraborti, Sylvia Zhao, Jin -Ji Yang

      • Abstract
      • Presentation
      • Slides

      Background
      Several genetically altered signaling pathways have been profiled in NSCLC, enabling advanced management of NSCLC using targeted therapies. This study investigated the therapeutic spectrum of NSCLC with uncommon molecular alterations by allocating patients to treatment arms based on molecular aberrations; targeted therapies alpelisib (PI3Kαi), capmatinib (METi), ceritinib (ALKi), and binimetinib (MEKi) were evaluated.The study was based on the umbrella design. Key objectives: investigate feasibility of using one trial for different agents based on biomarker-integrated analysis, assess anti-tumor activity, characterize safety, tolerability and PK profiles of individual agents. Key eligibility criteria: age ≥18 years; ECOG PS ≤2; failed prior treatment/unsuitable for chemotherapy. Documentation of locally determined molecular alterations before treatment allocation was required (alpelisib, 350 mg QD: PIK3CA mutation/amplification; capmatinib, 400 mg BID (tablet): MET IHC overexpression/amplification; ceritinib, 750 mg QD: ALK or ROS1 rearrangement; binimetinib, 45 mg BID: KRAS, NRAS or BRAF mutation).Sixty-six patients with advNSCLC were enrolled (median age 58 years; 65.2% male: alpelisib, n=2; capmatinib, n=16; ceritinib, n=26; binimetinib, n=22). As of Feb 28, 2018, 10 patients in ceritinib and 2 in binimetinib arms were ongoing. Twenty-four patients had confirmed partial responses (36.4%): alpelisib, 0%; capmatinib, 18.8%; ceritinib, 73.1%; binimetinib, 9.1% (Figure). Longest mPFS (14.4 months) was in ceritinib arm. Among the most common treatment-related AEs: alpelisib: malaise, hyperglycemia, dysgeusia; capmatinib: nausea, anemia, peripheral edema, decreased appetite; ceritinib: diarrhea, vomiting, ALT/AST elevation; binimetinib: mouth ulceration, AST, blood CPK increased, rash. Most AEs were grade 1/2.

      abstract #1.jpg

      Objective responses/tumor shrinkage were observed in the study; highest ORR and mPFS were observed with ceritinib, although patient numbers differed between arms. All treatments were well tolerated; no new safety signals were observed. This study demonstrated the feasibility of an umbrella trial and importance of precision medicine in the management of advNSCLC with uncommon molecular alterations.

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      JCSE01.10 - A Ph3 Study of Niraparib as Maintenance Therapy in 1L Platinum Responsive Extensive Disease Small Cell Lung Cancer Patients (Now Available) (ID 11679)

      10:25 - 10:35  |  Presenting Author(s): Shun Lu  |  Author(s): Liyan Jiang, Xinghao Ai, Junling Li, Xiaorong Dong, Dan Zhang, Qi Liu

      • Abstract
      • Presentation
      • Slides

      Background
      Small cell lung cancer (SCLC) accounts for 15% of lung cancer, characterized by early dissemination and rapid development of chemo-resistant disease after platinum response (60-80%). Less than 2% of extensive disease SCLC (ED-SCLC) patients survive 5 years. The bi-allelic loss or inactivation of TP53 and RB1 is common in SCLC, the poly(ADP-ribose) polymerase-1 (PARP-1), a critical DNA damage repair enzyme, is highly expressed in SCLC, and SCLC is sensitive to platinum based chemotherapy, suggesting that the defect in DNA damage repair pathways plays an important role in SCLC. ZL2306/ Niraparib is a highly selective PARP-1/2 inhibitor which was exclusively licensed for development in China by Zai Laboratory from TESARO. In SCLC PDX model, niraparib demonstrated anti-tumor activities as monotherapy. In addition, niraparib demonstrated promising tumor growth inhibition in maintenance post platinum treatment in platinum sensitive SCLC PDX models. Clinically, in phase III NOVA study, niraparib demonstrated clear clinical benefit as maintenance treatment by significantly extending progression free survival in all platinum-sensitive recurrent ovarian cancer patients regardless gBRCA or HRD status which led to the approval by FDA and EMA in ovarian cancer. It is suggested that niraparib maintenance therapy could provide potential clinical benefit in platinum responsive SCLC. ZL-2306-005 is a randomized double-blind multi-center phase 3 study to evaluate the efficacy and safety of niraparib versus placebo as maintenance therapy in ED-SCLC patients who have had responses to platinum based chemotherapy.Approximately 590 Chinese patients with histologically or cytologically confirmed ED-SCLC who have achieved either complete response or partial response to their platinum based chemotherapy to their newly diagnosed disease will be randomized (2:1) to 2 groups, receiving either ZL-2306 or placebo in ZL-2306-005 study. Patients need to complete 4 cycles of etoposide + cisplatin/ carboplatin. All patients will be stratified by gender, LDH level and history of prophylactic cranial irradiation. ZL-2306 will be started with 300mg PO QD for patients with a baseline body weight ≥77 kg and a baseline platelet count ≥150,000/μL, or 200 mg PO QD for patients with a baseline body weight <77 kg or a baseline platelet count <150,000/μL based on RADAR analysis in NOVA study. Patients will remain on treatment until disease progression or intolerable toxicity. The co-primary endpoints are PFS assessed by independent central radiologic review and OS; the secondary endpoints are PFS assessed by investigator, CFI, QoL, safety and tolerability.

      Section not applicable

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      JCSE01.11 - Dynamic ctDNA Monitoring Revealed Novel Resistance Mechanisms and Response Predictors of Osimertinib Treatment in East Asian NSCLC Patients (Now Available) (ID 14716)

      10:35 - 10:45  |  Presenting Author(s): Jianhua Chang  |  Author(s): Zhihuang Hu, Dongmei Ji, Shannon Chuai, Weina Shen, Junning Cao, Jialei Wang, Xianghua Wu

      • Abstract
      • Presentation
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      Background

      Advanced NSCLC patients, harboring EGFR T790M, exhibit marked diversity in tumor behavior and response to AZD9291, yet a discriminable molecular profile remains elusive. In addition, although EGFRC797S was involved in 30% of AZD9291 resistance cases in Western patients, mechanisms for the rest patients remain unclear, especially for the East Asian population. We utilized circulating tumor DNA (ctDNA) profiling to conduct dynamic monitoring in patients undergoing AZD9291, thus characterizing mutational heterogeneity and genomic evolution.

      Longitudinal plasma samples were collected before, during and post of the AZD9291 treatment in Chinese NSCLC patients with acquired T790M mutation. A ctDNA panel, spanning 160KB of human genome, was used to perform capture-based targeted sequencing that comprises critical exons and introns of 168 genes. The EGFR mutation abundance and dynamic changes of allele fraction (AF) were analyzed with progression-free survival (PFS) after AZD9291 treatment.

      A total of 61 samples were collected longitudinally from 14 patients, of which 9 have experienced progressive disease (PD). Six patients exhibited a rebound of ctDNA prior to radiographic PD, suggesting the potential of ctDNA in early detection of PD. Several acquired mutations were detected with the AZD9291 resistance, including newly identified EGFR G796S, L792H/F/R/V, V802F, V843I mutations, expect for the previously reported RB1 and EGFR C797S, L718Q mutations. Patients with a higher ratio of T790M and EGFRactivating mutation at baseline had a significantly longer PFS (9.6m vs 4.5m, p=0.008). A lower ratio of EGFRactivating mutation AF compared to baseline at first follow-up was significantly correlated with a longer PFS (8.5m vs 5.0m, p=0.027). Furthermore, patients harboring other known driver mutations in addition to T790M at baseline had an inferior PFS (4.9m vs 7.8m, P=0.039).

      Several novel resistance mechanisms were identified by ctDNA monitoring in the East Asian patients treated with AZD9291. Relative AF of T790M, changes of AF after treatment and the presence of concurrent driver mutations at baseline could predict clinical benefit of AZD9291 treatment.

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      JCSE01.12 - Discussant Oral Abstracts (Now Available) (ID 11681)

      10:45 - 11:00  |  Presenting Author(s): Daniel S.W. Tan

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      Abstract not provided

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      JCSE01.13 - Discussant Poster Abstracts (Now Available) (ID 11682)

      11:00 - 11:15  |  Presenting Author(s): Bob T. Li

      • Abstract
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      Abstract not provided

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      JCSE01.14 - Effects of Neoadjuvant Chemotherapy on the Expression of Programmed Death Ligand-1 and Tumor Infiltrating Lymphocytes in Lung Cancer Tissues (ID 14703)

      11:15 - 11:15  |  Presenting Author(s): Xu Wang  |  Author(s): Wenyu Sun, Kewei Ma

      • Abstract

      Background
      Immune checkpoints programmed death 1(PD1)and its ligand PD-L1,PD-L2 pathways can mediate negative synergistic stimulation signals.Immunotherapy combined with chemotherapy can increase the objective response rate of cancer patients,but the mechanism of combination therapy is not clear.This study aims to analyze the changes of PD-L1,PD-L2 in lung cancer tissues and the changes of TILs ( CD4+,CD8+,CD28+,and CD56+ lymphocytes ) surrounding the tumor before and after neoadjuvant chemotherapy(platinum-based),in order to provide a theoretical basis for relevant clinical studies.Tumor samples were obtained from 26 patients who confirmed primary lung cancer before and after NAC from 2009 to 2016 in the First Hospital of Jilin University. The expression of PD-L1, PD-L2 in lung cancer specimens were assessed by IHC. 5%,10%,20%,30%,50% expression thresholds were used to define PD-L1, PD-L2 positive status, respectively. Of 16 patients ( since the biopsy tissue specimens were limited, only 16 cases of biopsy and postoperative tissue specimens were collected), the expression of TILs around the tumor before and after NAC were assessed by IHC. We analyze the changes of PD-L1 and PD-L2 in lung cancer tissues before and after NAC, the correlation between the changes of PD-L1 in lung cancer tissues and tumor shrink rate, the interval from the end of NAC to operation, pathological type, gender and smoking status. Of 16 patients, the changes of TILs around the tumor before and after NAC were also evaluated. P<0.05 was considered statistically significant.

      1. When using 5%, 10%, and 20% as expression threshold to define PD-L1 positive status, PD-L1 was up-regulated after NAC (P=0.008,P=0.016,P=0.016). However, there were no obviously statistical significance about the expression of PD-L1 when using 30%, 50% expression threshold. The expression of PD-L2 were not show any statistical significance before and after NAC.

      2. Of 16 patients, the expression of CD4+, CD8+ and CD28+ lymphocytes increased after NAC (P=0.014,P=0.038,P=0.021), whereas the change of CD56+ lymphocytes was not statistical significant.

      3. There were no significant difference between the changes of PD-L1 and tumor shrink rate, interval from the end of NAC to operation, pathological type, gender and smoking status .

      1. NAC up-regulates the expression of PD-L1 in lung cancer tissues when the expression thresholds are 5%, 10%, and 20%.

      2. NAC up-regulates the expression of CD4+, CD8+, and CD28+ lymphocytes.

      3. No correlation exists between the variation of PD-L1 and tumor shrink rate, interval from the end of NAC to operation, pathological type, gender and smoking status.

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      JCSE01.15 - Molecular Characteristics of ALK Primary Point Mutations Non-Small-Cell Lung Cancer in Chinese Patients (ID 14704)

      11:15 - 11:15  |  Presenting Author(s): Chunwei Xu  |  Author(s): Jinhuo Lai, Wenxian Wang, Quxia Zhang, Wu Zhuang, Yunjian Huang, Youcai Zhu, Yanping Chen, Gang Chen, Meiyu Fang, Tang Feng Lv, Yong Song

      • Abstract

      Background
      Anaplastic lymphoma kinase (ALK) gene rearrangements have been identified in lung cancer at 3-7% frequency, thus representing an important subset of genetic lesions that drive oncogenesis in this disease. While the genetic locus of ALK primary point mutations NSCLC patients is unclear. The aim of this study is to investigate mutations and prognosis of NSCLC harboring ALK primary point mutations.

      A total of 339 patients with non-small-cell lung cancer were recruited between July 2012 and December 2015. The status of ALK primary point mutation and other genes were detected by next generation sequencing.


      ALK gene primary point mutation rate was 8.55% (29/339) in non-small cell lung cancer, including V163L (3 patients), F921Gfs*16 (2 patients), K1416N (2 patients), A585T (2 patients), P1442Q (1 patient), A348T (1 patient), K1525E (1 patient), S737L (1 patient), P115L (1 patient), Q515E (1 patient), E314D (1 patient), R395H (1 patient), S1219F (1 patient), S341G (1 patient), P1543S (1 patient), G129V (1 patient), Q167H (1 patient), L550F (1 patient), T1012M (1 patient), D302Y (1 patient), H755Q (1 patient), H331Q (1 patient), G1474E (1 patient) and E119D (1 patient), and median overall survival (OS) for these patients was 20.0 months. Among them, 27 patients with co-occurring mutations had a median OS of 20.0 months, and median OS of the 2 patients without complex mutations was 8.5 months. Statistically significant difference was found between the two groups (P=0.02). Briefly, patients with (n=8) or without (n=21) co-occurring EGFR mutations had a median OS of 24.0 months and 20.0 months respectively (P=0.73); patients with (n=21) or without (n=8) co-occurring TP53 mutations had a median OS of 20.0 months and 17.0 months respectively (P=0.83).

      EGFR and TP53 gene accompanied may have less correlation with ALK primary point mutation in NSCLC patients. Results of ongoing studies will provide a platform for further research to offer individualized therapy with the purpose of improving outcomes.

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      JCSE01.16 - Positive Correlation Between Whole Genomic Copy Number Variant Scoring and the Grading System in Lung Non-Mucinous Invasive Adenocarcinoma  (ID 14705)

      11:15 - 11:15  |  Presenting Author(s): Zheng Wang  |  Author(s): Shenglei Li, Lin Zhang, Lei He, Di Cui, Chenglong Liu, Yuyan Gong, Bi Liu, Xiaoyu Li, Wang Wu, David Cram, Dongge Liu

      • Abstract

      Background
      Grading systems of Lung adenocarcinoma have been proposed by Sica and Kadota in stage I tumors,but the predominant architectural subtypes grading system is applicable for resection samples mostly. The correlation between the histological subtypes and grading with whole genomic copy number variation(WGCNV) is unknown, and was investigated in lung non-mucinous invasive adenocarcinoma (LNMIA) at this study.The predominant histological subtype from 58 resection specimens of LNMIA and 20 para-cancerous lung tissues were collected by laser microdissection from HE staining FrameSlides PEN-Membrane slides.7 of 58 specimens,two predominant subtypes in one cancerous nodule were collected simultaneously. Whole genome amplification followed by high-throughput sequencing was used to deteted WGCNV with the para-cancerous lung tissues as normal reference set and WGCNV was scored by a particular formula.
      abstract #1.jpgabstract #2.jpg

      The letters above the figure show the results of Chi-squared test, and same letters mean no significant difference.

      WGCNV median scores of 5 histological subtypes of LNMIA with three tiered architectural grades are shown in Table1. The WGCNV scores have a positive correlation with either histological subtypes and architectural grading system (Figure1 A and B). The differences of WGCNV scores are detected betweem two predominant subtypes in one cancerous nodule.

      GWCNV scores display a positive correlation with three tiered architectural grading system and may has a potential value to predict prognosis in LNMIA.

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      JCSE01.17 - Weekly Nab-Paclitaxel Plus Carboplatin as Neoadjuvant Therapy for IIIA-N2 Lung Squamous Cell Carcinoma: A Prospective Phase II Study (ID 14706)

      11:15 - 11:15  |  Presenting Author(s): Changli Wang  |  Author(s): Yu Zhang, Jian Quan Zhu, Dongsheng Yue, Xiaoliang Zhao, qiang Zhang, Hui Chen

      • Abstract

      Background
      To evaluate the safety and antitumor activity of weekly nab-paclitaxel combined with carboplatin in patients with advanced stage IIIA-N2 NSCLC patients with squamous histologyFrom April 2015 to August 2017, 36 treatment-naive, pathologically diagnosed IIIA-N2 lung squamous cell carcinoma patients were enrolled and given two cycles of weekly nab-paclitaxel (100mg/m2, day1,8,15 of a 21-day cycle) plus Carboplatin (AUC = 5 at day 1, q3w) as neoadjuvant therapy. Then resectability was assessed and surgery was performed for resectable lesions. Post-operative adjuvant chemotherapy regimens is the combination of Nab-paclitaxel (100mg/m2, qw x 6) and carboplatin (AUC 5, Q3W x 2) for patients with PD, adjuvant chemotherapy regimen will be changed. The primary objective is the safety and efficacy, and the secondary objectives are quality of life and the role of prognostic biomarker SPARC.

      Of 36 patients, 3 stopped treatment due to patient decision. 33 were finally evaluated and 1 is still on treatment. Significant tumor volume shrinkage was seen in some patients after the neoadjuvant therapy. 66.7% patients achieved partial response (PR), 21.2% patients achieved stable disease (SD). Disease control (PR +SD) rate was 87.9%. Finally, 23 patients underwent surgical resection, the respectability rate was 69.7%. 12.1% occurred disease progress and failed to achieve resection, including 3 with local progress and 1 with pulmonary metastatic nodule; Among 22 PR pts, 4 failed to achieve resection, in which 1 was due to heart function, the other 3 due to personal unwillingness. 2 of 7 with stable disease failed to achieve resection; the pathological improvement in T stage and N stage before and after treatment was 81.8% (18/22) and 50% (11/22) respectively. The major adverse event was neutropenia (grade I and II) and no serious AE was found.

      Nab-paclitaxel in combination with Carboplatin showed promising ORR rate and resection rate in of IIIA-N2 lung squamous cell carcinoma. The regimen could be a new chemo option as the neoadjuvant treatment. PFS and OS data will be reported after follow up completing.

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      JCSE01.18 - A Multicenter Survey of One Year Survival Among Chinese Patients with Advanced Nonsquamous Non-Small Cell Lung Cancer (CTONG1506) (ID 14707)

      11:15 - 11:15  |  Presenting Author(s): Qing Zhou  |  Author(s): Ping Yu, Yong Song, Xin Zhang, Gongyan Chen, Yi Ping Zhang, Jianhua Chen, Zhuang Yu, Yi Hu, Xia Song, Diansheng Zhong, Guosheng Feng, Lulu Yang, Lujing Zhan, Luan Di Yao, Yun Chen, Yue Gao, Yi-Long Wu

      • Abstract

      Background
      Previous results of CTONG1506 study showed that gene aberration test rate was increasing in Chinese NSCLC patients and first-line treatment was standardized accordingly. This survey further described one year survival of patients with different gene aberration status and under different first-line treatments.

      CTONG1506 was a two-year series cross-sectional study. Patients with advanced nonsquamous NSCLC who were admitted from August 2015 to March 2016 and who received first-line anti-cancer treatment at one of 12 tertiary hospitals across China were included. Data extracted from medical charts were entered into medical record abstraction forms, which were collated for analysis. Survival information was collected one year after patients were admitted to hospital. One year survival rate and its 95% confidence interval were analysed by Kaplan-Meier method.

      A total of 707 patients were analysed, with mean age of 57 years and 56.7% were male. Among the 487 patients who had survival data, 192 were EGFR- mutation positive (86 mutated in exon 19 [one year survival rate 0.90, 95% CI: 0.81-0.94] and 88 mutated in exon 21 [one year survival rate 0.84, 95% CI: 0.75-0.90]), 27 patients were ALK positive and 164 patients were EGFR and ALK wild type. Most EGFRmutation positive patients (128/192) received tyrosine kinase inhibitors (TKIs) as first-line treatment and most EGFR wild type patients (155/175) received first-line chemotherapy (Chemo). Pemetrexed was the most common non-platinum chemotherapy-backbone agent (120/155) in platinum doublet regimens. One year survival rates are shown in the table.

      abstract 12337 ctogn1506 one-year survival.png

      This national-wide real world study of tertiary hospitals in China revealed that a majority of (>75%) advanced nonsquamous NSCLC patients survived more than one year and was comparable to well-controlled clinical trial results, indicating survival benefits by gene aberration status guided standard of care. This result may be further validated by our on-going two-year survey.

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      JCSE01.19 - ALTER-0303 Study: Tumor Mutation Index (TMI) For Clinical Response to Anlotinib in Advanced NSCLC Patients at 3rd Line (ID 14708)

      11:15 - 11:15  |  Presenting Author(s): Baohui Han  |  Author(s): Jun Lu, Wei Zhang, Bo Yan, Lele Zhang, Jie Qian, Bo Zhang, Shuyuan Wang

      • Abstract

      Background

      Anlotinib is an effective multi-targeted receptor tyrosin kinase inhibitor (TKI) for refractory advanced Non-Small Cell Lung Cancer (NSCLC) therapy at 3rd line. ALTER-0303 clinical trial has been revealed that Anlotinib significantly prolongs progression free survival (PFS; Anlotinib: 5.37 months vs Placebo: 1.40 months) and overall survival (OS; Anlotinib: 9.63 months vs Placebo: 6.30 months) with the objective response rate (ORR) of 9.18% and the disease control rate (DCR) of 80.95%. Here, we sought to understand the gene mutation determinants for clinical response to Anlotinib via next generation sequencing (NGS) upon cell-free DNA (cfDNA) and circulating tumor DNA (ctDNA) at baseline.

      Totally 437 advanced NSCLC patients enrolled in ALTER-0303 study, and 294 patients received Anlotinib therapy. Of the 294 patients, 80 patients were analyzed in the present study. Capture-based targeted ultradeep sequencing was performed to obtain germline and somatic mutations in cfDNA and ctDNA. Response analyses upon discovery cohort (n = 62) and validation cohort (n = 80) were performed by use of germline and somatic (G+S) mutation burden, somatic mutation burden, nonsynonymous mutation burden, and unfavorable mutation score (UMS), respectively. Based on the above independent biomarkers and their subtype factors, tumor mutation index (TMI) was developed, and then used for response analysis.

      Our data indicated that the patients harbouring less mutations are better response to Anlotinib therapy (G+S muatation burden, cutoff = 4000, Median PFS: 210 days vs 127 days, p = 0.0056; somatic mutation burden, cutoff = 800, Median PFS: 210 days vs 130 days; p = 0.0052; nonsynonymous mutation burden, cutoff = 50, Median PFS: 209 days vs 130 days; p = 0.0155; UMS, cutoff = 1, Median PFS: 210 days vs 131 days; p = 0.0016). TMI is an effective biomarker for Anlotinib responsive stratification (Median PFS: 210 days vs 126 days; p= 0.0008; AUC = 0.76, 95% CI: 0.62 to 0.89) upon discovery cohort and validation cohort (Median PFS: 210 days vs 127 days; p = 0.0006). Lastly, integrative analysis of TMI and IDH1 mutation suggested a more promising result for Anlotinib responsive stratification upon validation cohort (Median PFS: 244 days vs 87 days; p < 0.0001; AUC = 0.90, 95% CI: 0.82 to 0.97).This study provide a biomarker of TMI to stratify Anlotinib underlying responders, that may improve clinical outcome for Anlotinib therapy on refractory advanced NSCLC patients at 3rd line. Clinical trial information: NCT02388919.

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      JCSE01.20 - Outcome in Small Cell Lung Cancer Patients with Cerebral Recurrence After Prior Prophylactic Cranial Irradiation  (ID 14710)

      11:15 - 11:15  |  Presenting Author(s): Lei Zhao  |  Author(s): Jindong Guo, Xuwei Cai, Xiaolong Fu

      • Abstract

      Background
      Prophylactic cranial irradiation (PCI) is a standard therapy for both limited small cell lung cancer (SCLC) and extensive SCLC patients with good responses to first-line treatment. The aim of this study was to examine outcomes in SCLC patients in a single institution who underwent cerebral recurrence after prior PCI.

      We retrospectively examined the medical records of 219 consecutive SCLC patients who had initially received PCI(25 Gray in 10 fractions) between June 2007 to June 2017. Data were analyzed with regard to age, sex, smoking status, treatment, disease stage, data of PCI, time to cerebral recurrence, site of cerebral recurrence, re-irradiation after cerebral recurrence and time to death. Survival was estimated by the Kaplan-Meier method. Multivariate analyses were performed by the log-rank and Cox’s proportional hazard model test.

      Of the 219 patients undergoing PCI, 180(82.2%) were LD-SCLC and 39(17.8%) were ED-SCLC. The median age was 59 years and the median follow-up time was 23.7 months. The median overall survival (OS) of all patients from the time of diagnosis was 39.0 months (95%CI, 29.6–48.4), in LD-SCLC it was 47.0 months (95%CI, 35.4–58.6), and in ED-SCLC it was 19.0 months (95%CI, 17.0–21.0). The difference was statistically significant with P=0.000.

      Forty-six patients (21.0%) were diagnosed with cerebral recurrence. 30(65.2%) of these presented with oligometastatic disease and 16(34.8%) had non-oligometastatic disease. Cox multivariate analysis identified disease stage (P=0.043) was the only significantly favorable prognostic factor for cerebral recurrence. The median survival time from PCI was 21.0 months (95%CI, 12.5–29.5), in oligmetastatic disease it was 35.0 months (95%CI, 19.0–51.0), and in non-oligometastatic disease it was 16.0 months (95%CI, 12.1–19.9). The difference was statistically significant with P=0.007. Meanwhile, the median time from PCI to cerebral recurrence was 11.0 months (95%CI, 9.5–12.5), in oligmetastatic disease it was 11.0 months (95%CI, 6.7–15.3), and in non-oligometastatic disease it was 10.0 months (95%CI, 8.4–11.6). There was no statistical significance between the two.

      Among forty-six patients with cerebral recurrence, 34 patients underwent re-irradiation using either Re-WBRT (11patients, 23.9%) or SRS /SRT (23patients, 50.0%), another 12 patients (26.1%) did not accept radiotherapy to brain. The median survival time from cerebral recurrence was 10 months (95%CI, 4.1-16.0) for re-irradiation and 4 months (95%CI, 2.3-5.8) for no radiotherapy group, respectively. The difference was statistically significant with P=0.000.

      PCI remains standard therapy for SCLC patients with good responses to first-line treatment. Cerebral recurrence is inevitable, however, cerebral re-irradiation after recurrence is proven to be beneficial for survival.


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      JCSE01.21 - Different Responses to Osimertinib in Primary and Acquired EGFR T790M-Mutant NSCLC Patients (ID 14711)

      11:15 - 11:15  |  Presenting Author(s): Shuyuan Wang  |  Author(s): Bo Zhang, Baohui Han

      • Abstract

      Background
      Primary EGFR T790M could be occasionally identified by routine molecular testing in tyrosine kinase inhibitor TKI-naive non-small cell lung cancer (NSCLC) patients. This study was aimed to compare clinical characteristics of primary and acquired T790M mutations and their responses to Osimertinib in NSCLC patients.
      We collected clinical characteristics of patients diagnosed with epidermal growth factor receptor (EGFR) mutation from 2012 to 2017 in Shanghai Chest Hospital. For patients with primary and acquired T790M mutations, the responses to Osimertinib were analyzed.Primary T790M was identified in 1.03% (61/5900) of TKI-naive patients. Acquired T790M was detected in 45.50% (96/211) of TKI-treated patients. T790M always coexisted with sensitizing EGFR mutations. Primary T790M was always coexisted with 21L858R (45/61) whereas acquired T790M was coexisted with 19del (61/96). Among them, 18 patients with primary T790M mutation acquired Osimertinib and 75 patients with acquired T790M mutation received Osimertinib. The median progression-free survival (mPFS) of Osimertinib in primary T790M group was greatly longer than that in acquired T790M group (18.0 months:95% CI:15.0-21.0 VS 10.0months:95% CI:8.3-11.7, P=0.016). The DCR of both groups were 89.3% and 100%. In primary T790M group, the mPFS of concomitant occurrence of 20 T790M and 21 L858R or 19del were 15.7m and 24.0 m, respectively. In acquired T790M group, the mPFS of concomitant occurrence of 20 T790M and 21 L858R or 19del were 11.0m and 10.0m, respectively.

      Primary and acquired T790M-mutation patients showed different molecular characteristics. Both of them may respond to Osimertinib. However, primary T790M patients showed greater survival benefits from Osimertinib than acquired T790M patients.

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      JCSE01.22 - Differential Molecular Mechanisms Associated with Dramatic and Gradual Progression in NSCLC Patients with Intrathoracic Dissemination (ID 14713)

      11:15 - 11:15  |  Presenting Author(s): Ying Chen  |  Author(s): Bao Hua, Wei Li, Chao Zhang, Wen-Fang Tang, Ao Wang, Xue Wu, Jing-Hua Chen, Jian Su, Yang W. Shao, Yi-Long Wu, Wen-Zhao Zhong

      • Abstract

      Background
      Lung cancer is a highly heterogeneous disease with diverse clinical outcomes. The pleural cavity is a frequent metastasis site of proximal lung cancer. Better understanding of its underlining molecular mechanisms associated with dramatic and gradual progression of pleural metastasis in patients with non-small cell lung cancer (NSCLC) is essential for prognosis, intervention and new therapy development.We performed whole-exome sequencing (WES) of matched primary lung adenocarcinoma and pleural metastatic tumors from 26 lung cancer patients with dramatic progression (DP, n=13) or gradual progression (GP, n=13). Somatic alterations at both genome-wide level and gene level were detected. Kaplan-Meier survival analysis and multivariate Cox regression models were applied to analyze the association between different somatic alterations and clinical parameters.We first analyzed the differences in somatic alterations between AP and RP group in the primary tumors, and identified higher somatic copy number alteration (SCNA) level in DP group compared to GP group, which is significantly (p=0.016) associated with poorer progression-free survival (PFS). More specifically, patients with chromosome 18q loss in the primary tumor showed a trend (p=0.107) towards poorer PFS. PTEN (p=0.002) and GNAS (p=0.002) mutations are enriched in the primary tumors of DP group, and are associated with poorer PFS. Furthermore, pleural metastatic tumors harbor a relatively higher level of mutation burden (p=0.105) and significantly increased SCNA (p=0.035) compared to the primary tumors.NSCLC patients in the attenuated progression group have more stable genomes. High level of genomic instability, GNAS and PTENmutations, as well as chromosome 18q loss are associated with rapid progression.

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      JCSE01.22a - Tislelizumab Combined With Chemotherapy as First-Line Treatment in Chinese Patients With Advanced Lung Cancer (ID 14702)

      11:15 - 11:15  |  Presenting Author(s): Jie Wang  |  Author(s): Jun Zhao, Zhijie Wang, Zhiyong Ma, Jiuwei Cui, Yongqian Shu, Zhe Liu, Ying Cheng, Shiang Jiin Leaw, Jian Li, Fan Xia

      • Abstract

      Background
      Immune checkpoint inhibitors have shown efficacy in patients with NSCLC as monotherapy and in combination with chemotherapy. Tislelizumab is a humanized IgG4 monoclonal antibody to PD‑1 specifically engineered to minimize FcϒR binding on macrophages, possibly minimizing negative interactions with other immune cells. In a phase 1 study, tislelizumab was generally well tolerated and showed antitumor activity; 200mg IV Q3W was established as the recommended dose.

      This multi-arm phase 2 study, consisting of safety run-in and dose-extension phases, assessed tislelizumab in combination with platinum-based chemotherapy (by tumor histology) as a potential first-line treatment for Chinese patients with lung cancer. All patients received tislelizumab at 200mg Q3W in combination with 4–6 cycles of platinum-doublet until disease progression. Nonsquamous (nsq) NSCLC patients received pemetrexed + platinum Q3W for 4 cycles followed by pemetrexed maintenance, while squamous (sq) NSCLC patients received paclitaxel + platinum (A) or gemcitabine + platinum (B) Q3W, and small-cell lung cancer (SCLC) patients received etoposide + platinum Q3W. Tumor response (RECIST v1.1) and safety/tolerability were evaluated.

      As of 21 Feb 2018, 48 patients (median age, 62 years [range: 36–75], 71% male, 71% current/former smokers) received tislelizumab treatment (median, 3 cycles [range: 1–7]); 44 patients remain on the study. Across the four cohorts, confirmed and unconfirmed partial responses were observed in 13 and 9 patients, respectively (Table). The most frequent AEs were chemotherapy-related hematologic toxicities. The most commonly reported grade ≥3 treatment-related AEs were neutropenia (20.8%) and anemia (12.5%); the most common grade 3 immune-related AEs were pyrexia (6.3%) and rash (6.3%). One sq‑NSCLC patient experienced a fatal myocarditis/myositis following one cycle of paclitaxel/cisplatin; all other treatment-related AEs were managed/resolved by study-drug interruption (n=15) or discontinuation (n=4) and appropriate treatment.

      Best Overall Response (Patients With ≥1 Post-Baseline Tumor Assessment)

      nsq-NSCLC (n=9)

      sq-NSCLC [A] (n=12 )

      sq-NSCLC [B] (n=5 )

      SCLC (n=8)

      Total

      (N=34)

      PR

      4 (44.4)

      9 (75)

      4 (80)

      5 (62.5)

      22 (64.7)

      Confirmed PR

      1 (11.1)

      4 (33.3)

      4 (80)

      4 (50)

      13 (38.2)

      Unconfirmed PR

      3 (33.3)

      5 (41.7)

      0 (0)

      1 (12.5)

      9 (26.5)

      SD

      3 (33.3)

      2 (16.7)

      1 (20)

      2 (25)

      8 (23.5)

      PD

      1 (11.1)

      0 (0)

      0 (0)

      1 (12.5)

      2 (5.9)

      NE

      1 (11.1)

      1 (8.3)

      0 (0)

      0 (0)

      2 (5.9)

      Data presented as n (%).

      Abbreviations: nsq-NSCLC, non-squamous non-small cell lung cancer; NE, not evaluable; PD, progressive disease; PR, partial response; SCLC, small cell lung cancer; SD, stable disease; sq-NSCLC, squamous non-small cell lung cancer.

      Tislelizumab, in combination with platinum doublets, demonstrated preliminary antitumor activity and was generally well tolerated in patients with advanced lung cancer.

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    WS02 - Mesothelioma Workshop (ID 996)

    • Type: Workshop
    • Track: Mesothelioma
    • Presentations: 15
    • Now Available
    • Moderators:
    • Coordinates: 9/23/2018, 08:00 - 11:15, Room 205 AC
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      WS02.01 - Session 1: Surgery for Mesothelioma (Now Available) (ID 14745)

      08:00 - 08:00  |  Presenting Author(s): Harvey Pass

      • Abstract
      • Presentation

      Abstract not provided

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      WS02.02 - What Are the Most Important Unmet Needs in the Surgical Management of Mesothelioma? (Now Available) (ID 14746)

      08:00 - 08:15  |  Presenting Author(s): Valerie W Rusch

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      WS02.03 - Who Are the High Risk Patients for Surgical Failure in Mesothelioma? (Now Available) (ID 14747)

      08:15 - 08:30  |  Presenting Author(s): Harvey Pass

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      WS02.04 - SMART, Where It Is Going (Now Available) (ID 14748)

      08:30 - 08:45  |  Presenting Author(s): Marc De Perrot

      • Abstract
      • Presentation
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      Abstract not provided

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      WS02.05 - Reliability of MM Diagnosis and Role of BAP1 Staining (Now Available) (ID 14749)

      08:45 - 09:00  |  Presenting Author(s): Francoise Galateau-Salle

      • Abstract
      • Presentation
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      Abstract not provided

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      WS02.07 - Session 2: Immunotherapy in Mesothelioma (Now Available) (ID 14750)

      09:05 - 09:05  |  Presenting Author(s): Paul Baas

      • Abstract
      • Presentation

      Abstract not provided

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      WS02.08 - The Microenvironment and Mesothelioma (Now Available) (ID 14751)

      09:05 - 09:20  |  Presenting Author(s): Prasad S. Adusumilli

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      WS02.09 - PDL-1 and Mesothelioma (Now Available) (ID 14752)

      09:20 - 09:35  |  Presenting Author(s): Raphael Bueno

      • Abstract
      • Presentation
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      Abstract not provided

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      WS02.10 - An Overview of Present and Future Immunotherapy Trials in Mesothelioma: Progress and Problems (Now Available) (ID 14753)

      09:35 - 09:50  |  Presenting Author(s): Aaron S. Mansfield

      • Abstract
      • Presentation
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      Abstract not provided

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      WS02.11 - Window of Opportunity Immunotherapy Trials in Mesothelioma: Design and Translation (Now Available) (ID 14754)

      09:50 - 10:05  |  Presenting Author(s): Anne S. Tsao

      • Abstract
      • Presentation
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      Abstract not provided

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      WS02.13 - Session 3: Transcriptome Changes and Mutations in Mesothelioma - Somatic, Germline, BAP1 and more (Now Available) (ID 14757)

      10:10 - 10:10  |  Presenting Author(s): David Mark Jablons

      • Abstract
      • Presentation
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      Abstract not provided

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      WS02.14 - BAP1 Mutations: Mechanisms and Significance (Now Available) (ID 14758)

      10:10 - 10:25  |  Presenting Author(s): Michele Carbone

      • Abstract
      • Presentation
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      Abstract not provided

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      WS02.15 - Novel Approaches for Targeting BAP1 (Now Available) (ID 14759)

      10:25 - 10:40  |  Presenting Author(s): Marjorie G. Zauderer

      • Abstract
      • Presentation
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      Abstract not provided

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      WS02.16 - Genome-wide Silencing Screen in Mesothelioma Cells Reveals that Loss of Function of BAP1 Induces Chemoresistance to Ribonucleotide Reductase Inhibition: Implication for Therapy (Now Available) (ID 14760)

      10:40 - 10:55  |  Presenting Author(s): Emanuela Felley-Bosco

      • Abstract
      • Presentation
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      Abstract not provided

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      WS02.17 - A Subset of Mesotheliomas with Improved Survival Occurring in Carriers of BAP1 and of other Germline Mutations (Now Available) (ID 14761)

      10:55 - 11:10  |  Presenting Author(s): Haining Yang

      • Abstract
      • Presentation
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      Abstract not provided

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    WS03 - Endoscopic Diagnosis and Staging of Lung Cancer – Interventional Pulmonology Hands-On Workshop (Ticketed Session) (ID 986)

    • Type: Workshop
    • Track: Interventional Diagnostics/Pulmonology
    • Presentations: 4
    • Now Available
    • Moderators:
    • Coordinates: 9/23/2018, 08:00 - 11:30, Room 205 BD
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    YI01 - Young Investigators Session (ID 988)

    • Type: Young Investigator Session
    • Track:
    • Presentations: 14
    • Now Available
    • Moderators:
    • Coordinates: 9/23/2018, 08:00 - 11:30, Room 106
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    WS05 - ITONF Workshop: Excellence in Thoracic Oncology Care (ID 889)

    • Type: Workshop
    • Track: Nursing and Allied Professionals
    • Presentations: 9
    • Now Available
    • Moderators:
    • Coordinates: 9/23/2018, 12:00 - 18:00, Room 206 BD
  • +

    PR01 - Press Conference (ID 872)

    • Type: Press Conference
    • Track:
    • Presentations: 3
    • Now Available
    • Moderators:
    • Coordinates: 9/23/2018, 16:00 - 17:30, Room 202 BD
  • +

    OC01 - Opening Ceremony (ID 839)

    • Type: Opening Ceremony
    • Track:
    • Presentations: 1
    • Now Available
    • Moderators:
    • Coordinates: 9/23/2018, 19:00 - 20:30, Plenary Hall
    • +

      OC01.01 - Welcome Addresses (ID 14928)

      19:00 - 19:30  |  Presenting Author(s): General Presenter

      • Abstract

      Abstract not provided

    • +

      OC01.02 - Global Effects of Smoking, of Quitting, and of Taxing Tobacco on Lung Cancer and Other Diseases (Now Available) (ID 11596)

      19:30 - 19:45  |  Presenting Author(s): Prabhat Jha

      • Abstract
      • Presentation
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      Abstract not provided

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      OC01.03 - IASLC Distinguished Award Presentations (ID 14929)

      19:45 - 20:20  |  Presenting Author(s): General Presenter

      • Abstract

      Abstract not provided

    • +

      OC01.04 - WCLC 2018 – At a Glance (ID 14930)

      20:20 - 20:30  |  Presenting Author(s): General Presenter

      • Abstract

      Abstract not provided

  • +

    MTE01 - Preclinical Models of Lung Cancer (Ticketed Session) (ID 811)

    • Type: Meet the Expert Session
    • Track: Biology
    • Presentations: 2
    • Now Available
    • Moderators:
    • Coordinates: 9/24/2018, 07:00 - 08:00, Room 206 F
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      MTE01.01 - GEMM of Lung Cancer (Now Available) (ID 11546)

      07:00 - 07:30  |  Presenting Author(s): Sarah Ann Best

      • Abstract
      • Presentation
      • Slides

      Abstract

      The primary induction of lung cancer is difficult to study in humans because patients often present very late in the course of their disease. Genetically engineered mouse models (GEMMs) have therefore emerged as crucial bridging strategies between understanding pathogenic mechanisms and clinical translation. Importantly, they reveal insights on the events and processes underlying tumor initiation and progression, studies which are not possible when employing transplantation or chemically-induced model systems.

      The recent advent of next-generation sequencing technologies has provided us with an in-depth characterization of the cancer genome of lung adenocarcinoma (LUAD) (1), squamous cell carcinoma (LUSC) (2) and small cell lung cancer (SCLC) (3). While these studies have highlighted the genetic complexities of lung cancers, attention is now focused on elucidating “driver” mutations that confer a growth advantage, from “passenger” mutations that have little impact on malignant transformation. Investigating the loss or gain-of-function of individual genes, alone or in combination, can be directly addressed using GEMM systems.

      The “gold-standard” lung cancer models are based on Cre-LoxP recombination technology that enable the formation of autochthonous tumors from a limited number of somatic cells in a spatial and temporal fashion. Critically, tumors arise sporadically within the lung, in the setting of an intact immune microenvironment. GEMMs are designed to harbor genetic mutations frequently identified in human lung cancer. Cre-inducible alleles are engineered to disrupt tumor suppressor genes (LoxP sites flanking key exons (floxed), that are removed upon recombination) and/or activate oncogenes (LoxP-flanked stop codons (lox-stop-lox) that result in gene expression upon recombination). Cre-recombinase is delivered to the lung via inhalation or intra-tracheal injection of a recombinant adenovirus (Ad5) expressing Cre-recombinase under the control of a ubiquitous cytomegalovirus (CMV) promoter. Expression of Cre-recombinase directs the recombination of floxed alleles in a variety of epithelial cell types in the adult mouse lung (4,5). Utilizing this approach enabled investigators to interrogate the functional consequences of genetic alterations found in human lung cancer through the generation of models of LUAD, SCLC and more recently lung LUSC (6). Moreover, the recent advent of CRISPR-Cas9 gene-editing technology now enables us to interrogate the functional interaction between multiple genetic alterations in a high-throughput setting (7). Furthermore, the generation of cell type specific Ad5-Cre viruses, that restrict Cre expression, and thus recombination, to alveolar type II (ATII) (Ad5-SPC-Cre), club (Ad5-CC10-Cre), neuroendocrine (Ad5-CGRP-Cre) and basal (Ad5-K5-Cre, Ad5-K14-Cre) (8) cells, have provided insights into the cellular origins of different subtypes of lung cancer (9,10). Critically, unlike patient-derived xenograft (PDX) models, one additional advantage of GEMMs is the ability to interrogate the interplay between tumor cells and immune cells present in the tumor microenvironment. Such studies are crucial given the success of immune checkpoint inhibitors in lung cancer patients.

      This presentation will outline lung cancer GEMMs commonly used in the field and how these models can be utilized to identify cancer initiating cells, understand the molecular pathways underlying tumorigenesis, the immune microenvironment of lung cancer, and importantly to identify vulnerabilities that can be exploited for the design of improved treatment modalities for patients.

      References

      1. The Cancer Genome Atlas Research Network, Comprehensive molecular profiling of lung adenocarcinoma (2014) Nature, 511 (7511) 543-550.

      2. The Cancer Genome Atlas Research Network, Comprehensive genomic characterization of squamous cell lung cancers (2012) Nature, 489 (7417) 519-525.

      3. George et al., Comprehensive genomic profiles of small cell lung cancer (2015) Nature, 524 (7563) 47-53.

      4. Best et al., Combining cell type-restricted adenoviral targeting with immunostaining and flow cytometry to identify cells-of-origin of lung cancer (2018) Methods in Molecular Biology, 1725 15-29.

      5. DuPage et al., Conditional mouse lung cancer models using adenoviral or lentiviral delivery of Cre recombinase (2009) Nature Protocols, 4 (7) 1064-1072.

      6. Farago et al., SnapShot: Lung cancer models (2012) Cell, 149 (1) 246-246e1.

      7.Rogers et al., A quantitative and multiplexed approach to uncover the fitness landscape of tumor suppression in vivo (2017) Nature Methods, 14 (7) 737-742.

      8. Ferone et al., SOX2 is the determining oncogenic switch in promoting lung squamous cell carcinoma from different cells of origin (2016) Cancer Cell, 30 (4) 519-532.

      9. Sutherland et al., Cell of origin of small cell lung cancer: inactivation of Trp53 and Rb1 in distinct cell types of adult mouse lung (2011) Cancer Cell, 19 (6) 754-764.

      10. Sutherland et al., Multiple cells-of-origin of mutant K-Ras-induced mouse lung adenocarcinoma (2014) Proc. Natl. Acad. Sci. USA, 111 (13) 4952-2957.

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      • Abstract
      • Presentation
      • Slides

      Abstract

      Establishment of preclinical lung cancer models that closely match patient tumor biology is imperative for developing therapeutic strategies with the most translational relevance. Non small cell lung cancer (NSCLC) cell lines grown under 2D conditions or as cell line-derived xenografts (CDXs) are the most widely used models. They have been complemented with murine models engineered to develop lung cancer after introduction of specific genetic alterations (GEMMs). Lung cancer cell lines are readily amenable to mechanistic studies and economical high-throughput drug screening. However, for many NSCLC cell lines, the spectrum of mutations and copy number alterations have drifted considerably relative to patient tumors 1. This finding, in conjunction with long-term adaption to heterologous in vitro growth conditions, raise concerns about the extent to which cell line biology and potential drug responses may have deviated from clinical tumors. GEMMs are powerful tools for studying specific oncogenic mechanisms in isolation in vivo, but these models lack the intratumoral heterogeneity of patient tumors, which is thought to play a major role in the development of drug resistance. Furthermore, ideally, GEMMs should be constructed using the appropriate cell of origin context, which is challenging, as there are differences in the compositions of human and murine airways, and the cellular origins for most forms of lung cancer have not been established.

      NSCLC patient-derived xenografts (PDXs) overcome some of the limitations of these other models. They show much less genetic drift than cell lines, and their mRNA expression and the phospho-tyrosyl proteome more closely match patient tumors 1, 2. We have established a large collection of NSCLC PDXs from surgically resected tumors and endobronchial ultrasound-guided (EBUS) and CT-guided biopsies. Tumor specimens were initially implanted in the subcutaneous flanks of NSG mice (NOD SCID gamma, non-obese diabetic severe combined immunodeficiency, gamma). The PDX tumors have been viably cryopreserved and can be serially passaged in NOD SCID mice. Most of our collection comprises the major histologic subtypes of NSCLC [52 adenocarcinomas (LUAD) and 62 squamous cell carcinomas (LUSC)]. They, along with the primary patient tumors, are being molecularly profiled at multiple levels so that they can be optimally used for personalized medicine studies and novel integrated approaches to understand NSCLC pathogenesis, prognosis, and treatment. These levels include copy number variations, exome mutations, DNA methylation, mRNA and miRNA expression, and proteomics. In general, the PDX models recapitulate the mutation spectrum, copy number variations, and gene expression of matched patient histologies. They also recapitulate sensitivity and resistance to known targeted therapeutics (e.g. EGFR inhibitors), and thus, can be used to dissect mechanisms underlying differential drug responses. Such studies are ongoing, including investigation of potentially new biomarker-targeted therapeutic combinations. We have also found that not all patient tumor fragments engraft successfully, and that successful engraftment correlates with poor prognosis of the patient 3. We are using this relationship to discover a new molecular fingerprint to predict clinical outcome, as well as understand the bases that distinguish less and more aggressive tumor behavior.

      In parallel, we have developed methods to grow organoids from primary patient tumors and PDX models in 3D culture using Matrigel (PDO and XDO, respectively). For LUAD, both the PDO and XDO success rate of establishing bona fide organoid models is ~20%. Our stringent criteria include a minimum capacity of 10 passages and a split ratio of at least 1:3. LUSC has been more difficult to establish as organoid models, with a success rate of 17%, and only from PDXs, so far. Using these methods, we have established 4 models of each histology, which we have confirmed form tumors when transplanted into mice. Molecular profiling indicates that the organoids maintain the same mutation spectrum and copy number variations of their parental tumor tissue. These models offer distinct advantages over PDXs and cell lines. As compared to standard 2D cultures, they recapitulate the appropriate tissue histology, and thus, possibly clinically relevant growth control mechanisms, even while growing ex vivo. This notion is further supported by the ex vivo conditions supporting gene expression patterns, which allows the organoids to be segregated into their respective tumor histologies when using signatures derived from patient or PDX material. Given the low cost, rapid growth rates, and ease of in vitro manipulation, these models are ideally suited for rapid discovery and testing of new therapeutic strategies that can be matched to specific patient molecular profiles.

      In summary, generation of molecularly profiled PDX and organoid models offer great opportunity for translational and personalized medicine in NSCLC.

      1. Gao, H. et al. High-throughput screening using patient-derived tumor xenografts to predict clinical trial drug response. Nat. Med. 21, 1318-1325 (2015).

      2. Wang, D. et al. Molecular heterogeneity of non-small cell lung carcinoma patient-derived xenografts closely reflect their primary tumors. Int. J. Cancer 140, 662-673 (2017).

      3. John, T. et al. The ability to form primary tumor xenografts is predictive of increased risk of disease recurrence in early-stage non-small cell lung cancer. Clin. Cancer Res. 17, 134-141 (2011).

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    MTE02 - Update on WHO Classification and Staging of Lung Cancer (Ticketed Session) (ID 812)

    • Type: Meet the Expert Session
    • Track: Pathology
    • Presentations: 2
    • Now Available
    • Moderators:
    • Coordinates: 9/24/2018, 07:00 - 08:00, Room 203 BD
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      MTE02.01 - Update on WHO Classification and Staging of Lung Cancer (Now Available) (ID 11548)

      07:00 - 07:30  |  Presenting Author(s): Sanja Dacic

      • Abstract
      • Presentation
      • Slides

      Abstract

      The most significant changes in the 2015 WHO classification of the lung tumors include classification criteria for small biopsy and cytology specimens, use of immunohistochemistry, integration of molecular testing, adoption of the IASLC/ATS/ERS adenocarcinoma classification and a strict definition of large cell carcinoma limited to surgical resection specimens only. 1,2 Tumors that show unequivocal morphology of adenocarcinoma or squamous cell carcinoma on a small specimen should be diagnosed without immunohistochemistry. Immunohistochemical work up of poorly differentiated tumors should be limited to TTF-1and p40/p63, while neuroendocrine markers should be used only if morphologically indicated. This approach should reduce the diagnosis of NSCC, NOS to less than 5 % and preserve tissue for molecular testing. 1,2

      Major changes in the adenocarcinoma classification for resected specimens include addition of adenocarcinoma in situ (AIS) to preinvasive group that already includes atypical adenomatous hyperplasia. Minimally invasive adenocarcinoma (MIA) defined as a solitary, lepidic predominant adenocarcinoma presenting measuring in gross size 3 cm or less and with invasion of ≤
5 mm was added as a new category. These tumors are also recognized by the 8th edition of the AJCC staging of lung cancer and include Tis(adenocarcinoma) and T1a-mi. T stage of non-mucinous lepidic predominant adenocarcinomas is based on the microscopic size of invasion, but gross size should be recorded in the pathology reports. Multifocal ground glass opacities/lung nodules most frequently present as MIAs and should be classified by the T category of the lesion with the highest T along with the number of lesions (#) or simply (m) for multiple indicated in parentheses, and with a single N and M category that applies to all of the multiple tumor foci. This approach should be applied to grossly or microscopically identified lesions occurring in the same or in different ipsilateral or contralateral lobes.3 For non-lepidic adenocarcinoma T stage is determined by gross size in 1.0 cm increments as each size subgroup carries prognostic significance.

      Former mucinous BAC are reclassified as invasive mucinous adenocarcinoma, excluding tumors that meet criteria for AIS or MIA. Signet ring and clear cell carcinomas are considered to represent cytologic variants rather than specific subtypes.

      Invasive adenocarcinomas should be subtyped by semi-quantitatively estimating the percentage of the various subtypes in 5% increments. 1,2 Reproducibility for lung adenocarcinoma predominant subtypes among pulmonary pathologists was good to moderate (κ-values 0.44 to 0.72).4 For untrained pathologists, κ-values were lower ranging from 0.38 to 0.47, but these improved after a training session and particularly for individual reviewer. 5

      The 2015 WHO classification defines large cell carcinomas based on morphology, as carcinomas without morphologic evidence of glandular, squamous or neuroendocrine differentiation, and also based on null immunophenotype and genotype. 1This change in definition reflect what was already happening in the pathology practice. According to National Cancer Institute (NCI) Surveillance Epidemiology and End Results registry the diagnosis of large cell carcinoma started to decline about the time that TTF-1 was introduced into clinical diagnosis. 6

      References:

      Travis WD, Brambilla E, Burke AP, Marx A, Nicholson AG. WHO Classification of Tumours of the Lung, Pleura, Thymus and Heart. Lyon: International Agency for Research on Cancer, 2015.

      
Travis WD. Et al. The 2015 World Health Organization Classification of Lung Tumors Impact of Genetic, Clinical and Radiologic Advances Since the 2004 Classification. J Thorac Oncol 2015; 10 (9); 1243-1260

      Frank C. Detterbeck, MD et al. The IASLC Lung Cancer Staging Project: Summary of Proposals for Revisions of the Classification of Lung Cancers with Multiple Pulmonary Sites of Involvement in the Forthcoming Eighth Edition of the TNM Classification . J Thorac Oncol 2016;11(5): 639-650

      Thunnissen E, Beasley MB, Borczuk AC, et al. Reproducibility of histopathological subtypes and invasion in pulmonary adenocarcinoma. An international interobserver study. Mod Pathol 2012;25:1574–1583. 


      Warth A, Cortis J, Fink L, et al.; Pulmonary Pathology Working Group of the German Society of Pathology. Training increases concordance in classifying pulmonary adenocarcinomas according to the novel IASLC/ ATS/ERS classification. Virchows Arch 2012;461:185–193. 


      Lewis DR, Check DP, Caporaso NE, Travis WD, Devesa SS. US lung cancer trends by histologic type. Cancer 2014;120:2883–2892. 


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      MTE02.02 - Update on WHO Classification and Staging of Lung Cancer (Now Available) (ID 11549)

      07:30 - 08:00  |  Presenting Author(s): Teh-Ying Chou

      • Abstract
      • Presentation
      • Slides

      Abstract

      Squamous cell carcinoma comprises approximately 20% of lung cancer cases and is classified into keratinizing, non-keratinizing and basaloid types (1,2,3). The p40 (or p63) immunohistochemical stain is helpful in diagnosing squamous cell carcinoma, if keratinization of the tumor cells is not appreciable.

      Neuroendocrine tumors comprises of four categories: small cell carcinoma, large cell carcinoma, typical carcinoid and atypical carcinoid (1), with variable degrees of malignant potential. Small cell carcinoma comprises approximately 14% of lung cancer cases and is further categorized into small cell carcinoma and combined small cell carcinoma (1,4,5). The tumor is composed of densely packed small-size tumor cells with scant cytoplasm, finely granular chromatin, and absence of distinct nucleoli. Mitotic figures and apoptotic bodies are frequently seen. Nuclear molding and smearing may be observed. Rosette formation and peripheral palisading, characteristics of neuroendocrine tumors, are consistently found. Large cell neuroendocrine carcinoma has the cytological morphology of large cell carcinoma and the growth pattern of neuroendocrine tumor. Both small cell carcinoma and large cell neuroendocrine carcinoma are high grade tumors. Carcinoid tumors are usually centrally located with endobronchial growth and are further divided into two categories: typical carcinoid (intermediate grade) and atypical carcinoid (low grade).

      Adenosquamous carcinoma is rare and comprises 0.4-4% of lung cancer cases (1,6,7). Presence of both adenocarcinoma and squamous cell carcinoma components and each component comprising more than 10% is required.

      Sarcomatoid carcinoma comprises less than 1% of lung cancer cases and is further subcategorized into pleomorphic carcinoma, spindle cell carcinoma, giant cell carcinoma, carcinosarcoma, and pulmonary blastoma (1,8). Given the marked histological heterogeneity, sarcomatoid carcinoma need to be thoroughly sampled before the final diagnoses are made.

      Salivary gland-type carcinomas include mucoepidermoid carcinoma, adenoid cystic carcinoma, and epithelial-myoepithelial carcinoma, arising from the salivary-type glands of the bronchial mucosa (1).

      In summary, the major types of lung carcinomas are outlined in Figure 1.

      180629 histology lung cancer classification.jpg

      References:

      1. William D. Travis EB, Allen P. Burke, Alexander Marx, Andrew G. Nicholson (Eds.). WHO Classification of Tumours of the Lung, Pleura, Thymus and Heart (4th Edition). 4 ed: IARC: Lyon; 2015.

      2. Tomashefski JF, Jr., Connors AF, Jr., Rosenthal ES, Hsiue IL. Peripheral vs central squamous cell carcinoma of the lung. A comparison of clinical features, histopathology, and survival. Archives of pathology & laboratory medicine. 1990;114(5):468-74.

      3. Funai K, Yokose T, Ishii G, Araki K, Yoshida J, Nishimura M, et al. Clinicopathologic characteristics of peripheral squamous cell carcinoma of the lung. The American journal of surgical pathology. 2003;27(7):978-84.

      4. Fraire AE, Johnson EH, Yesner R, Zhang XB, Spjut HJ, Greenberg SD. Prognostic significance of histopathologic subtype and stage in small cell lung cancer. Hum Pathol. 1992;23(5):520-8.

      5. Mangum MD, Greco FA, Hainsworth JD, Hande KR, Johnson DH. Combined small-cell and non-small-cell lung cancer. Journal of clinical oncology : official journal of the American Society of Clinical Oncology. 1989;7(5):607-12.

      6. Fitzgibbons PL, Kern WH. Adenosquamous carcinoma of the lung: a clinical and pathologic study of seven cases. Hum Pathol. 1985;16(5):463-6.

      7. Ishida T, Kaneko S, Yokoyama H, Inoue T, Sugio K, Sugimachi K. Adenosquamous carcinoma of the lung. Clinicopathologic and immunohistochemical features. Am J Clin Pathol. 1992;97(5):678-85.

      8. Travis WD. Sarcomatoid neoplasms of the lung and pleura. Archives of pathology & laboratory medicine. 2010;134(11):1645-58

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