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Enriqueta Felip

Moderator of

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    PL01 - New Questions with Imaginative Answers (ID 88)

    • Event: WCLC 2019
    • Type: Plenary Session
    • Track: Advanced NSCLC
    • Presentations: 4
    • Now Available
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      PL01.01 - Tumor-Agnostic Biologically Driven Treatments: An Endless Dream? (Now Available) (ID 3580)

      08:15 - 09:45  |  Presenting Author(s): Robert C. Doebele

      • Abstract
      • Presentation
      • Slides

      Abstract

      The identification of several oncogenes in non-small cell lung cancer (NSCLC) along with the development of cognate, targeted tyrosine kinase inhibitors (TKIs) has revolutionized the treatment approach for patients with this disease. Several oncogene targets have been successfully deployed in other malignancies, including melanoma (BRAF), GIST (KIT), CML (BCR-ABL) and other malignancies. However, until recently, the conventional wisdom has said that targeted therapies will not have similar efficacy for the same class of oncogenes across different tumor histologies. This point of view was likely largely grounded in two perceptions: 1) certain oncogenes are heavily associated with certain tumor histologies (e.g., BCR-ABL in CML or EGFR in NSCLC) and 2) based on the differential activity of BRAF/MEK inhibition in melanoma compared to colorectal cancers (CRC) harboring BRAF V600E mutations. Since then, BRAF +/- MEK inhibition has demonstrated remarkable response rates in NSCLC, anaplastic thyroid cancer, and hairy cell leukemia suggesting that CRC may be the exception rather than the rule. In 2012, we identified the first NTRK1 fusion in NSCLC,1 and while prior reports of NTRK gene fusions existed,2 there were no therapies developed for this oncogene. Preclinical in vitro and in vivo models suggested that ATP-competitive inhibitors had activity irrespective of NTRK1/2/3 gene (TRKA/B/C kinases) and also irrespective of tumor histology.3 Clinical trial data with the two lead TRK inhibitors, larotrectinib4 and entrectinib,5 confirmed both of these preclinical findings of activity in NTRK1/2/3 across tumor histologies, validating the concept of tumor (or tissue) agnostic therapeutic strategies in cancer. Similar to NTRK gene fusions, ALK, ROS1 and RET gene fusions have not only been identified in NSCLC, but also in other tumor histologies. Clinical data suggest similar opportunities for these oncogene targets. For examples, entrectinib generated a robust and durable response in a patient with GOPC-ROS1 fusion melanoma6 and similar responses have been noted in ROS1 fusion IMT.7 Basket clinical trials of ROS1 inhibitors are now ongoing. RET gene fusions are targetable alterations in NSCLC as well as other malignancies, and now improved, highly RET-selective inhibitors under development with encouraging activity.8 NRG1 gene fusions represent another opportunity for a tumor agnostic development. Although first described in NSCLC (specifically, invasive mucinous adenocarcinomas),9 these novel fusion genes that signal via HER2/HER3 heterodimers have been described across numerous tumor types, including pancreatic, ovarian, and other cancers, albeit at a low estimated frequency of 0.2%.10 This low frequency is a common reason cited to not pursue such strategies, but given the immense heterogeneity of cancer it is likely that we will further fragment cancer types based on their underlying biology. Additional tumor agnostic targets include ALK gene fusions, HER2 mutations, EGFR mutations (including exon 20 insertions), FGFR1/2/3 fusions, BRAF fusions, MET (exon 14 skipping, gene amplification, and fusions), and others. Indeed, several KRAS mutant selective inhibitors are under development and may open the flood gates for tumor agnostic trials given the frequency of mutations in this oncogene. Success of tumor agnostic strategies will be dictated by appropriate biomarker selection, which may differ for each tumor types, robust testing methods that capture the majority of oncogenic variants (NRG1 is a good example that is not currently covered on many assays), and implementation of panel-based next generation sequencing applications in more routine practice. While it is likely that we already have the testing capability and even the appropriate drugs to to target these tumor agnostic oncogenes, infrastructure changes at institutions may need to be enacted to allow for clinical trial teams that enroll from many disease types, similar to existing phase I teams. The NSCLC community of oncologists, researchers, pathologists, patient advocates, and commercial partners has had immense success in realizing the dream of precision oncology strategies and can lead the way to distribute the knowledge gained over the last decade in precision oncology strategies.tumor agnostic.png

      References

      1. Vaishnavi A, Capelletti M, Le AT, et al: Oncogenic and drug-sensitive NTRK1 rearrangements in lung cancer. Nat Med 19:1469-1472, 2013

      2. Vaishnavi A, Le AT, Doebele RC: TRKing down an old oncogene in a new era of targeted therapy. Cancer Discov 5:25-34, 2015

      3. Doebele RC, Davis LE, Vaishnavi A, et al: An Oncogenic NTRK Fusion in a Patient with Soft-Tissue Sarcoma with Response to the Tropomyosin-Related Kinase Inhibitor LOXO-101. Cancer Discov 5:1049-57, 2015

      4. Drilon A, Laetsch TW, Kummar S, et al: Efficacy of Larotrectinib in TRK Fusion-Positive Cancers in Adults and Children. N Engl J Med 378:731-739, 2018

      5. Drilon A, Siena S, Ou SI, et al: Safety and Antitumor Activity of the Multitargeted Pan-TRK, ROS1, and ALK Inhibitor Entrectinib: Combined Results from Two Phase I Trials (ALKA-372-001 and STARTRK-1). Cancer Discov 7:400-409, 2017

      6. Couts KL, McCoach CE, Murphy D, et al: Acral Lentiginous Melanoma Harboring a ROS1 Gene Fusion With Clinical Response to Entrectinib. JCO Precision Oncology:1-7, 2017

      7. Lovly CM, Gupta A, Lipson D, et al: Inflammatory myofibroblastic tumors harbor multiple potentially actionable kinase fusions. Cancer Discov 4:889-95, 2014

      8. Subbiah V, Gainor JF, Rahal R, et al: Precision Targeted Therapy with BLU-667 for RET-Driven Cancers. Cancer Discov 8:836-849, 2018

      9. Fernandez-Cuesta L, Plenker D, Osada H, et al: CD74-NRG1 fusions in lung adenocarcinoma. Cancer Discov 4:415-22, 2014

      10. Jonna S, Feldman RA, Swensen J, et al: Detection of NRG1 Gene Fusions in Solid Tumors. Clin Cancer Res, 2019

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      PL01.02 - The Evolution of Tissue Testing for Immunotherapy - Where Next? (Now Available) (ID 3581)

      08:15 - 09:45  |  Presenting Author(s): Keith Kerr

      • Abstract
      • Presentation
      • Slides

      Abstract

      Biomarkers have, to date, had an uneasy relationship with immunotherapy in lung cancer, a conflict between the degree of biomarker expression (largely PD-L1) being related to treatment efficacy, and a desire to give these drugs to everyone, either as monotherapy or, increasingly, in combination with other drugs. PD-L1 immunohistochemistry (IHC) is well established as a companion or complementary diagnostic, depending on indication, and tumour mutational burden (TMB) is an item of interest, with a surrogate, MSI-high, approved by the FDA in a tumour-type agnostic setting for second/greater line therapy.

      Where is PD-L1 testing going?

      PD-L1 IHC will remain a useful test. PD-L1 IHC scoring in cytology-type samples has been validated outside clinical trials and will become accepted in daily practice. New IHC clones will challenge the place of existing ones, hopefully validated by comparative study and EQA. Data are emerging on the clinical validity of PD-L1 scoring on small amounts of tumour (the heterogeneity issue), how few cells can be used, and the clinical impact of scoring PD-L1 on insufficient material.

      Tumour Mutational Burden

      Difficulties with the PD-L1 IHC biomarker drove the search for alternatives and TMB, as a several times removed surrogate of tumour immunogenicity, emerged. The place for TMB in the diagnostic algorithm remains uncertain but clinical trials looking at tumour tissue or blood TMB continue to provide promising, if confusing, results. Many of the issues with PD-L1 IHC are also in play with TMB. There is no consensus about what is ‘high TMB’? TMB is another biological continuum, like PD-L1 expression, so the creation of a binary high vs low categorization potentially ignores relative biological significance of different levels. There is huge variability in the methodology used to derive or predict TMB, the amount of the genome screened, different definitions of a ‘mutation’, different next generation sequencing platforms, different contexts (tumour tissue vs blood) and a lack of published data on how these different TMB assessment approaches vary. Anecdotal reports so far indicate substantial variation.

      As a predictive biomarker in this setting, TMB works; it enriches a treatment group for benefit. But we have seen relatively little comparative data to suggest superiority over any other singular biomarker in this treatment area. TMB is a crude predictor of tumour neo-antigenicity and perhaps we should look to more specific measures of this aspect of sensitivity to immunotherapy. It is possible to predict probable neo-antigenicity from deep analysis of sequencing data. Neo-antigens should be clonal, rather than subclonal, to maximize their immune impact. Are their particular genes whose alteration would predict greater (or lesser) tumour ‘visbility’ to the immune system, be they involved in DNA repair, maintaining genome stability or integrity, antigen processing and presentation, or more likely to generate immunogenic proteins? Other factors such as loss of heterozygosity at MHC coding genes may also provide useful information.

      So, it may well be possible to refine our assessment of TMB into a more specific and meaningful metric. This then raises the question of whether it is practical to do so, and whether this provides clinically useful information.

      Tumour inflammation

      For immune checkpoint inhibitors (ICI) to work, a tumour specific immune response must be ‘available’ and somehow inhibited by the checkpoints being therapeutically targeted. Assessments of tumour inflammation, as a presumptive sign of such an available but inhibited immune response, have been successfully used to enrich a treatment group for benefit from ICI therapy. In lung cancer, these assessments of inflammation have been relatively complex assays of immune gene signature expression using mRNA extracted for fresh/frozen tumour tissue. Initially large panels of immune response-related genes have been reduced to single digit-sized panels. Interferon gamma seems to be important as is, unsurprisingly, PD-L1.

      The same questions arise with respect to immune gene signatures. Is this any better than a more simplistic approach such as PD-L1 IHC? Evidence is at best marginal, that it would be superior. Is this practical and affordable in a daily practice setting? Probably not. Are there alternative ways to derive the same information? Probably yes. In other tumour sites, a morphological assessment of tumour inflammation has been more keenly pursued than in lung cancer. This approach has tended to focus on the presence and location of the immune cell infiltrate and to some extent, on the nature of the infiltrating cells. When tumour sample area allows, immune cell activity at the tumour-stromal interface, and the presence of CD8-expressing T cells have been associated with better responses to ICI. There is much more that could be investigated, especially in relation to other immune-active or immune-suppressive cell types and their location within the tumour and its microenvironment (TME). Immunohistochemistry is readily available, but in order to understand the complexity of this process and find new biomarkers, in limited tissue samples, multiplex IHC and digital pathology analysis tools will almost certainly be required. These tools already exist but the challenge will be generating the data in relation to clinical response and then deployment in daily practice.

      Other regulation in the TME

      Other factors in the TME, such as tissue hypoxia and lactate dehydrogenase, are relevant biomarkers, indicating an immune-suppressive environment, and potential resistance to ICI therapy. Other factors like IDO, and other immune checkpoints like LAG3 and TIM3 may also confer resistance to current ICI therapy and provide new therapeutic targets.

      Conclusion

      There is much more to be learned about factors that regulate responsiveness to ICI therapy. The multifactorial complexity of the immune response suggests that combinations of biomarkers are more likely to provide better prediction of therapeutic benefit. Many of these factors are more likely to be continuous variables rather than binary metrics, and oncology will have to learn to deal with this situation, perhaps more akin to a complementary rather than a companion diagnostic, leading to more nuanced therapeutic decisions. It remains to be seen whether oncology, regulatory authorities or industry has an appetite for such an approach.

      References

      Blank CU et al. Science 2016;352,658

      Camidge DR et al. Nat Rev Clin Oncol 2019;16,341

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      PL01.03 - Will the Immunotherapy with Newer Biomarkers, Combination Therapy or New Technology Eventually Cure Lung Cancer? (Now Available) (ID 3582)

      08:15 - 09:45  |  Presenting Author(s): Tetsuya Mitsudomi

      • Abstract
      • Presentation
      • Slides

      Abstract

      The recent introduction of immune checkpoint therapy has greatly changed the clinical practice of non-small cell lung cancer (NSCLC). A battery of clinical trials showed the superiority of either PD-1 antibody monotherapy or PD-1/L1 antibody combined with chemotherapy as a first-line treatment of NSCLC over standard platinum doublet chemotherapy that has long been a standard of care. Hence, most if not all of NSCLC patients receive PD-1/L1 antibodies unless contraindicated due to coexisting immune-related comorbidities.

      The recent update of the Keynote-001 trial showed that 5-year survival of the high expressors of PD-L1 treated with pembrolizumab as a first-line treatment was 23%. Especially, the 5-year survival rate of patients who received the first-line pembrolizumab more than 2 years was 79%. This really indicates that at least some of the NSCLC patients may be cured by monotherapy of PD-1 antibodies.

      Conversely, about three fourth of patients, even with high expression of PD-L1 cannot survive for more than 5 years. This is natural considering the complexity of immunologic mechanisms against cancer. To be eliminated effectively by PD-1/L1 treatment, cancers should express their unique antigens typically generated by somatic mutations in the context of MHC. Therefore, the adequate quantity as well as the adequate quality of somatic mutations and intact antigen presentation, are prerequisite for immune response. When abnormal peptide is recognized by immune cells, adaptive expression of PD-L1 on the tumor cells occurs by secretion of interferon γ by T cells as a negative feedback that dampens antitumor immunity, Upon binding of PD-L1 with PD-1 on T cells downregulates T cell function. This tumor microenvironment (TME) is the best candidate for anti-PD-1/PD-L1 therapy. However, not all cancer has this TME. Besides PD-1/L1 systems, there are many other molecules such as CTLA4, TIGIT, TIM3, LAG3, etc. that negatively regulate the immune response. Regulatory T cells and myeloid-derived suppressor cells (MDSC) are also major players of immunosuppressive TME

      To overcome these immunologic evasions, many strategies are being extensively sought. To enhance immune recognition of mutations and to prime new response, polypeptide or RNA-based vaccines that contain mutation-derived epitopes are being tested. For tumor cells that lost HLA molecules, enhancement of NK cell activities through NKG2A antibody or anti KIR antibody may be effective. To overcome adaptive immune resistance by molecules other that PD-1, use of blocking antibodies against above-mentioned other co-inhibitory molecules or agonistic antibodies against co-stimulatory molecules such as ICOS, GITR, 4-1BB, OX40, etc. is a rational way. Finally, to reverse immune suppressive TME, use of antibodies against CSF-1R and CCR4 to suppress MDSC and regulatory T cells, respectively, may be effective. Antagonists for immunosuppressive molecules such as adenosine A2AR, IDO, TGFb, etc are also expected to enhance tumor immunity.

      Will the Immunotherapy eventually cure lung cancer? Currently, I have to say "Yes, for some but not sure for every patient". In this talk, I would like to discuss ongoing efforts to further improve outcomes of immune-therapy of lung cancer and future perspectives.

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      PL01.04 - Artificial Intelligence, Big Data and Lung Cancer: Ready to Implement? (Now Available) (ID 3583)

      08:15 - 09:45  |  Presenting Author(s): Hugo Aerts

      • Abstract
      • Presentation
      • Slides

      Abstract

      A critical barrier present in cancer research and treatment today is when and how to act based on the information provided from tumor data. One important reason for the slow progress in the fight against cancer, is the fact that cancer is a “moving target”. It is constantly evolving and diversifying, changing its phenotype, its genomic composition, and through metastatic spread, even its location. This is even more true when subjected to the pressure of therapeutic intervention, where cancer evolution rapidly explores and exploits resistance mechanisms, potentially even aided by the mutagenic nature of cancer treatments, leaving the treating oncologist chasing a constantly changing disease.

      Artificial Intelligence (AI) and Deep Learning technologies have recently led to revolutionary advances in areas ranging from computer vision to speech recognition - tasks that up to a few years ago could only be done by humans. AI has the potential to fundamentally alter the way medicine is practiced, as it excels in recognizing complex patterns in medical data and provides a quantitative, rather than qualitative, assessment of clinical conditions. AI-powered radiographic-biomarkers (“radiomics”) may quantify non-invasive information of the cancer phenotype that is clinically actionable, and may further improve diagnosis, characterization, and longitudinal tracking through therapy. AI methods are precise and allow specific quantification of features not otherwise quantifiable by human experts. Radiomic-analysis is performed on the entire tumor as compared to just a small sample for molecular analysis and provides a non-invasive window into internal growth pattern of the tumor (including internal textural heterogeneity, macroscopic necrosis, and viable tumor mass). Radiomics can thus quantify the phenotypic state of a tumor within its evolutionary process, thereby sidestepping issues relating to biopsies.

      This is particularly important for patients with cancer, where different cancer lesions can express different microenvironments that could ultimately lead to heterogeneous response patterns. Despite the remarkable success of novel cancer therapies, the clinical benefit remains limited to a subset. Cancer therapies are often expensive and could bring unnecessary toxicity, there is a direct need to identify beneficial patients, but this remains difficult in the clinic today. Radiomics biomarkers could provide this information on a lesion and patient level using standard-of-care CT scans. Unlike biopsy assays that - by definition - only represent a sample within the tumor, imaging can depict a full picture of the entire tumor burden, providing information of each cancer lesion within a single non-invasive examination.

      Another field that will be impacted by AI and big data is radiation oncology. Radiation oncology as a therapeutic specialty presents itself as an exemplary field that will be impacted by AI automation. Especially as much of the current radiation therapy work flow requires time-consuming, manual labor by both radiation oncologists and a team of medical staff including medical physicists, certified medical dosimetrists, and radiation therapists. The growing complexity of the human-machine and human-software interactions in conjunction with the increasing incidences of cancer have created a workforce shortage throughout the world. In fact, variations in the radiation treatment planning process can lead to significant differences in the quality of care, and negatively impact overall survival even in clinical settings where extra care is given to standardizing segmentation and planning approaches. Furthermore, the knowledge and experience gap between more developed and under-resourced health care environments poses an enormous public health challenge and represents one of the great global inequities in cancer care.

      In this talk, Dr. Aerts will discuss recent developments from his group and collaborators performing research at the intersection of artificial intelligence big data, and oncology. Also, he will discuss recent work of building a computational image analysis system to extract deep learning algorithms and use these to build radiomic signatures. The presentation will conclude with a discussion of future work on building integrative systems incorporating both molecular and phenotypic data to improve cancer therapies.

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Author of

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    MA03 - Clinomics and Genomics (ID 119)

    • Event: WCLC 2019
    • Type: Mini Oral Session
    • Track: Advanced NSCLC
    • Presentations: 1
    • Now Available
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      MA03.06 - Efficacy Results of Selective AXL Inhibitor Bemcentinib with Pembrolizumab Following Chemotherapy in Patients with NSCLC (Now Available) (ID 2271)

      10:30 - 12:00  |  Presenting Author(s): Enriqueta Felip

      • Abstract
      • Presentation
      • Slides

      Background

      The RTK AXL is implicated in epithelial-to-mesenchymal transition, negative regulation of anti-tumour immunity and resistance to multiple therapies including immune checkpoint inhibitors.

      Bemcentinib (BGB324) is a first-in-class, oral, highly selective and potent AXL inhibitor which has been demonstrated to enhance anti-PD1 therapy.

      Method

      This phase II trial (Cohort A, NCT03184571) enrolled 48 advanced lung adenocarcinoma patients with progression on or after no more than one prior line of platinum-based chemotherapy. Patients with EGFR/ALK mutations were included in this study and must have progressed on or after at least one standard targeted therapy. The primary endpoint was ORR according to RECIST v1.1. Additional endpoints included efficacy according to biomarker expression, DCR, PFS, OS, and safety. Tumour biopsies were analysed for PD-L1 expression (22C3 pharmDx), AXL by IHC, and infiltrating immune cells.

      Result

      As of April 2019, the trial was fully recruited: median age 65 (range 39-82) yrs, 61% male, 76% smokers or ex-smokers.

      At time of writing, a total of 210 treatment cycles had been completed by all patients. 17 patients were ongoing.

      17 of 32 biomarker-evaluable patients (53%) were PD-L1 negative, 13 (41%) had TPS 1-49%, and 2 (6%) had TPS >50%. Of 28 biomarker-evaluable patients, 14 (50%) expressed AXL on their tumours.

      Among patients who had at least 1 evaluable on-treatment scan: 5 responses were observed in 13 AXL positive patients (38%), and 7 in 30 patients with TPS 0-49% (23%). There were 10 responses observed among 34 evaluable patients overall (29%).

      In Stage 1, two of the 4 AXL positive responses are ongoing; mDoR is not mature in the AXL positive patients. mPFS was 5.9 mo in AXL positive patients (n=10, 3.0-NR) and 4.0 mo (95% CI 1.9-NR) overall (n=24). mOS was not mature.

      The most common TRAEs (occurring in >10% of patient in both stages) were transaminase increases (34%), asthenia/fatigue (30%), diarrhoea (26%), nausea (13%), anaemia (11%), decreased appetite (11%), and pruritus (11%). All cases of transaminase increase were reversible and resolved with concomitant administration of systemic corticosteroids and interruption of study treatments.

      Conclusion

      Patients had predominantly low or no PD-L1 expression; approximately half were AXL positive. The combination of bemcentinib and pembrolizumab was well tolerated and showed promising efficacy in previously treated IO-naïve NSCLC patients, particularly in those with AXL positive disease, including PD-L1 negative patients. Mature ORR for both stages, as well as 12-month OS for stage 1 will be presented at the meeting.

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    MA21 - Non EGFR/MET Targeted Therapies (ID 153)

    • Event: WCLC 2019
    • Type: Mini Oral Session
    • Track: Targeted Therapy
    • Presentations: 1
    • Now Available
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      MA21.03 - The International Association for the Study of Lung Cancer (IASLC) Global Survey on Molecular Testing in Lung Cancer (Now Available) (ID 1198)

      14:30 - 16:00  |  Author(s): Enriqueta Felip

      • Abstract
      • Presentation
      • Slides

      Background

      Evidence-based standards for molecular testing of lung cancer have been established, but the global frequency and practice of testing are not well understood. The IASLC conducted an international survey to evaluate current practice and barriers to molecular testing.

      Method

      Distributed to IASLC members and other healthcare professionals, content included: 7-question introduction, 32 questions for those requesting tests/treating patients, 45 questions on performing/interpreting assays, and 24 questions on tissue acquisition. All respondents were asked to provide 3-5 barriers to implementing/offering molecular testing.

      Respondents’ countries were grouped by geography or developing/developed using IASLC and World Bank criteria. Surveys were available in 7 languages. Regional comparisons used the Chi-squared test or ANOVA; free-text was analyzed with Nvivo.

      Result

      We obtained 2,537 responses from 102 countries. Respondents were 45% Medical Oncologists, 12% Pulmonologists, 12% Thoracic Surgeons, 9% Pathologists, and 22% scientists or other. 56% of responses were from developing countries, 44% developed. Regions included: 52% Asia, 19% Europe, 11% Latin America, 11% US/Canada, 7% Other.

      1683 (66%) chose the requesting/treating track (50% government, 42% academic, 8% other). 61% reported most patients in their country do not receive molecular testing, with the lowest rates in Latin America/Other (p<0.0001). 39% were not satisfied with the conditions of molecular testing in their country. Indications for requesting testing included: adenocarcinoma (89%), never-smoker (61%), female (57%), and young (54%) (variable by region, p<0.0001). 99% ordered EGFR, 95% ALK, 84% PDL1, 79% ROS1, all other tests <50%. 56% typically received results within 10 days. Only 67% were aware of CAP/IASLC/AMP guidelines, least frequently in Asia/Other (p=0.041). 37% have trouble understanding molecular testing result reports, most of whom cited a need for more technical and scientific knowledge. 75% had multidisciplinary tumor boards, but 23% met <1/month.

      The 316 (12%) testing track respondents were from laboratories that were 49% academic, 35% government, and 16% private/other. 94% of laboratories offered EGFR, 83% ALK, 69% KRAS, 68% BRAF, 64% ROS1, 56% HER2, and others <50%; 68% tested for PDL1. 57% offered Multiplex assays, less frequently in Latin America/Asia (p=0.0294). 69% tested blood-derived DNA, less frequently in US/Canada/Other (0.0013). 23% of respondents reported >10% of cases are rejected due to inadequate samples; however, 47% stated there is no policy or strategy to improve the quality of the tissue samples in their country. 52% reported patients/physicians are not satisfied with the state of molecular testing in their country. Respondents performing/interpreting assays (334, 14%) were typically informed of biopsy results (91%), and notified when the sample was inadequate (84%).

      The most frequent barrier to molecular testing in every region was cost, followed by quality/standards, turnaround-time, access, and awareness. After cost, time was the most common barrier in developed countries, while it was quality in developing countries. The second largest barrier was quality in Asia, access in Europe/Latin America/Other, and turn-around time in US/Canada.

      Conclusion

      These preliminary analyses show molecular testing usage varies across the globe. Barriers vary by region, and one-third of respondents were unaware of evidence-based guidelines. Global and regional strategies should be developed to address barriers.

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    MA22 - Partnering with Patients to Understand Stigma, Disparities and Values Leading to Improved Lung Cancer Care (ID 154)

    • Event: WCLC 2019
    • Type: Mini Oral Session
    • Track: Advocacy
    • Presentations: 1
    • Now Available
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      MA22.05 - Assessment of Gender Differences in the Psychosocial and Economic Impact on Patients with Stage IV Non-Small Cell Lung Cancer (Now Available) (ID 718)

      15:45 - 17:15  |  Author(s): Enriqueta Felip

      • Abstract
      • Presentation
      • Slides

      Background

      Incidence of lung cancer in women is rising overtime reporting evident gender-based differences in epidemiology, biology, and treatment outcome. However, little is known about gender-differences regarding psychological, economic and social aspects. The objectives of this prospective study are to evaluate the psychosocial and economic impact of metastatic non-small cell lung cancer (NSCLC), according to gender. Additionally, to assess the emotional burden and the economic impact of the disease on the primary caregiver from a gender perspective

      Method

      Multicenter, prospective, observational, study of two cohorts of patients with metastatic NSCLC (male and female) in Oncology departments of 20 Spanish hospitals. The following measurement tools were used: the APGAR questionnaire (family functionality: adaptability, partnership, growth, affection, and resolve), the Relationship impact scale, the DUKE-UNC scale (perceived socio-affective support), the patient and the caregiver economic impact scale and the Zarit scale (caregiver burden). All questionnaires were performed at the first visit, repeated 4 months later and following the first and second disease progression.

      Result

      Of the 333 pts included, 104 were females and 229 male, of whom 63% and 97%, respectively, were smokers/ex-smokers (p=0.0001). More women than men (85% vs 70%) had adenocarcinomas . The median overall survival was longer in women but did not reach statistical significance [17.1 vs 11.0 months, HR 0.732 (95% CI 0.534 to 1.005), p=0.0524]. Most families considered themselves functional (high score in APGAR questionnaire) with no changes in their partner relationship and social support was evaluated as optimal for majority of patients. Around a quarter of interviewed patients said their economic situation was a little worse after the lung cancer diagnosis, without remarkable differences by gender. Statistically significant differences were found between both groups regarding the caregiver´s relationship to the patient (more parents were the caregiver in females than in males) (p <0.0001) and the caregiver’s employment situation (more employed caregivers in females) (p<0.0001). Most caregivers of both sexes considered that taking care of their relative did not pose a significant burden. No remarkable differences by gender were found between the different variables across the study.

      Conclusion

      This study provides a preliminary insight into gender-related characteristics in the management of advanced NSCLC and its impact on the emotional, social and economic burden of patients and their caregivers, and recall the high priority of researching in cancer from a gender perspective

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    OA04 - Immuno Combinations and the Role of TMB (ID 126)

    • Event: WCLC 2019
    • Type: Oral Session
    • Track: Immuno-oncology
    • Presentations: 2
    • Now Available
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      OA04.02 - CheckMate 817: First-Line Nivolumab + Ipilimumab in Patients with ECOG PS 2 and Other Special Populations with Advanced NSCLC (Now Available) (ID 1876)

      15:15 - 16:45  |  Author(s): Enriqueta Felip

      • Abstract
      • Presentation
      • Slides

      Background

      Data are limited for immunotherapy in patients with advanced NSCLC and poor performance status or other comorbidities. CheckMate 817 is a multi-cohort, open-label phase 3b/4 study investigating safety and efficacy of flat-dose nivolumab plus weight-based low-dose ipilimumab in advanced NSCLC. Here we evaluate this regimen as first-line treatment in special populations (cohort A1) and a reference population (cohort A; previously reported).

      Method

      Patients had previously untreated advanced NSCLC. Cohort A1 (n=198) had ECOG PS 2 or ECOG PS 0–1 with 1 of: asymptomatic untreated brain metastases, hepatic or renal impairment, or HIV. Cohort A (n=391) had ECOG PS 0–1. Patients with known EGFR mutations or ALK translocations sensitive to available targeted therapy were excluded from both cohorts. Nivolumab 240 mg Q2W plus ipilimumab 1 mg/kg Q6W was administered for two years or until disease progression/unacceptable toxicity. Safety and efficacy endpoints were assessed; cohort A1 analyses were exploratory.

      Result

      Cohort A1 patients were grouped as: ECOG PS 2 (n=139) and all other special populations (AOSP; n=59). Baseline characteristics were generally balanced between cohorts. Rates of grade 3–4 treatment-related adverse events (TRAEs) were similar between cohorts; within cohort A1, grade 3–4 TRAEs were numerically higher in AOSP versus the ECOG PS 2 subgroup; TRAEs leading to discontinuation were similar across populations (Table). ORR was 25% in cohort A1 (patients with ECOG PS 2, 20%; AOSP, 37%) and 35% in cohort A. PFS was numerically shorter in cohort A1 than cohort A; high TMB (≥10 mut/Mb) and higher PD-L1 expression (≥1% or ≥50%) were associated with numerically longer PFS in both cohorts (Table).

      table_v3.jpg

      Conclusion

      First-line flat-dose nivolumab plus weight-based ipilimumab showed a consistent safety profile in special populations with advanced NSCLC, including those with ECOG PS 2. Patients with either high TMB or higher tumor PD-L1 expression appeared to exhibit improved efficacy.

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      OA04.06 - Evaluation of TMB in KEYNOTE-189: Pembrolizumab Plus Chemotherapy vs Placebo Plus Chemotherapy for Nonsquamous NSCLC (Now Available) (ID 1936)

      15:15 - 16:45  |  Author(s): Enriqueta Felip

      • Abstract
      • Presentation
      • Slides

      Background

      First-line pembrolizumab plus chemotherapy with pemetrexed and platinum significantly improved OS (HR 0.49, P < .001), PFS (HR 0.52, P < .001) and ORR (47.6% vs 18.9%, P < .001) vs placebo plus chemotherapy with pemetrexed and platinum for metastatic nonsquamous NSCLC in the double-blind phase 3 KEYNOTE-189 study (NCT02578680); benefit was observed in all analyzed subgroups, including PD-L1 TPS <1%, 1-49%, and ≥50%. We explored the association of TMB with efficacy in KEYNOTE-189.

      Method

      616 patients were randomized 2:1 to pembrolizumab plus chemotherapy or placebo plus chemotherapy. TMB was determined by whole-exome sequencing of tumor and matched normal DNA. Association of TMB (continuous log10 transformed) with outcomes in each arm was assessed using Cox proportional hazards models (OS, PFS) and logistic regression (ORR); statistical significance was determined at the 0.05 level without multiplicity adjustment. The clinical utility of TMB on outcomes was assessed using prespecified TMB cutpoints of 175 and 150 Mut/exome (~13 and ~10 Mut/Mb by FoundationOne CDx). Data cutoff was 21 Sep 2018.

      Result

      293 (48.3%) treated patients had evaluable TMB data: 207 for pembrolizumab plus chemotherapy, 86 for placebo plus chemotherapy. Baseline characteristics and outcomes were generally similar in the TMB-evaluable and total populations. TMB as a continuous variable was not significantly associated with OS, PFS, or ORR for pembrolizumab plus chemotherapy (one-sided P = .174, .075 and .072, respectively) or placebo plus chemotherapy (two-sided P = .856, .055 and .434, respectively). Pembrolizumab plus chemotherapy improved OS, PFS, and ORR for TMB ≥175 and <175 (Table). Results were similar for TMB ≥150 and <150.

      Conclusion

      TMB was not significantly associated with efficacy of pembrolizumab plus chemotherapy or placebo plus chemotherapy as first-line therapy for metastatic nonsquamous NSCLC. Pembrolizumab plus chemotherapy had a similar OS benefit in the TMB-high and low subgroups.

      TMB ≥175 TMB <175

      Pembrolizumab plus Chemotherapy

      n = 100

      Placebo plus Chemotherapy

      n = 34

      Pembrolizumab plus Chemotherapy

      n = 107

      Placebo plus Chemotherapy

      n = 52
      Median OS (95% CI), mo 23.5
      (20.2-NE)
      13.5
      (7.0-NE)
      20.2
      (15.8-NE)
      9.9
      (7.4-19.1)
      HR (95% CI) 0.64 (0.38-1.07) 0.64 (0.42-0.97)
      Median PFS (95% CI), mo 9.2
      (7.6-14.0)
      4.7
      (4.0-5.5)
      9.0
      (6.7-11.1)
      4.8
      (4.5-6.6)
      HR (95% CI) 0.32 (0.21-0.51) 0.51 (0.35-0.74)
      ORR, % (95% CI) 50.0
      (39.8-60.2)
      11.8
      (3.3-27.5)
      40.2
      (30.8-50.1)
      19.2
      (9.6-32.5)

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    OA14 - Update of Phase 3 Trials and the Role of HPD (ID 148)

    • Event: WCLC 2019
    • Type: Oral Session
    • Track: Immuno-oncology
    • Presentations: 1
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      OA14.04 - Five-Year Outcomes From the Randomized, Phase 3 Trials CheckMate 017/057: Nivolumab vs Docetaxel in Previously Treated NSCLC (ID 894)

      11:30 - 13:00  |  Author(s): Enriqueta Felip

      • Abstract
      • Slides

      Background

      Historically, outcomes for advanced non-small cell lung cancer (NSCLC) have been poor, with 5-year survival rates < 5% with conventional chemotherapy. Nivolumab, a programmed death-1 (PD-1) inhibitor, was approved in 2015 for patients with previously treated advanced NSCLC based on two randomized phase 3 trials, CheckMate 017 (NCT01642004; squamous) and CheckMate 057 (NCT01673867; non-squamous), which demonstrated improved overall survival (OS) vs docetaxel. We report 5-year pooled efficacy and safety from these trials, representing the longest survival follow-up for randomized phase 3 trials of an immune checkpoint inhibitor in advanced NSCLC.

      Method

      Patients (N = 854; CheckMate 017/057 pooled) with advanced NSCLC, ECOG performance status (PS) ≤ 1, and progression during or after first-line platinum-based chemotherapy, were randomized 1:1 to nivolumab 3 mg/kg Q2W or docetaxel 75 mg/m2 Q3W until progression or unacceptable toxicity. After completion of the primary analyses, patients in the docetaxel arm no longer receiving benefit could cross over to receive nivolumab. OS was the primary endpoint for both studies.

      Result

      At 5-year follow-up, 50 nivolumab patients and 9 docetaxel patients were alive. Baseline characteristics of 5-year survivors in both arms were similar to the overall population and patients who survived < 1 year, except for a higher percentage of patients with ECOG PS 0 or tumor programmed death ligand-1 (PD-L1) expression ≥ 1% on nivolumab and ECOG PS 0 and Stage IIIB NSCLC on docetaxel. Nivolumab continued to show long-term OS and progression-free survival (PFS) benefit vs docetaxel with 5-year OS rates 13% vs 3% (HR, 0.68 [95% CI, 0.59–0.78]) and PFS rates 8% vs 0% (0.79 [0.68–0.92]). OS benefit with nivolumab vs docetaxel was observed across subgroups including patients with tumor PD-L1 expression < 1%, baseline liver and adrenal metastases, neutrophil-to-lymphocyte ratio < median, lactate dehydrogenase ≥ upper limit of normal or no baseline proton-pump inhibitor use. Among patients with an objective response to nivolumab (20%) or docetaxel (11%), 32% remained in response at 5 years vs none on docetaxel, with a median duration of response of 19.9 vs 5.6 months, respectively. Of the 5-year nivolumab vs docetaxel survivors, 36% vs 0% were on study drug, 20% vs 67% received subsequent immunotherapy (on or off study), and 10% vs 0% were off study drug, progression free, with no subsequent therapy. No new safety signals were observed with longer follow-up. Between 3 and 5 years’ follow-up, 8 of the 31 (26%) nivolumab-treated patients reported a treatment-related adverse event, 1 (3%) grade 3–4. The most common select adverse events (events with a potential immunological cause) were related to skin, in 4 (13%) patients, none of which were grade 3–4.

      Conclusion

      CheckMate 017 and 057 are the first phase 3 trials to report 5-year outcomes for a PD-1 inhibitor in previously treated advanced NSCLC, demonstrating a greater than 4-fold increase in 5-year OS rates with nivolumab (13%) over docetaxel (3%). Nivolumab remained well tolerated with no new safety signals.

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    OC01 - Opening Ceremony (ID 82)

    • Event: WCLC 2019
    • Type: Opening Ceremony
    • Track:
    • Presentations: 2
    • Now Available
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      OC01.01 - Welcome Addresses (Now Available) (ID 3551)

      19:00 - 20:30  |  Presenting Author(s): Enriqueta Felip

      • Abstract
      • Presentation

      Abstract not provided

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      OC01.03 - Conference Presidents Announce New Things at WCLC 2019 (Now Available) (ID 3554)

      19:00 - 20:30  |  Presenting Author(s): Enriqueta Felip

      • Abstract
      • Presentation

      Abstract not provided

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    P1.01 - Advanced NSCLC (ID 158)

    • Event: WCLC 2019
    • Type: Poster Viewing in the Exhibit Hall
    • Track: Advanced NSCLC
    • Presentations: 5
    • Now Available
    • Moderators:
    • Coordinates: 9/08/2019, 09:45 - 18:00, Exhibit Hall
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      P1.01-107 - KEYNOTE-495/KeyImPaCT: Phase 2 Biomarker-Directed Study of Pembrolizumab-Based Therapy for Non–Small Cell Lung Cancer (ID 1355)

      09:45 - 18:00  |  Author(s): Enriqueta Felip

      • Abstract

      Background

      Immune checkpoint–based therapy has revolutionized the care of patients with non–small cell lung cancer (NSCLC). Pembrolizumab-based combination therapy aims to improve clinical outcomes over pembrolizumab monotherapy. Identification of biomarkers associated with improved response to different combination therapies may improve overall outcomes and yield a more precise approach to the use of immunotherapies in NSCLC. To test the clinical usefulness of a biomarker-informed, pembrolizumab-based combination therapy, this phase 2 KEYNOTE-495 trial (NCT03516981) will be carried out in patients with treatment-naive, advanced NSCLC.

      Method

      KEYNOTE-495 is a randomized, multicenter, open-label, phase 2 trial. Tumor tissue from patients with treatment-naive, advanced NSCLC will be initially screened for 2 validated, independent, next-generation biomarkers: T cell–inflamed gene expression profile (GEP) and tumor mutational burden (TMB). Based on the results of this biomarker screening, patients will be assigned to 1 of 4 groups: TMBlowGEPlow, TMBhighGEPlow, TMBlowGEPhigh, and TMBhighGEPhigh. Within each group, patients will be randomly assigned to receive pembrolizumab combined with MK-4280 (anti–LAG-3), lenvatinib, or MK-1308 (anti–CTLA-4). This is a group-sequential, adaptive randomization trial. Patients will be randomly assigned to MK-4280 or lenvatinib first, after which MK-1308 will be introduced; randomization has been modified to accommodate the delayed introduction of MK-1308. Response will be assessed by tumor imaging every 9 weeks for the first year, then every 12 weeks thereafter using RECIST v1.1. Treatment will continue for 35 cycles (~2 years). Patients in the pembrolizumab + lenvatinib arm who complete 35 treatments may continue with lenvatinib monotherapy until disease progression or toxicity. After a patient experiences disease progression or starts new anticancer therapy, the patient will be followed up and contacted every 12 weeks until death, withdrawal of consent, or study end, whichever occurs first. Safety will be monitored throughout the study and for 30 days after treatment or before initiation of a new anticancer treatment, whichever occurs first. Treatment arms may be terminated during the interim analysis because of safety, prespecified futility criteria, or both. The primary end point is investigator-assessed objective response rate (RECIST v1.1). Secondary end points are progression-free survival, overall survival, and safety. Recruitment and screening are ongoing in more than 14 countries and will continue until ~288 patients are randomly assigned across the biomarker-defined groups to determine the optimal treatment for each subgroup.

      Result

      Section not applicable

      Conclusion

      Section not applicable

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      P1.01-111 - ATEZO-BRAIN, A Single-Arm Phase II Study of Atezolizumab Combined with Chemotherapy in Stage IV NSCLC Patients with Untreated Brain Metastases (ID 733)

      09:45 - 18:00  |  Author(s): Enriqueta Felip

      • Abstract
      • Slides

      Background

      Brain metastases (BM) are a frequent complication in non-small cell lung cancer (NSCLC), have significant impact on quality of life and are associated with poor prognosis. Systemic therapies might be an alternative approach to whole brain radiotherapy (WBRT) to avoid cognitive-related adverse events. Immune checkpoint inhibitors (ICI) showed intracranial activity in advanced NSCLC patients with BM. However clinical data about efficacy and safety of immune checkpoint inhibitors in combination with chemotherapy in patients with untreated BM are limited and further research in this setting is needed. We hypothesize that addition of ICI to conventional platinum-based chemotherapy may increase intracranial tumor response and provide clinically relevant benefit in terms of PFS, OS and quality of life to the patients with asymptomatic and non-previously treated BM.

      Method

      This is an ongoing multicenter, open-label, single-arm phase 2 study (EUDRACT: 2017-005154-11) to evaluate the efficacy and safety of atezolizumab 1200 mg combined with 4-6 cycles of carboplatin AUC 5 and pemetrexed 500mg/m2 every 3 weeks followed by maintenance with atezolizumab 1200 mg plus pemetrexed 500mg/m2 every 3 weeks in stage IV non-squamous NSCLC patients with untreated synchronous BM. Patients should have multiple and measurable BM, adequate performance status and organic function, do not harbor EGFR or ALK genomic alterations, be treatment naïve and do not have any contraindication to receive immunotherapy. Exclusion criteria consist of active neurological symptoms, dexamethasone dose ≥ 4 mg QD, prior treatment with brain radiotherapy, presence of leptomeningeal carcinomatosis, spinal or hemorrhagic metastases in the central nervous system. Primary endpoints are progression-free survival (PFS) at 12 weeks according to RANO-BM and RECIST v1.1 criteria and safety based on CTCAE v4. Both primary endpoints will be assessed in 40 patients in 15 sites using a Bayesian approach. Patients will undergo tumor assessments by body CT scan and brain MRI at baseline every 6 weeks for the first 12 weeks and thereafter tumor assessments will be performed every 9 weeks until disease progression or loss of clinical benefit. Secondary endpoints: intracranial and systemic objective response rate and duration of response. Exploratory endpoints: to assess neurocognitive function and quality of life; to determine time to neurological deterioration and time to need of salvage brain radiotherapy. Enrollment started on August 2018 and currently 12 patients have been included in the study.

      Result

      Clinical trial in progress

      Conclusion

      Clinical trial in progress

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      P1.01-133 - Randomized Open-Label Study of Bintrafusp Alfa (M7824) vs Pembrolizumab in Patients with PD-L1 Expressing Advanced 1L NSCLC (Now Available) (ID 741)

      09:45 - 18:00  |  Author(s): Enriqueta Felip

      • Abstract
      • Slides

      Background

      Transforming growth factor β (TGF- β) promotes tumor progression via immune- and non–immune-related processes. Bintrafusp alfa* (M7824) is an innovative first-in-class bifunctional fusion protein composed of 2 extracellular domains of TGF-βRII (a TGF-β “trap”) fused to a human IgG1 monoclonal antibody against PD-L1. Targeting these independent and complementary pathways may restore and enhance antitumor responses. An expansion cohort of the NCT02517398 study of patients with advanced NSCLC (n=80) treated with bintrafusp alfa in the second-line setting presented at ESMO 2018 showed an objective response rate of 86% in the subgroup with high PD-L1 tumor expression at the recommended phase 2 dose (1200 mg intravenously [IV] every 2 weeks [Q2W]). Observed data support the hypothesis that bintrafusp alfa may be superior to other PD-(L)1 inhibitors, including pembrolizumab, for the treatment of NSCLC. Based on the promising antitumor activity and manageable safety profile, this study will evaluate bintrafusp alfa treatment in patients with advanced NSCLC in the 1L setting.

      Method

      Here we present a global, randomized trial comparing bintrafusp alfa vs pembrolizumab in the 1L treatment of patients with metastatic NSCLC with high PD-L1 expression levels. Patients in this study must have a histologically confirmed diagnosis of advanced NSCLC with high PD-L1 expression on tumor cells (defined as either ≥80% by the Dako 73-10 pharmDx kit or ≥50% by the Dako 22C3 pharmDx kit since both assays are expected to select a similar patient population at their respective cut-offs). ECOG performance status must be 0 or 1. Patients must not have received prior systemic treatment for advanced NSCLC. Patients with tumors with actionable mutations (for which targeted therapy is locally approved) are not eligible. Patients will receive 1200 mg Q2W or pembrolizumab 200 mg Q3W as an IV infusion until confirmed disease progression, unacceptable toxicity, or trial withdrawal. Dual primary endpoints are progression-free survival and best overall response; key secondary endpoints include overall survival, duration of response, and safety. Estimated enrollment is 300 patients. Clinical trial information: NCT03631706. *Proposed INN.

      © 2019 American Society of Clinical Oncology, Inc. Reused with permission. This abstract was accepted and previously presented at the 2019 ASCO-SITC Clinical Immuno-Oncology Meeting. All rights reserved.

      Result

      Section not applicable

      Conclusion

      Section not applicable

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      P1.01-72 - A Phase II Study of Selective AXL Inhibitor Bemcentinib and Pembrolizumab in Patients with NSCLC Refractory to Anti-PD(L)1 (ID 1632)

      09:45 - 18:00  |  Author(s): Enriqueta Felip

      • Abstract

      Background

      The RTK AXL is implicated in epithelial-to-mesenchymal transition, negative regulation of anti-tumour immunity and resistance to multiple therapies including immune checkpoint inhibitors.

      Bemcentinib (BGB324) is a first-in-class, oral, highly selective and potent AXL inhibitor which has been demonstrated to enhance anti-PD1 therapy.

      The combination of bemcentinib and pembrolizumab was well tolerated and showed promising efficacy in previously treated IO-naïve NSCLC patients (Cohort A, NCT03184571), particularly in those with AXL positive disease, including PD-L1 negative patients.

      The novel combination is now being assessed in patients refractory to anti-PD-(L)1 therapy, considering the emerging need in this population and AXL’s role as a mediator of resistance.

      Method

      This is an open-label, single-arm, 2-stage phase II study (Cohort B, NCT03184571) to evaluate the safety and efficacy of bemcentinib (200mg/d) in combination with pembrolizumab (200mg/q3wk) in patients post anti-PD-(L)1 therapy. The primary endpoint is overall response rate (ORR), and additional endpoints include efficacy by biomarker expression, duration of response (DoR), disease control rate (DCR), progression free survival (PFS), overall survival (OS), and safety. Clinical efficacy endpoints are based on tumour imaging evaluable by RECIST v1.1.

      Eligible patients received a maximum of 2 prior lines of therapy, with the most recent course having included a PD-(L)1 inhibitor. To be eligible, patients must have exhibited disease control (CR/PR/SD) for at least 6 months on prior PD-(L)1 inhibitor therapy with disease progression occurring within 12 weeks since last dose.

      Bemcentinib will be administered as a loading dose of 400mg on days 1, 2 and 3 followed by a dose of 200mg once daily. A fixed dose of 200 mg pembrolizumab will be given by intravenous infusion over 30 minutes every 3 weeks. Bemcentinib and pembrolizumab will be given until disease progression, unacceptable dose toxicity, or for a maximum of 35 cycles.

      Tumour specimens will be analysed for PD-L1 expression (22C3 pharmDx), AXL by IHC, and infiltrating immune cells.

      The pre-specified efficacy threshold for continuation into the second stage is 1 objective response among the first 13 patients, at which point up to a further 16 patients may be evaluated, for a total of 29 patients.

      Result

      Section not applicable

      Conclusion

      Section not applicable

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      P1.01-84 - Interaction of Lorlatinib with CYP2B6, CYP2C9, UGT, and P-gp Probe Drugs in Patients with Advanced Non-Small Cell Lung Cancer (ID 293)

      09:45 - 18:00  |  Author(s): Enriqueta Felip

      • Abstract
      • Slides

      Background

      Lorlatinib is a small-molecule anaplastic lymphoma kinase (ALK) inhibitor approved for treatment of patients with ALK-positive advanced non-small cell lung cancer (NSCLC). Because lorlatinib is an inducer and inhibitor of various cytochrome P450 (CYP) enzymes and transporters, an evaluation of its effect on these substrates at steady state is warranted. A drug-drug interaction (DDI) sub-study was conducted in patients with advanced NSCLC to evaluate the net effect of these interactions.

      Method

      Probe drugs utilized included bupropion for CYP2B6, tolbutamide for CYP2C9, acetaminophen for uridine 5'-diphospho-glucuronosyltransferase (UDP-glucuronosyltransferase, UGT), and fexofenadine for P-glycoprotein-1 (P-gp). Thirty-two patients (to have at least 6 evaluable patients per probe drug) were administered a single dose of a probe drug alone on Day −2 to determine plasma exposure of the probe drug alone. Starting on Cycle 1 Day 1, patients began lorlatinib tablets 100 mg daily. On Cycle 1 Day 15, another single dose of the same probe drug was administered concurrently with lorlatinib.

      Result

      Co-administration of lorlatinib 100 mg with bupropion, a sensitive CYP2B6 probe drug, decreased bupropion geometric mean plasma AUCinf and Cmax by 25% and 27%, respectively. For tolbutamide, a sensitive CYP2C9 probe drug, lorlatinib decreased tolbutamide AUCinf and Cmax by 43% and 15%, respectively. Likewise, for acetaminophen, a sensitive UGT substrate, lorlatinib decreased acetaminophen AUCinf and Cmax by 45% and 28%, respectively. Finally, for fexofenadine, a sensitive P-gp substrate, lorlatinib decreased fexofenadine AUCinf and Cmax by 67% and 63%, respectively.

      Conclusion

      Critical steady-state–based DDI evaluations can be conducted in patients with cancer in carefully designed studies. Per FDA guidance, strong, moderate, and weak inducers are drugs that decrease the AUC of sensitive index substrates by ≥80%, ≥50% to <80%, and ≥20% to <50%, respectively. Based on these criteria, lorlatinib behaved as a net weak inducer of CYP2B6, CYP2C9, and UGT; and a net moderate inducer of P-gp. The results of this sub-study can help guide recommendations for dose modifications when lorlatinib is given concomitantly with drugs that are metabolized by these enzymes or transporters. Based on the current results, only drugs that are P-gp substrates of narrow therapeutic index may require dose adjustments when used concomitantly with lorlatinib.

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    P1.03 - Biology (ID 161)

    • Event: WCLC 2019
    • Type: Poster Viewing in the Exhibit Hall
    • Track: Biology
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/08/2019, 09:45 - 18:00, Exhibit Hall
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      P1.03-26 - Genetic and Molecular Profiling of Non-Smoking Related Lung Adenocarcinomas (ID 1701)

      09:45 - 18:00  |  Author(s): Enriqueta Felip

      • Abstract
      • Slides

      Background

      The etiology and many details of the genomic profile and molecular basis of lung adenocarcinomas (LuADs) in nonsmoker patients remain elusive. Further, the scarcity of primary cultures available from non-smoking related lung adenocarcinomas (NSK-LuADs) contributes to hamper our biological understanding of these tumors.

      Method

      We established patient-derived cancer cell (PDCs) cultures from NSK-LuADs, and performed whole exome sequencing (WES) and RNA sequencing (RNA-seq) analysis to delineate their genomic architecture. For validations, we analyzed independent cohorts of LuADs.

      Result

      The analysis revealed non-smoker related alterations such as those at the growth factor receptors RET, ALK, EGFR and ERBB2. There were also mutations affecting signal transduction molecules such as AKT1, BRAF and KRAS, and mutations in tumor suppressor genes, including TP53, CDKN2A, RB1, ARID1A, ATM and STK11. We also identified new fusions and recurrent mutations in some genes, one of them, a possible regulator of gene expression, affecting ten percent of the LuADs, thus constituting a potentially relevant tumor suppressor gene. We also report a predominance of RB1-inactivation, mostly complex intragenic rearrangements (homozygous deletions or duplications) in EGFR-mutant tumors. Three EGFR-/RB1-mutant tumors, treated with EGFR-TKIs, and one EGFR-wild type tumor, treated with standard chemotherapy, developed small cell lung cancer and/or squamous cell carcinoma transformation, evident in the re-biopsies and/or PDCs. Finally, we found pathogenic germ-line mutations at genes associated to familiar-cancer syndromes, especially the TP53-associated Li Fraumeni syndrome, affecting ten percent of EGFR-mutant LuADs patients, underscoring a genetic predisposition origin for a subset of NSK-LuADs.

      Conclusion

      The recurrent gene inactivation found in candidate gene in LuADs heralds a tumor suppressor role which deserves further exploration. The pre-existent inactivation of RB1 predominates in EGFR-mutant tumors and may underlie an extremely ductile nature, albeit additional gene alterations are required to overcome sensitivity to the TKIs. Given their potential clinical and therapeutic implications, testing for RB1-alterations and for the Li-Fraumeni syndrome in EGFR-mutant LuADs patients may need to be incorporated in the clinical settings.

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    P1.16 - Treatment in the Real World - Support, Survivorship, Systems Research (ID 186)

    • Event: WCLC 2019
    • Type: Poster Viewing in the Exhibit Hall
    • Track: Treatment in the Real World - Support, Survivorship, Systems Research
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/08/2019, 09:45 - 18:00, Exhibit Hall
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      P1.16-05 - Incidence and Outcome of Multiple Primary Cancers (MPC) in a Series of Lung Cancer (LC) Patients (ID 1030)

      09:45 - 18:00  |  Author(s): Enriqueta Felip

      • Abstract
      • Slides

      Background

      The number of cancer survivors has increased as a result of significant progress in prevention, diagnosis and treatment of malignant tumors. The risk of developing a second neoplasm, after treatment of an initial primary cancer, is increasing and indeed lung cancer represents a commonly diagnosed second primary malignancy. This study investigates the co-occurrence of MPC among patients (p) diagnosed with lung cancer (LC).

      Method

      Review of clinical data of all consecutive patients with histologically confirmed LC visited at our institution between October 2017 and August 2018

      Result

      Out of 1386 p with LC, two primary cancers occurred in 206 cases (15%), including 41 p (3%) with three primary cancers. Patients with MPC were predominantly males (67%), smokers (88%), statin users (40%) and 28% had known family history. Second cancer was detected in a routine follow-up in 62%, whereas 27% were symptomatic patients. Median age at the first tumor diagnosis was 61 years (27-85). LC occurred as first neoplasm in 34% of the cases, as subsequent neoplasm in 41% and as two consecutive primary neoplasm in 25%. The most common primary cancer was LC in 34%, followed by breast (16%), colorectal (15%), prostate (9%), bladder (8%) and head and neck (6%). Treatment received for the first cancer included surgery in 80%, chemotherapy in 47% and radiotherapy in 32%. As a second tumor LC represented 41%, followed by bladder (19%), colorectal (10%), prostate (9%) and breast (7%). Surgery was performed in 70% of the cases with a second cancer. Regarding only patients with LC as two primary tumours (first and second tumour), 25 pts (89%) were not metastatic at second tumour, surgery was performed in 82% and 7 pts (24%) developed a third tumour. Overall, median time of diagnosis between the first and the second neoplasm was 4.2 years (CI95% 3.2-5.2), without significant differences if primary tumor was LC or another neoplasm (p=0.82). Smoking was associated with a shorter time of the second neoplasm diagnosis (3.8 years vs 7.9 years for non-smokers, p=0.09), whereas taking statins exhibited longer time of diagnosis of the second neoplasm (5.1 vs 3.3 year, p=0.05). With a median follow up of 7.3 years after diagnosis of the first neoplasm, the 5-year survival rate was 97.2% (94.8-99.7%).

      Conclusion

      In our series, the frequency of the MPC co-occurrence among LC p is 15%, indicating that surveillance strategies are recommended. Many p are treated with curative intent. Moreover, smoking and taking statins influences the time interval between tumors

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    P2.01 - Advanced NSCLC (ID 159)

    • Event: WCLC 2019
    • Type: Poster Viewing in the Exhibit Hall
    • Track: Advanced NSCLC
    • Presentations: 3
    • Now Available
    • Moderators:
    • Coordinates: 9/09/2019, 10:15 - 18:15, Exhibit Hall
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      P2.01-10 - Real Clinical Practice Study to Evaluate 2 Line Treatment Based on Comprenhensive Genomic Profiling in NSCLC. LungONE Study (Now Available) (ID 1558)

      10:15 - 18:15  |  Author(s): Enriqueta Felip

      • Abstract
      • Slides

      Background

      Cancer is a genomic disease and molecular-targeted therapy plays an increasingly important role in the treatment of advanced NSCLC. The current standard of care (SoC) indication for NSCLC is defined by genomic biomarkers to classify the tumor as a carrier of a therapeutic approved target. However, the current standard of practice for molecular testing in NSCLC in Spain is highly heterogeneous, depending on several factors such as hospital size, resources, laboratory equipment and experience. In addition, there are several other markers and/or genomic signatures which are not determined due to the current lack of scientific evidence, i.e. MSI, TMB, KRAS, BRAF, RET, MET, HER2 and NTKR, which could guide physician second line treatment choice, including clinical trial options. The aim of this study is to evaluate the impact on decision making in the 2nd line treatment using a comprehensive genomic profiling (CGP) in advanced/metastatic NSCLC with adenocarcinoma histology.

      Method

      Section not applicable

      Result

      Section not applicable

      Conclusion

      This is a multicenter, prospective, single-cohort study to describe the clinical management of the 2nd line SoC treatment in patients with locally advanced/metastatic NSCLC with adenocarcinoma histology, when a comprehensive genomic profile based on FoundationOne®CDx or FoundationOne® Liquid test, is provided. 12 academic institutions in Spain were selected and 180 patients were planned to be recruited. The principal objective is to evaluate if there is any change in planned 2nd line treatment decisions after receiving the CGP report. Secondary objectives for this study are:1) to identify non-previously detected actionable molecular aberrations by conventional molecular assays; 2) to evaluate the economic impact in terms of use of healthcare resources of the CGP vs. standard diagnostic panels; and 3) to describe each patient’s status 2 years after the inclusion of the last patient in the study. Patients will follow usual clinical pathways for biomarker analysis and a comprehensive genomic profiling in the remaining tissue through FoundationOne® CDx, will be conducted or liquid biopsy with FoundationOne® Liquid, if exhausted. To be enrolled in the study, patients must have an ECOG between 0 and 2 and biomarkers ALK, EGFR, ROS1 must have been assayed (negative or unknown results). Enrolment begun on October 2018 and, to date, a total of 110 patients have been included.

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      P2.01-12 - A Phase I/II Trial of IO102 and Pembrolizumab With/Without Chemotherapy as First-line Treatment of Metastatic NSCLC (ID 706)

      10:15 - 18:15  |  Author(s): Enriqueta Felip

      • Abstract
      • Slides

      Background

      Immunotherapy has significantly changed the treatment landscape of non-small cell lung cancer (NSCLC) with no driver mutations. However, despite the addition of anti-PD-1/PD-L1 therapies to the clinical armamentarium only a subset of patients derives durable benefit. IO102 is a novel, second generation, HLA-A unrestricted immune modulating T-win® vaccine targeting IDO. IO102 has a dual mode of action; remodulation of the tumour micro-environment through elimination of immune suppressive cells, and induction of CD8 T-cell mediated killing of IDO-expressing tumor cells. Our first-generation IDO vaccine (IO101) has shown promising antitumor activity and a favorable safety in heavily pretreated NSCLC patients (Iversen, CCR 2013).

      Method

      Phase I/II, international, multicenter, open-label, randomized trial with two parallel cohorts. Cohort A: IO102 (100µg s.c.) and pembrolizumab (200 mg) (PD-L1 ≥ 50%); Cohort B: IO102, pembrolizumab and carboplatin plus pemetrexed (PD-L1 < 50%). The maximum treatment duration is 35 cycles (app. 2 years). Key eligibility criteria include metastatic NSCLC or non-squamous NSCLC (cohort B) with no prior treatment for metastatic NSCLC and no driver mutations.

      Phase I is a non-randomized safety run-in with 6 patients per cohort investigating one dose level of the experimental arms. Only one DLT is allowed in each cohort. Phase II is following Sargent’s two-stage, three-outcome optimum design (Sargent, ClinTrial2001) with a 2:1 randomization in the cohorts. Cohort A: IO102 and pembrolizumab versus pembrolizumab alone; Cohort B: IO102, pembrolizumab and chemotherapy vs. pembrolizumab and chemotherapy. Provision of blood and tumour tissue is required for biomarker studies.

      The primary endpoint is safety and objective response rate (ORR) per RECIST 1.1 in Phases I and II, respectively. Secondary endpoints include ORR per iRECIST, duration of response, progression free survival, overall survival, and biomarkers including immunoscore in tissue, tumour mutational burden and immunomonitoring in blood.

      The study is enrolling in Europe. First patient was entered in September 2018 and recruitment is expected to continue throughout 2019: EudraCT Number 2018-000139-28 / IND Number: 018081.

      Result

      Section not applicable

      Conclusion

      Section not applicable

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      P2.01-17 - CANOPY-1: Phase 3 Study of Canakinumab/Placebo+Pembrolizumab+Platinum-Chemotherapy in Untreated Stage IIIB-IV NSCLC Pts (ID 1209)

      10:15 - 18:15  |  Presenting Author(s): Enriqueta Felip

      • Abstract

      Background

      Interleukin-1β (IL-1β) inhibition with canakinumab reduced the incidence of and mortality due to lung cancer among patients with atherosclerosis in CANTOS trial. Inhibition of IL-1β driven inflammation may lead to a tumor microenvironment more susceptible to anti-PD-(L)1 therapies. Recent studies have shown that low levels of CRP at baseline or decreased levels over time correlated with improved responses to anti-PD-(L)1 agents, providing rationale for combination of canakinumab and Pembrolizumab (PEM).

      Method

      CANOPY-1 (NCT03631199) is a double-blind, randomized, placebo (Pb)-controlled, phase III trial to determine efficacy and safety of PEM + platinum-based chemotherapy (Ctx) ± canakinumab in untreated stage IIIB/IIIC-IV squamous and non-squamous NSCLC pts. It is a 2 part study- In Part 1 [open-label safety run-in with 3 cohorts of ~9 pts each to confirm recommended phase 3 canakinumab regimen], pts will receive canakinumab 200 mg s.c (Q3W) + PEM 200 mg i.v (Q3W) + platinum-based Ctx [Cohort A (non-squamous), carboplatin (CBCDA) + pemetrexed (PTX); Cohort B (non-squamous), cisplatin + PTX; Cohort C (squamous or non-squamous), CBCDA + paclitaxel]. In Part 2 [with ~600 pts) to evaluate efficacy and safety of canakinumab combination], pts will be randomized to receive canakinumab/Pb + PEM + platinum-based Ctx (non-squamous, CBCDA or cisplatin + PTX; squamous, CBCDA + paclitaxel or nab-paclitaxel). PEM and platinum-based Ctx will be administered at their approved doses. Randomization (1:1) will be stratified by PD-L1 status, region and histology. In both parts, pts will receive 4 cycles of induction therapy (canakinumab/Pb + PEM + Ctx) followed by maintenance therapy (PEM + canakinumab/Pb +/- PTX) until progressive disease. Primary objectives: confirm recommended phase 3 regimen for canakinumab combination (Part 1), compare PFS and OS between treatment arms (Part 2). Secondary objectives (Part 1 and 2): ORR, DCR, safety, PK and DOR.

      Result

      Section not applicable

      Conclusion

      Section not applicable

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    P2.18 - Treatment of Locoregional Disease - NSCLC (ID 191)

    • Event: WCLC 2019
    • Type: Poster Viewing in the Exhibit Hall
    • Track: Treatment of Locoregional Disease - NSCLC
    • Presentations: 1
    • Now Available
    • Moderators:
    • Coordinates: 9/09/2019, 10:15 - 18:15, Exhibit Hall
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      P2.18-01 - A Multicenter, Double-Blind, Randomized, Controlled Study of Bintrafusp Alfa (M7824) in Unresectable Stage III NSCLC (Now Available) (ID 2200)

      10:15 - 18:15  |  Author(s): Enriqueta Felip

      • Abstract
      • Slides

      Background

      The TGF-β pathway promotes tumor immunosuppression, and its inhibition may enhance the antitumor activity of PD-(L)1 monoclonal antibodies and reduce radiation-induced lung fibrosis. Bintrafusp alfa is an innovative first-in-class bifunctional fusion protein composed of the extracellular domain of TGF-βRII (a TGF-β “trap”) fused to a human IgG1 mAb blocking PD-L1. In a phase 1 study, second-line bintrafusp alfa therapy demonstrated promising antitumor activity in advanced non-small cell lung cancer (NSCLC) (NCT02517398). In preclinical studies, bintrafusp alfa plus radiotherapy showed enhanced antitumor activity compared with radiotherapy alone in mouse models. This study is evaluating the efficacy and safety of bintrafusp alfa with concurrent chemoradiation (cCRT) followed by bintrafusp alfa vs cCRT plus placebo followed by durvalumab in patients with unresectable stage III NSCLC.

      Method

      This global, multicenter, double-blind, randomized, controlled study of bintrafusp alfa (NCT03840902) includes adults with histologically documented stage III locally advanced, unresectable NSCLC, ECOG performance status ≤1, adequate pulmonary function, and life expectancy ≥12 weeks. Patients with tumors with actionable mutations (EGFR, ALK translocation, ROS-1 rearrangement) are also eligible. Mixed small cell lung cancer and NSCLC histology; pleural effusions greater than minimal, exudative, or cytologically positive; significant acute or chronic infections; prior chemotherapy or immune checkpoint inhibitor therapy for NSCLC; and current use of immunosuppressive medication are exclusion criteria. Patients are randomized to receive either bintrafusp alfa 1200 mg IV every 2 weeks (Q2W) with cCRT for 6 weeks followed by bintrafusp alfa 1200 mg IV Q2W (arm A) or placebo with cCRT for 6 weeks followed by durvalumab 10 mg/kg IV Q2W (arm B) until confirmed disease progression, unacceptable toxicity, or treatment ≤1 year. The primary endpoint is progression-free survival; secondary endpoints include overall survival, safety, lung function assessment, objective response, duration of response, pharmacokinetics, and immunogenicity. This phase 2 trial was activated on April 2, 2019 and first patient in is anticipated for May 22, 2019. Target enrollment: 350 patients.

      Result

      Section not applicable

      Conclusion

      Section not applicable

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    PL04 - Food for Thought in the Management of Thoracic Malignancies (ID 91)

    • Event: WCLC 2019
    • Type: Plenary Session
    • Track: Advanced NSCLC
    • Presentations: 1
    • Now Available
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      PL04.01 - Epidemiology and Clinical Characteristics of Lung Cancer in Women (Now Available) (ID 3595)

      16:15 - 17:00  |  Presenting Author(s): Enriqueta Felip

      • Abstract
      • Presentation
      • Slides

      Abstract

      "Non applicable"

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    PR02 - Press Conference (ID 387)

    • Event: WCLC 2019
    • Type: Press Conference
    • Track: Immuno-oncology
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/08/2019, 09:45 - 10:30, CC7.1 A&B
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      PR02.01 - Summary of Day's Plenary (ID 4071)

      09:45 - 10:30  |  Presenting Author(s): Enriqueta Felip

      • Abstract

      Abstract not provided

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    WS06 - Women in Thoracic Oncology Networking Event (ID 355)

    • Event: WCLC 2019
    • Type: Workshop
    • Track: Thymoma/Other Thoracic Malignancies
    • Presentations: 3
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      WS06.01 - Welcome (ID 3828)

      07:00 - 08:00  |  Presenting Author(s): Enriqueta Felip

      • Abstract

      Abstract not provided

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      WS06.02 - Lessons Learned – Women Leaders in Thoracic Oncology (ID 3829)

      07:00 - 08:00  |  Presenting Author(s): Enriqueta Felip

      • Abstract
      • Slides

      Abstract not provided

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      WS06.04 - Networking Table 2: How to Negotiate Successfully (ID 4066)

      07:00 - 08:00  |  Presenting Author(s): Enriqueta Felip

      • Abstract

      Abstract not provided