Virtual Library

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    ISS07 - Industry Supported Symposium: Immuno-Oncology and Lung Cancer: Emerging Data and Recent Developments - Bristol-Myers Squibb (ID 440)

    • Event: WCLC 2016
    • Type: Industry Supported Symposium
    • Track:
    • Presentations: 5
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      ISS07.01 - Welcome & Introduction (ID 7140)

      12:45 - 14:15  |  Author(s): M.D. Hellmann

      • Abstract
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      Abstract not provided

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      ISS07.02 - Developments in the Use of I-O Monotherapy in Lung Cancers (ID 7141)

      12:45 - 14:15  |  Author(s): E. Felip

      • Abstract

      Abstract not provided

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      ISS07.03 - Rationale for Studying I-O Combo Therapies to Address Unmet Needs in Lung Cancer (ID 7142)

      12:45 - 14:15  |  Author(s): M.D. Hellmann

      • Abstract

      Abstract not provided

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      ISS07.04 - Clinical Lessons Learned for the Use of I-O Therapies (ID 7143)

      12:45 - 14:15  |  Author(s): J. Wolf

      • Abstract

      Abstract not provided

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      ISS07.05 - Close & Outlook (ID 7144)

      12:45 - 14:15  |  Author(s): M.D. Hellmann

      • Abstract

      Abstract not provided

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    PL01 - Opening Plenary Session (ID 419)

    • Event: WCLC 2016
    • Type: Plenary
    • Track:
    • Presentations: 1
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      PL01.01 - Keynote Lecture: Is Smoking a Sole Factor in Lung Cancer Development? (ID 6927)

      19:00 - 20:45  |  Author(s): H. zur Hausen

      • Abstract
      • Presentation
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      Abstract not provided

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    PL02a - Distinguished Lecture (ID 480)

    • Event: WCLC 2016
    • Type: Plenary
    • Track:
    • Presentations: 1
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      Welcome Address (ID 7160)

      08:45 - 09:00  |  Author(s): H. Fischer

      • Abstract
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      Abstract not provided

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    PL02b - Tobacco Control (ID 425)

    • Event: WCLC 2016
    • Type: Plenary
    • Track: Epidemiology/Tobacco Control and Cessation/Prevention
    • Presentations: 4
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      PL02b.01 - Implementing Tobacco Control Measures in Uruguay (ID 6864)

      09:00 - 10:20  |  Author(s): T. Vázquez

      • Abstract
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      Abstract not provided

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      PL02b.02 - Framework Convention on Tobacco Control: Its impact on Global Health (ID 7052)

      09:00 - 10:20  |  Author(s): V. Da Costa E Silva

      • Abstract
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      Abstract not provided

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      PL02b.03 - Free Trade & Investment Agreement Threatens Public Health (ID 6464)

      09:00 - 10:20  |  Author(s): Z. Zain

      • Abstract
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      Abstract not provided

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      PL02b.04 - Tobacco Control (ID 6865)

      09:00 - 10:20  |  Author(s): L. Clancy

      • Abstract
      • Presentation
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      Abstract:
      Tobacco Control Tobacco is the biggest preventable cause of cancer in the world. Estimates suggest that approximately one-third of all cancers are caused by tobacco use. Although 80%–90% of all lung cancers are attributable to tobacco, it also has a causative role in malignancies of the mouth, larynx, pharynx, nose and sinuses, oesophagus, stomach, liver, pancreas, kidney, bladder, cervix, and bowel as well as on one type of ovarian cancer and some types of leukaemia. Tobacco is a widely and legally available product which, through the drug nicotine, is highly addictive and is promoted by a powerful and highly profitable industry. It has several marketing advantages over other addictive drugs. Other addictive drugs are mostly illegal, their method of administration is often by injection, they are socially disruptive, and they have very low social acceptability. In contrast, tobacco use has been the norm in the past and still has social acceptability in certain societies. Thousands of harmful chemicals are present in tobacco and particularly in tobacco smoke, which has documented serious adverse health effects. There are 70 known carcinogens in cigarette smoke including nitrosamines, polycyclic aromatic hydrocarbons, benzene, cadmium, toluidine, and vinyl chloride Industry access to policymakers Tobacco control policies, and therefore the health of the public, suffer when policy-makers maintain connections with the Transnational Tobacco Companies (TTC), as this provides a direct avenue for policy influence. TTCs still meet with and hope to influence government officials responsible for tobacco control policy in many countries. This is in direct violation of those countries commitments under the FCTC which is a legally binding WHO treaty. Through these contacts, industry has been able to offer ‘help’ to national governments to negotiate e.g. a later excise harmonization deadline and influence the speed of increase to meet these requirements. Political links such as this contravene the FCTC Article 5.3, which seeks to protect policymaking from industry influence. What can we do to reduce death and disability from Tobacco use? The prevalence—at approximately 29% of the adult population—remains stubbornly high in Europe and is increasing among females in some European countries. This despite the fact that effective and cost effective interventions to control and eliminate tobacco use exist and are well known. The World Health Organization (WHO) has validated several strategies which are effective in curtailing the use of tobacco .These approaches include using increased price, through taxation, as a tool to reduce tobacco use. The use of smoke-free legislation to prevent exposure to second-hand smoke (SHS) in the workplace is also important in preventing cancer because SHS is also a known carcinogen. The banning of advertising, sponsorship, and promotion of tobacco is an effective and a widespread intervention to help reduce tobacco use and the use of strong antismoking advertising has also been shown to be effective. WHO recommends the monitoring of smoking and the provision of cessation programs to help smokers stop smoking. This treatment of tobacco dependence is particularly covered by Article 14 of the FCTC. In Art.14 of the FCTC governments are urged to ‘facilitate accessibility and affordability for treatment of tobacco dependence’ (World Health Organization, 2015). According to the 2014 FCTC implementation report, the implementation of services to support cessation of tobacco use in line with Article 14 can and should be significantly improved (World Health Organization, 2014). Yet there seems to date to be little progress. Price as a control intervention The relationship between a rise in price and a fall in tobacco consumption is clear; however, a number of important aspects of this relationship must be considered. Lower socioeconomic groups and younger people are most sensitive to price increase as a deterrent, whereas in higher socioeconomic groups, price is not necessarily a determining factor. The use of price as an instrument to reduce tobacco use is usually opposed by the tobacco industry and its allies. The industry and its representatives usually try to persuade finance ministers that a price increase will lead to a loss of revenue through an increase in smuggling, although the evidence from many studies is that a rise in tobacco price leads to an increase in revenue and a reduction in cigarette consumption. Taxation is an effective, highly cost-effective and very powerful tool available to governments if they want to prevent cancer and the many other diseases which are caused by tobacco. Smoke free policies Since Ireland introduced its comprehensive national smoke-free legislation in 2004, many European countries have followed Ireland’s lead, but not all of those have introduced laws as comprehensive as Ireland’s. Nevertheless, all 27 EU member state countries have initiated some form of smokefree strategy. To date, 14 EU member states have enacted laws which ban smoking in all indoor workplaces including bars, restaurants, and clubs; however, a number of countries with significant populations such as Germany and Poland have only limited smoke-free laws. It is encouraging that Russia, where smoking prevalence is very high (more than 50%), introduced its smoke-free measure on June 1, 2013, banning smoking in airports, train stations, stadiums, schools, playgrounds, hospitals, government institutions, beaches, and places of employment. Tougher smoking fines were signed into law by President Vladimir Putin on October 21, 201 The importance of smoke-free policies for cancer prevention is high. SHS is a definite cause of cancer and is defined as Class 1 carcinogen by the International Agency for Research on Cancer. The number of cancers caused by SHS can be calculated, but smoke-free policies have other cancer prevention benefits. They discourage young people from starting to smoke, encourage smokers to quit, and help former smokers stay off smoking and promote an attitude of denormalisation of smoking. Smoking has often been regarded as a normal social activity despite the fact that it is addictive, is a cause of great inequality, and contributes significantly to disease, disability, and death. Smoke-free policies can achieve their positive effect by educating about the health benefits, limiting opportunities to smoke, and promoting an attitude of denormalisation of smoking.

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    PL03 - Presidential Symposium (ID 428)

    • Event: WCLC 2016
    • Type: Plenary
    • Track:
    • Presentations: 10
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      PL03.01 - Presidential Address (ID 6881)

      08:35 - 10:25  |  Author(s): D.P. Carbone

      • Abstract
      • Presentation
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      Abstract not provided

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      PL03.02 - Lung Cancer Staging – Changing the Clinical Practice (ID 6866)

      08:35 - 10:25  |  Author(s): R. Rami-Porta

      • Abstract
      • Presentation
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      Abstract:
      Introduction At the time of the 17[th] World Conference on Lung Cancer, the 8[th] edition of the tumor, node and metastasis (TNM) classification of lung cancer will have been published by the Union for International Cancer Control, the American Joint Committee on Cancer and the International Association for the Study of Lung Cancer (IASLC) in their respective staging manuals. The innovations introduced, based on the analyses of the new IASLC database that includes 70,967 evaluable patients with non-small cell lung cancer and 6,189 with small cell lung cancer are described in the table. (1-9) These innovations will lead to some changes in clinical practice that are worth reflecting on. Table. Innovations introduced in the 8[th] edition of the TNM classification of lung cancer.

      Descriptor 8[th] edition
      T component
      >/= 1cm T1a
      >1 – 2cm T1b
      >2 – 3cm T1c
      >3 – 4cm T2a
      >4 – 5cm T2b
      >5 – 7cm T3
      >7cm T4
      Brochus <2cm from carina T2
      Total atelectasis/pneumonitis T2
      Diaphragm inasion T4
      Mediastinal pleura invasion -
      M component
      Metastases in thoracic cavity M1a
      Single extrathoracic metastasis M1b
      Multiple extrathoracic metastases M1c
      Other innovations in classification
      Second primaries One TNM for each
      Separate tumor nodules T3, T4 and M1a
      Multifocal adenocarcinomas with ground glass opacity/lepidic features Highest T (#/m) and global N and M
      Pneumonic type adenocarcinoma T3, T4 and M1a
      The T component Tumor size is a much more relevant prognostic factor than in previous editions and is now a descriptor in all T categories. Therefore, tumor size measurement should be carefully performed because small changes in size mean important changes in prognosis. (2) In part-solid tumors, only the solid/invasive part counts to measure tumor size. (7) The fact that adenocarcinoma in situ –Tis(AIS) – and minimally invasive adenocarcinoma –T1mi– have their own coding in the TNM classification will increase their awareness. (7) These, together with the smallest coded solid tumors, those of one cm or less in largest dimension –T1a– can become the base from which to study therapeutic options, such as sublobar resections, stereotactic radiotherapy, radiofrequency ablation; tumor biology, including tumor growth, tumor density and intensity of the standardized uptake value, as well as molecular profile and genetic signatures. Visceral pleural invasion and its two categories (PL1: invasion beyond its elastic layer; and PL2: invasion of the pleural surface) have been confirmed as important prognostic factors. (2) This means that pathologists should intensively investigate the identification of visceral pleural invasion, and, if it is not evident by the standard hematoxylin and eosine stains, elastic stains should be used, as recommended in the 7[th] edition of the TNM classification. (10) The N component Although there will be no changes in the N categories, the analyses for the 8[th] edition have shown that quantification of nodal disease has prognostic implications. This had already been evident in the 7[th] edition, when it was found that the number of involved nodal zones was prognostic. The analyses for the 8[th] edition have considered the number of involved nodal stations and have found that the more nodal stations involved, the worse the prognosis; and that the prognosis of tumors with involvement of multiple N1 stations was similar to that of tumors with single station N2 without concomitant N1 disease (skip metastases). (3) The findings of the 7[th] edition already raised the issue of indicating upfront resection in patients with tumors with single N2 zone involvement, because their prognosis was the same as that of tumors with multiple N1 zones. The question will be raised again in the light of the results of the 8[th] edition. However, in both occasions, the quantification of nodal disease derived from pathological staging of those tumors that had been resected and the resection had been accompanied by a properly performed systematic nodal dissection. This is difficult to replicate at clinical staging, the moment at which therapeutic decisions are made, unless a transcervical mediastinoscopic lymphadenectomy is performed. This lymphadenectomy has been found to be equivalent to that performed at the time of resection, either by thoracoscopic or open surgery, and is the only pre-resection test that can define single station or single zone N2 disease reliably. The M component There is no change in the metastasis within the thoracic cavity (M1a), but single extrathoracic metastases have better prognosis than multiple extrathoracic metastasis in one or in several organs, and different categories have been defined for them: M1b for single and M1c for multiple extrathoracic metastases. (4) The fact that single extrathoracic metastasis have their own category will facilitate the redefinition of oligometastatic and oligoprogressive disease, the establishment of therapeutic protocols with radical intention, and the investigation of all therapeutic modalities to eliminate the advance disease. However, clinical staging will have to be precise and will have to determine the number and the organ location of the metastatic deposits. The stages Some TNM subsets have moved from one stage to another and new stages and sub-stages have been created to accommodate groups of tumors with similar prognosis. (5) As it occurred with the 7[th] edition, the question of how to treat patients whose tumors have changed stage will be raised at multidisciplinary team meetings. Taxonomic changes do not necessarily mean an automatic change in therapy if the clinical trials performed to test therapeutic options did not include the tumors that are now included in the selected stages for study. Therefore, in the absence of results from clinical trials, clinical judgment will have to determine what the best options are for a given patient with a given tumor. Lung cancer with multiple lesions The 8[th] edition will provide a set of rules with the intention to classify lung cancers with multiple lesions in a homogeneous way. (8) It is our responsibility to follow the rules to collect prospective data uniformly and validate the given recommendations with international data. Conclusion The 8[th] edition will help us refine prognosis both at clinical and pathologic staging and stratify tumors in future clinical trials, but will require more attention from us at measuring tumor size, at determining nodal disease, at searching for metastases, and at using clinical judgment to indicate treatment. References 1. Rami-Porta R, Bolejack V, Giroux DJ et al. The IASLC lung cancer staging project: the new database to inform the eighth edition of the TNM classification of lung cancer. J Thorac Oncol 2014; 9: 1618-1624. 2. Rami-Porta R, Bolejack V, Crowley J et al. The IASLC lung cancer staging project: proposals for the revisions of the T descriptors in the forthcoming 8[th] edition of the TNM classification for lung cancer. J Thorac Oncol 2015; 10: 990-1003. 3. Asamura H, Chansky K, Crowley J et al. The IASLC Lung Cancer Staging Project: proposals for the revisions of the N descriptors in the forthcoming 8[th] edition of the TNM classification for lung cancer. J Thorac Oncol 2015; 10: 1675-1684. 4. Eberhardt WEE, Mitchell A, Crowley J et al. The IASLC lung cancer staging project: proposals for the revisions of the M descriptors in the forthcoming 8[th] edition of the TNM classification for lung cancer. J Thorac Oncol 2015; 10: 1515-1522. 5. Goldstraw P, Chansky K, Crowley J et al. The IASLC lung cancer staging project: proposals for the revision of the stage grouping in the forthcoming (8th) edition of the TNM classification of lung cancer. J Thorac Oncol 2016; 11: 39-51. 6. Nicholson AG, Chansky K, Crowley J et al. The International Association for the Study of Lung Cancer Lung Cancer Staging Project: proposals for the revision of the clinical and pathologic staging of small cell lung cancer in the forthcoming eighth edition of the TNM classification for lung cancer. J Thorac Oncol 2016; 11: 300-311. 7. Travis WD, Asamura H, Bankier A et al. The IASLC Lung Cancer Staging Project: proposals for coding T categories for subsolid nodules and assessment of tumor size in part-solid tumors in the forthcoming eighth edition of the TNM classification of lung cancer. J Thorac Oncol 2016; 11: 1204-1223. 8. Detterbeck FC, Nicholson AG, Franklin WA 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: 539-650. 9. Detterbeck FC, Chansky K, Groome P et al. The IASLC Lung Cancer Staging Project: methodology and validation used in the development of proposals for revision of the stage classification of NSCLC in the forthcoming (eighth) edition of the TNM classification of lung cancer. J Thorac Oncol 2016; 11: 1433-1446. 10. Travis WD, Brambilla E, Rami-Porta R et al. Visceral pleural invasion: pathologic criteria and use of elastic stains. Proposal for the 7[th] edition of the TNM classification for lung cancer. J Thorac Oncol 2008; 3: 1384-1390.

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      PL03.03 - Randomised Phase III Study of Osimertinib vs Platinum-Pemetrexed for EGFR T790M-Positive Advanced NSCLC (AURA3) (Abstract under Embargo until December 6, 7:00 CET) (ID 4452)

      08:35 - 10:25  |  Author(s): V. Papadimitrakopoulou, Y.-. Wu, M. Ahn, S.S. Ramalingam, M.C. Garassino, H.R. Kim, F. Shepherd, H. Akamatsu, W.S. Theelen, C.K. Lee, M. Sebastian, A. Templeton, M. Marotti, S. Ghiorghiu, T. Mok

      • Abstract
      • Presentation
      • Slides

      Background:
      Osimertinib is a potent, irreversible, CNS active, epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) selective for sensitising (EGFRm) and T790M resistance mutations. Osimertinib is indicated for the treatment of patients with locally advanced or metastatic EGFR T790M-positive NSCLC. AURA3 (NCT02151981) is a Phase III, open-label, randomised study assessing the efficacy and safety of osimertinib versus platinum-based chemotherapy plus pemetrexed in patients with EGFR T790M-positive advanced NSCLC, whose tumours progressed on first-line EGFR-TKI therapy.

      Methods:
      Eligible patients were ≥18 years with documented EGFRm, radiological disease progression following first-line EGFR-TKI and centrally confirmed T790M-positive (by cobas® EGFR Mutation Test) from a tissue biopsy after disease progression. Asymptomatic, stable CNS metastases were allowed. Patients were randomised 2:1 to osimertinib 80 mg orally, once daily or platinum-pemetrexed (pemetrexed 500 mg/m[2] plus either cisplatin 75 mg/m[2] or carboplatin AUC5) every three weeks for up to six cycles; pemetrexed could be continued as maintenance treatment. Primary endpoint was progression-free survival (PFS) by investigator assessment according to RECIST v1.1; sensitivity analysis was by blinded independent central review (BICR).

      Results:
      A total of 419 patients were randomised to treatment (osimertinib, n=279; platinum-pemetrexed, n=140). Baseline characteristics were generally balanced across treatment groups: female 64%, Asian 65%, never smoker 68%, CNS metastases 34%, EGFR exon 19 deletion 66%. Osimertinib significantly improved PFS compared with platinum-pemetrexed: hazard ratio [HR] 0.30; 95% CI: 0.23, 0.41; p<0.001 (median 10.1 months vs 4.4 months). The result was consistent with PFS analysis by BICR: HR 0.28; 95% CI: 0.20, 0.38; p<0.001 (11.0 months vs 4.2 months). Objective response rate was significantly improved with osimertinib (71%) vs platinum-pemetrexed (31%); odds ratio 5.39 (95% CI: 3.47, 8.48; p<0.001). Median duration of response was 9.7 months (95% CI 8.3, 11.6) with osimertinib and 4.1 months (95% CI 3.0, 5.6) with platinum-pemetrexed. Grade ≥3 causally-related adverse events (AEs) as assessed by the investigator were reported in 6% of patients (n=16) treated with osimertinib and 34% (n=46) treated with platinum-pemetrexed. Most common causally-related AEs in the osimertinib group: diarrhoea (29% [grade ≥3, 1%]), rash (28% [<1%]); in the platinum-pemetrexed group: nausea (47% [3%]), decreased appetite (32% [3%]).

      Conclusion:
      In patients with EGFR T790M-positive advanced NSCLC following progression on EGFR-TKI treatment, osimertinib demonstrated a superior clinically-meaningful efficacy over platinum-pemetrexed, with a 70% reduction in the risk of disease progression, and well-characterised safety profile, establishing the new standard of care for these patients.

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      PL03.04 - Discussant for PL03.02, PL03.03 (ID 7156)

      08:35 - 10:25  |  Author(s): T. Mitsudomi

      • Abstract
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      Abstract not provided

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      PL03.05 - BRAIN: A Phase Ⅲ Trial Comparing WBI and Chemotherapy with Icotinib in NSCLC with Brain Metastases Harboring EGFR Mutations (CTONG 1201) (Abstract under Embargo until December 6, 7:00 CET) (ID 4570)

      08:35 - 10:25  |  Author(s): Y.-. Wu, J.-. Yang, C. Zhou, J. Feng, S. Lu, Y. Song, C. Huang, G. Wu, Y. Cheng, C. Hu, L. Zhang, G. Chen, L. Zhang, X. Liu, H. Yan, F. Tan, Y. Huang

      • Abstract
      • Presentation
      • Slides

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

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

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

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

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      PL03.06 - Discussant for PL03.05 (ID 7154)

      08:35 - 10:25  |  Author(s): J. Jassem

      • Abstract
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      Abstract not provided

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      PL03.07 - First-line Ceritinib Versus Chemotherapy in Patients With ALK-rearranged (ALK+) NSCLC: A Randomized, Phase 3 Study (ASCEND-4) (Abstract under Embargo until December 6, 7:00 CET) (ID 4987)

      08:35 - 10:25  |  Author(s): G. De Castro Jr, D. Tan, L. Crinò, Y.-. Wu, L. Paz-Arez, J. Wolf, S.L. Geater, S. Orlov, D. Cortinovis, C. Yu, M.J. Hochmair, A.B. Cortot, C. Tsai, D. Moro-Sibilot, R. García Campelo, F. Branle, P. Sen, T. McCulloch, J. Soria

      • Abstract
      • Presentation
      • Slides

      Background:
      Here, we report results of ceritinib versus chemotherapy as first-line treatment for advanced ALK+ NSCLC.

      Methods:
      Untreated ALK+ (IHC confirmed), advanced, nonsquamous NSCLC patients (N=376; median age, 54 years) were randomized (1:1) to ceritinib 750 mg/day (n=189 [59 with brain metastases (BM)]) or chemotherapy (n=187 [62 with BM]; [pemetrexed 500 mg/m[2] plus cisplatin 75 mg/m[2] or carboplatin AUC 5-6] for 4 cycles followed by maintenance pemetrexed), stratified by WHO PS (0 vs 1-2), BM at screening, and prior neo-/adjuvant chemotherapy. Crossover from chemotherapy to ceritinib was allowed at progression (n=80 crossed-over).

      Results:
      Median treatment exposure was 66.4 weeks for ceritinib and 26.9 weeks for chemotherapy. Median follow-up duration was 19.7 months (randomization to cut-off date). The study met its primary objective, with ceritinib demonstrating statistically significant improvement in BIRC PFS (RECIST 1.1; median, 16.6 [12.6, 27.2] vs 8.1 months [5.8, 11.1], HR=0.55, P<0.001) versus chemotherapy. OS was immature (HR, 0.73 [0.50, 1.08]; P=0.056) with 42.3% of required events at interim analysis. ORR (BIRC, 72.5% vs 26.7%) and DOR (BIRC, median, 23.9 vs 11.1 months) were also higher with ceritinib versus chemotherapy. Among patients with measurable baseline BM and ≥1 postbaseline assessment, intracranial ORR (BIRC neuroradiologist; modified RECIST v1.1) was higher with ceritinib (72.7% [49.8, 89.3] vs 27.3% [10.7, 50.2]) versus chemotherapy (Table). Most common AEs (>50%) with ceritinib were diarrhea (84.7%), nausea (68.8%), vomiting (66.1%), ALT increase (60.3%), and AST increase (52.9%). Overall, 5.3% ceritinib- and 11.4% chemotherapy-treated patients discontinued due to AEs suspected to be drug-related. Figure 1



      Conclusion:
      First-line ceritinib achieved statistically significant and clinically meaningful improvement in median PFS with an estimated 45% risk reduction in advanced ALK+ NSCLC versus chemotherapy including maintenance. Moreover, ceritinib achieved high and durable systemic responses and high OIRR in patients with measurable BM. Safety profile of ceritinib is consistent with previously reported.

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      PL03.08 - Discussant for PL03.07 (ID 7155)

      08:35 - 10:25  |  Author(s): F. Blackhall

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      PL03.09 - Phase 3 Study of Ganetespib, a Heat Shock Protein 90 Inhibitor, with Docetaxel versus Docetaxel in Advanced Non-Small Cell Lung Cancer (GALAXY-2) (Abstract under Embargo until December 6, 7:00 CET) (ID 5232)

      08:35 - 10:25  |  Author(s): R.N. Pillai, D.A. Fennell, V. Kovcin, T.E. Ciuleanu, R. Ramlau, D. Kowalski, M. Schenker, B. Perin, I. Yalcin, F. Teofilovici, V.M. Vukovic, S.S. Ramalingam

      • Abstract
      • Presentation
      • Slides

      Background:
      Heat shock protein 90 functions as a chaperone to stabilize oncoproteins. Ganetespib (G), a highly potent Hsp90 inhibitor, has demonstrated efficacy in combination with docetaxel (D) over D alone in the second-line therapy of patients with advanced adenocarcinoma of the lung in a phase 2 study.

      Methods:
      GALAXY-2 is a randomized (1:1), international, open-label study of D with or without G. Patients with advanced (stage IIIB/IV) non-small cell lung cancer (NSCLC) of adenocarcinoma histology, EGFR and ALK wild-type, diagnosed ≥ 6 months prior to study entry, one prior systemic therapy and ECOG PS 0-1 were eligible. D was given at 75 mg/m[2] on day 1 of three-week cycle; D was given on day 1 with G at 150 mg/m[2 ]on Days 1 and 15 of each cycle. Patients were stratified by performance status (PS), LDH, and geographic region. Primary endpoint was overall survival (OS). Secondary endpoints included progression free survival (PFS) and OS in elevated LDH (eLDH) patients. We report the results of a planned interim analysis at 336 events, which occurred on October 5, 2015, with type I error level set at 0.01 (2 sided stratified log-rank test).

      Results:
      677 patients were randomized with 335 patients in G+D arm and 337 patients in D arm. Baseline characteristics: females 60%, age < 65 68%; never-smoker 18%; PS 0 36%; eLDH 29%; North America/Western Europe 39%. The median number of cycles delivered was 5 in G+D and 4 in D arm. There was no difference in median OS (mOS) for the two arms: 10.9 months with G+D versus 10.5 months with D alone. The hazard ratio for OS was 1.111 (95% CI 0.899-1.372), which met the early stopping criteria for futility. Median PFS was similar in the two arms: 4.2 versus 4.3 months, G+D and D, respectively (HR 1.161, 95% CI 0.961-1.403). There was no improvement with the addition of G for any secondary endpoint, including survival in the eLDH and EGFR and ALK negative populations, response rate, or progression due to new metastatic lesions. The most common grade 3/4 treatment-emergent adverse event in both arms was neutropenia (31.1% versus 24.3%, G+D and D, respectively).

      Conclusion:
      The addition of ganetespib to docetaxel did not result in improved efficacy for salvage therapy of patients with advanced stage lung adenocarcinoma.

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      PL03.10 - Discussant for PL03.09 (ID 7157)

      08:35 - 10:25  |  Author(s): D.R. Gandara

      • Abstract
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      Abstract not provided

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    PL04a - Plenary Session: Immune Checkpoint Inhibitors in Advanced NSCLC (ID 430)

    • Event: WCLC 2016
    • Type: Plenary
    • Track: Chemotherapy/Targeted Therapy/Immunotherapy
    • Presentations: 5
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      PL04a.01 - Health-Related Quality of Life for Pembrolizumab vs Chemotherapy in Advanced NSCLC with PD-L1 TPS ≥50%: Data from KEYNOTE-024 (Abstract under Embargo until December 7, 7:00 CET) (ID 7153)

      08:45 - 09:40  |  Author(s): J.R. Brahmer, D. Rodriguez-Abreu, A.G. Robinson, R. Hui, T. Csoszi, A. Fülöp, M. Gottfried, N. Peled, A. Tafreshi, S. Cuffe, M. O’brien, S. Rao, K. Hotta, A.C. Deitz, G.M. Lubiniecki, J. Zhang, R. Rangwala, M. Reck

      • Abstract
      • Presentation
      • Slides

      Background:
      In KEYNOTE-024 (NCT02142738), pembrolizumab provided superior progression-free survival (PFS) over platinum-based chemotherapy as first-line therapy for patients with advanced non-small cell lung cancer (NSCLC) with PD-L1 expression on ≥50% of tumor cells (ie, PD-L1 tumor proportion score [TPS] ≥50%) and no sensitizing EGFR or ALK aberrations (HR 0.50, P < 0.001). Despite a 44% crossover rate from chemotherapy to pembrolizumab, pembrolizumab also significantly improved overall survival (OS) (HR 0.60, P = 0.005). Any-grade (73% vs 90%) and grade 3-5 (27% vs 53%) treatment-related adverse events were less frequent with pembrolizumab. Health-related quality of life (HRQoL) is an important consideration for anticancer therapy, particularly in the first-line setting. We present data from the prespecified exploratory patient-reported outcomes (PRO) analysis of KEYNOTE-024.

      Methods:
      305 patients were randomized to pembrolizumab 200 mg Q3W or investigator-choice platinum-doublet chemotherapy plus optional pemetrexed maintenance therapy for nonsquamous disease. The EORTC QLQ-C30 and QLQ-LC13 were administered at cycles 1-3 and every 9 weeks thereafter. The key PRO end points were change from baseline to week 15 in the QLQ-C30 global health status/QoL score and time to deterioration in the QLQ-LC13 composite of cough, chest pain, and dyspnea. PROs were analyzed for all patients who received study treatment and completed ≥1 PRO instrument (n = 299).

      Results:
      Across treatment arms, PRO compliance was >90% at baseline and ~80% at week 15. Least squares (LS) mean (95% CI) change from baseline to week 15 in QLQ-C30 global health status/QoL score was 6.95 (3.29 to10.58) for pembrolizumab (n = 151) and –0.88 (–4.78 to 3.02) for chemotherapy (n = 148). The difference in LS means was 7.82 (95% CI 2.85-12.79; nominal 2-sided P = 0.002). The proportion of improved global health status/QoL score at week 15 was 40.0% for pembrolizumab and 26.5% for chemotherapy. Fewer patients in the pembrolizumab arm had deterioration in the QLQ-LC13 composite of cough, dyspnea, and chest pain (30% vs 39%), and time to deterioration was also prolonged with pembrolizumab (HR 0.66, 95% CI 0.44-0.97; nominal 2-sided P = 0.029).

      Conclusion:
      Pembrolizumab was associated with a clinically meaningful improvement in HRQoL compared with platinum-based chemotherapy. Combined with the superior PFS and OS and manageable safety profile, these data suggest pembrolizumab may be a new standard of care for first-line treatment of PD-L1–expressing advanced NSCLC.

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      PL04a.02 - OAK, a Randomized Ph III Study of Atezolizumab vs Docetaxel in Patients with Advanced NSCLC: Results from Subgroup Analyses (Abstract under Embargo until December 7, 7:00 CET) (ID 5822)

      08:45 - 09:40  |  Author(s): S.M. Gadgeel, F. Ciardiello, A. Rittmeyer, F. Barlesi, D. Cortinovis, C. Barrios, T. Hida, K. Park, D. Kowalski, M. Cobo Dols, J. Leach, J. Polikoff, C. Matheny, P. He, M. Kowanetz, D.S. Chen, D. Waterkamp, M. Ballinger, A. Sandler, D.R. Gandara, J. Von Pawel

      • Abstract
      • Presentation
      • Slides

      Background:
      Atezolizumab inhibits PD-L1 binding to its receptors PD-1 and B7.1, thereby restoring tumor-specific T-cell immunity. Primary analysis of the Phase III OAK study in previously-treated NSCLC revealed superior survival for atezolizumab vs docetaxel in the ITT population (mOS, 13.8 vs 9.6 months; HR, 0.73) and in patients expressing ≥1% PD-L1 on TC or IC (TC1/2/3 or IC1/2/3; mOS, 15.7 vs 10.3; HR, 0.74). Here we present further subgroup analyses.

      Methods:
      OAK evaluated atezolizumab vs docetaxel in an unselected NSCLC population who had failed prior platinum-containing chemotherapy. Patients were stratified by PD-L1 expression, prior chemotherapy regimens and histology, and randomized 1:1 to atezolizumab (1200 mg) or docetaxel (75 mg/m[2]) IV q3w. PD-L1 expression by IHC and mRNA was centrally evaluated by VENTANA SP142 IHC assay and Fluidigm, respectively. Data cutoff, July 7, 2016.

      Results:
      For the first 850 of 1225 randomized patients (primary study population), OS was improved with atezolizumab vs docetaxel regardless of histology and this benefit was observed across PD-L1 subgroups within each histology (Table). PD-L1 gene expression showed a similar association with OS as PD-L1 IHC. In nonsquamous patients ORR was 14.4% vs 15.2%; in squamous patients ORR was 11.6% vs 8.2% (atezolizumab vs docetaxel). OS benefit vs docetaxel was seen across subgroups including patients with treated baseline brain metastases (n=85; mOS 20.1 vs 11.9 mo; HR 0.54, 95% CI 0.63-0.89) and never smokers (n=156; mOS 16.3 vs 12.6 mo, HR 0.71, 95% CI 0.47-1.08). Further secondary endpoints and exploratory biomarker analyses for these subgroups and by age and EGFR/KRAS status will be presented.

      Conclusion:
      OAK demonstrated clinically relevant improvements with atezolizumab in the ITT population, including in both histology subgroups regardless of PD-L1 expression (measured by IHC or tumor gene expression), and among other subgroups including never smokers and in patients with baseline brain metastases.

      OS
      Atezolizumab Docetaxel HR[a]95% CI
      n Median, mo n Median, mo
      Nonsquamous
      TC3 or IC3 49 22.5 47 8.7 0.35(0.21-0.61)
      TC2/3 or IC2/3 89 18.7 99 11.3 0.61(0.42-0.88)
      TC1/2/3 or IC1/2/3 171 17.6 162 11.3 0.72(0.55-0.95)
      TC0 and IC0 140 14.0 150 11.2 0.75(0.57-1.00)
      All 313 15.6 315 11.2 0.73(0.60-0.89)
      Squamous
      TC3 or IC3 23 17.5 18 11.6 0.57(0.27-1.20)
      TC2/3 or IC2/3 40 10.4 37 9.7 0.76(0.45-1.29)
      TC1/2/3 or IC1/2/3 70 9.9 60 8.7 0.71(0.48-1.06)
      TC0 and IC0 40 7.6 49 7.1 0.82(0.51-1.32)
      All 112 8.9 110 7.7 0.73(0.54-0.98)
      [a]Unstratified HRs. TC=tumor cell, IC=tumor-infiltrating immune cell


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      PL04a.03 - Durvalumab in ≥3rd-Line Locally Advanced or Metastatic, EGFR/ALK Wild-Type NSCLC: Results from the Phase 2 ATLANTIC Study (Abstract under Embargo until December 7, 7:00 CET) (ID 5336)

      08:45 - 09:40  |  Author(s): M.C. Garassino, J.F. Vansteenkiste, J. Kim, H. Léna, J. Mazières, J. Powderly, P. Dennis, Y. Huang, C. Wadsworth, N. Rizvi

      • Abstract
      • Presentation
      • Slides

      Background:
      Treatment with anti-PD-1/PD-L1 antibodies has demonstrated meaningful clinical benefit in patients with advanced NSCLC. Patients that progress after 2 lines of chemotherapy have few treatment options and poor outcomes. Durvalumab is an engineered human IgG1 mAb targeting programmed cell death ligand-1 (PD-L1).

      Methods:
      ATLANTIC (NCT02087423) is a Phase 2, open-label, single-arm trial in patients with locally advanced or metastatic Stage IIIB–IV NSCLC (WHO PS 0 or 1; ≥2 prior systemic treatment regimens, including one platinum-based). There was no maximum number of prior treatments. The study initially enrolled all-comers and then was restricted to patients with PD-L1 high tumours (≥25% of tumour cells with membrane staining). The study includes three cohorts; here we report final results in Cohorts 2 and 3 that had EGFR/ALK wild-type or unknown status. Patients enrolled in Cohort 3 had ≥90% of tumour cells with PD-L1 staining. The primary endpoint is ORR (RECIST v1.1), based on independent central review. Secondary endpoints include DCR, DoR, PFS, OS, and safety (CTCAE v4.03).

      Results:
      As of 3 June 2016, in Cohorts 2/3, 265/68 patients (median age 62/61 years, 67/72% PS 1, 21/29% squamous histology; mean of 3.2/2.6 prior therapies) had received durvalumab (10 mg/kg i.v. q2w). Responses were durable; in Cohort 2, patients with PD-L1 ≥25%, the ORR was similar in patients with squamous and non-squamous histology.

      Cohort 2 Cohort 3
      PD-L1 high (≥25%) PD-L1 low/negative (<25%) PD-L1 ≥90%
      n=146 n=93 n=68
      ORR,* %(95%CI) 16.4(10.8-23.5) 7.5(3.1-14.9) 30.9(20.2-43.3)
      DCR, %(95%CI) 28.8(21.6-36.8) 20.4(12.8-30.1) 38.2(26.7-50.8)
      mDoR, months(25[th], 75[th] percentile) 12.3(7.5-NR) NR(7.2-NR) NR; 18/21 responders progression free at DCO
      n=149 n=94 n=67
      mPFS, months(95%CI) 3.3(1.9-3.7) 1.9(1.8-1.9) 2.4(1.8-5.5)
      mOS, months(95%CI) 10.9(8.6-13.6) 9.3(5.9-10.8) NR(5.9-NC)
      1-year OS, %(95%CI) 47.7(39.3-55.5) 34.5(25.0-44.1) 50.8(36.9-63.2)
      mFollow-up for OS, months 9.4 9.3 7.0
      *Confirmed response per independent central review. DCO=data cutoff; DCR=disease control rate (complete response, partial response or stable disease ≥24 weeks); DoR=duration of response; m=median; NC=not calculated; NR=not reached; ORR=objective response rate; OS=overall survival; PFS=progression-free survival
      Most AEs were low grade and resolved with treatment delay and/or immunosuppressive interventions. Overall, 10.2% of patients had Grade ≥3 treatment-related AEs and 2.7% had treatment-related AEs leading to discontinuation.

      Conclusion:
      Durvalumab was active and led to durable responses in a heavily pretreated metastatic NSCLC population; activity was numerically greater for patients whose tumours exceeded the 25% PD-L1 cutoff. The tolerability profile was manageable. Results are consistent with other anti-PD-1/PD-L1 therapies in metastatic, relapsed NSCLC and support further development of durvalumab.

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      PL04a.04 - Multicentric French Harmonization Study for PD-L1 IHC Testing in NSCLC (Abstract under Embargo until December 7, 7:00 CET) (ID 4910)

      08:45 - 09:40  |  Author(s): J. Adam, I. Rouquette, D. Damotte, C. Badoual, C. Danel, F. Damiola, F. Penault-Llorca, S. Lantuejoul

      • Abstract
      • Presentation
      • Slides

      Background:
      PD-L1 immunohistochemistry (IHC) is considered as a predictive biomarker for most anti PD-1/PDL-1 therapies in non-small cell lung cancer, but different assays were used in clinical trials. Several studies have compared 4 assays (22C3, 28-8, SP142, SP263) performed in central laboratories on dedicated platforms. In order to harmonise and make PD-L1 testing widely available on most IHC platforms and centers, we compared PD-L1 Dako (22C3, 28-8) and Ventana (SP263) assays and laboratory-developed tests (LDT).

      Methods:
      IHC with five anti-PD-L1 clones (28-8, 22C3, E1L3N, SP142 and SP263) was performed concomitantly on 41 NSCLC surgical specimens in 7 centers. The IHC platforms used were Ventana BenchMark Ultra (2 centers), Leica Bond (2 centers) or Dako Autostainer Link 48 (3 centers). For each matching platform, 22C3, 28.8 and SP263 assays were performed. For non-matching platforms and other antibodies, LDT were developed in each center and harmonised based on tonsil tissue staining. A total of 35 stainings were performed across different platforms and antibodies for each case. Seven thoracic pathologists trained to PD-L1 scoring in expert courses participated. Each pathologist analysed 6 cases and compared the stainings obtained with the 5 antibodies on all platforms. Tumor cell and immune cell D-L1 stainings were scored semi-quantitatively as recommended in PD-L1 Dako and Ventana assays. For statistical analysis, 1, 5, 25, 50% and 1, 5, 10% thresholds were used for tumor cells and immune cells, respectively.

      Results:
      28-8, 22C3 and SP263 assays were highly concordant for tumor cell and immune cell stainings across the 5 Dako or Ventana platforms (R2=0.886 to 0.953). LDT demonstrated various levels of concordance as compared to those 3 assays. Notably, LDT using SP263 clone were the most concordant across all platforms for both immune cell and tumor cell stainings, whereas some selected LDT with clones 28-8, 22C3 and E1L3N, but not SP142, showed a good correlation with the 3 assays regarding tumor cells only.

      Conclusion:
      28-8, 22C3 and SP263 assays gave comparable results across dedicated platforms for tumor cells staining, as well as some selected LDT protocols using 28-8, 22C3, SP263 and E1L3N clones. These results will be further validated at the national level in order to provide recommendations for the use of assays and LDT for PD-L1 testing in NSCLC.

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      PL04a.05 - Discussant for PL04a.01, PL04a.02, PL04a.03, PL04a.04 (ID 7158)

      08:45 - 09:40  |  Author(s): M. Boyer

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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