International Meeting onLung Cancer · International Meeting on Lung Cancer International Meeting on Lung Cancer 11 SATURDAY, OCTOBER 24 09.00-10.00 SESSION V: NEWS FROM THE KINOME

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Congress & Event Planning2-4, Kastriotou str.

P.O.11476, Athens - Greece Τ +30 210 7294559

E [email protected] www.eventema.gr

InternationalMeetingonLungCancerOctober 23-242020

Divani Palace AcropolisAthens - G R E E C E

Organized by Under the auspices of

International Meeting on Lung Cancer International Meeting on Lung Cancer

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WELCOME LETTERDear colleagues, Dear friends,

As you know, the Covid-19 pandemic has affected all aspects of public life, including scientific activity in the field of Medicine in general and Oncology in particular, creating problems in scientific encounter and exchange of scientific views. In these difficult conditions, going “against” the adverse environment, we considered that it would be very important to have a closer contact between the scientific community in Greece and abroad in the field of Thoracic Oncology and so it was decided to organize this meeting on Developments in Biology and Treatment of Thoracic Malignancies.

This event falls within a general effort to mobilize Greek Scientists who live and work abroad dealing with Thoracic Tumors both researchers and clinicians. We believe that such an effort could only have positive results from the simple acquaintance and recording of our strengths to the human and comradely contact, the prospects for the development of research collabora-tions and, of course, the training of young scientists in European centers of excellence. We know that this effort will be difficult, but the positive response of that idea from our colleagues creates real optimism and encourages us to continue to achieve this goal.

This event on the subject of Thoracic Oncology also aims to be the basis for the creation of a general Network of scientists working abroad and in Greece and to highlight the possibilities of common interest and goals and collaborations both at clinical and laboratory level.

For this purpose, the structure of the program has been decided to include a small number of tutorial lectures and mainly to devote time to presenting the research interests and projects of the participants, both in the form of results and in the form of the basic design of the research program.

Within the grounds of the 1st International Meeting on Lung Cancer, we wish to welcome you and warmly thank you for your support.

T h e O r g a n i z i n g & S c i e n t i f i c C o m m i t t e e

P. Christopoulos

MD, PhD, Hematologist - Medical Oncologist,Thoraxklinik and National Center for

Tumor Diseases, Heidelberg University Hospital, Germany

N. Karachaliou

MD, PhD, Medical Director, Global Clinical Development,

Merck Healthcare KGaA, Darmstadt, Germany

M. Rovithi

Medical Oncologist, Agios Nikolaos General

Hospital, Crete, Greece

V. Georgoulias

MD, Emeritus Professor of Medical Oncology,School of Medicine, University of Crete,

Greece

D. Papadatos - Pastos

MRCP(UK), PhD, Consultant in Medical OncologyLung Cancer and Acute Oncology UniversityCollege London Hospitals and The Princess

Alexandra Hospital, UK

F. Dimitrakopoulos

MD, PhD, Medical Oncologist, Division of Oncology & Molecular Oncology Laboratory,

Department of Medicine, University of Patras,Greece

I. Mountzios

ΜD, MSc, PhD, Medical Oncologist,2nd Oncology Department and

Clinical Trials Unit, Henry DunantHospital Center, Athens, Greece


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ORGANIZING COMMITTEEP. Christopoulos (DE)

I. Mountzios (GR)

SCIENTIFIC COMMITTEEF.I. Dimitrakopoulos (GR)

V. Georgoulias (GR)

N. Karachaliou (DE)

D. Papadatos-Pastos (UK)

M. Rovithi (GR)


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FRIDAY, OCTOBER 2308.45-09.00 Welcome Address and Meeting Perspectives V. Georgoulias (GR)

09.00-10.20 SESSION I: BIOLOGICAL FUNDAMENTALS FROM BASICS TO CLINICS Chairs: E. Lianidou (GR), A. Klinakis (GR)

09.00-09.20 Heterogeneity, clonality and tumor evolution: Clinical implications I. Mountzios (GR) 09.20-09.40 Recent update on Liquid biopsy applications in lung cancer E. Lianidou (GR) 09.40-10.00 Current and future perspectives of ctDNA in NSCLC F. Papageorgiou (GR) 10.00-10.20 Beyond PD-L1: Biomarkers of immunotherapy efficacy M. Tsiatas (GR)

10.20-10.35 C o f f e e b r e a k

10.35-11.50 Oral Presentations (1) Chairs: E. Lianidou (GR), M. Tsiatas (GR)

01-1 10.35-10.50 Preliminary results on the molecular heterogeneity P. Makrythanasis - A. Voutsina (GR) from a cohort of early stage NSCLC by NGS 01-2 10.50-11.05 Preliminary results of liquid biopsy in early stage NSCLC patients A. Markou (GR) 01-3 11.05-11.20 Phenotypic characterization and clinical relevance of G. Kallergi (GR) Circulating Tumor Cells in NSCLC 01-4 11.20-11.35 Small extracellular vesicles in pre-therapy plasma predict clinical E.K. Vetsika (GR) outcome in non-small cell lung cancer patients 11.35-11.50 General Discussion

11.50-12.20 C o f f e e B r e a k

12.20-13.20 SESSION II: IMMUNOTHERAPY (I) Combinations and Resistance Chairs: A. Kotsakis (GR), M. Rovithi (GR)

12.20-12.40 Chemo-immunotherapy is feasible for all patients with NSCLC G. Lazaridis (GR) in the first line setting? 12.40-13.00 Immunotherapy in oncogene-addicted lung cancer N. Pistamaltzian (GR)* *Satellite lecture by 13.00-13.20 Immunotherapy Combo strategies D. Papadatos-Pastos (UK)

13.20-15.05 Oral Presentations (2) Chairs: A. Kotsakis (GR), N. Pistamaltzian (GR)

02-1 13.20-13.35 Biomarkers in NSCLC- taking into account tumor heterogeneity Ι. Pateras (GR) 02-2 13.35-13.50 Proteomic screening of bronchoscopic biopsies-on-chip for improved M. Tsoumakidou (GR) prediction of anti-PD-1 responses in real-time 02-3 13.50-14.05 Association of the Advanced Lung Cancer Inflammation Index (ALI score) I. Mountzios (GR) with Immune Checkpoint Inhibitor Outcomes in Patients with Advanced Non-Small Cell Lung Cancer 02-4 14.05-14.20 B-PREIMMUNE (Blood derived pre-immune platform) project Α. Xagara (GR)


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02-5 14.20-14.35 Discovery and quantitative measurement of biomarkers in Μ. Toki (GR) Tumor Microenvironment 14.35-14.50 Expanded tumor profiling to predict IO benefit in NSCLC P. Christopoulos (DE) 14.50-15.05 General Discussion

15.05-15.35 L i g h t L u n c h

15.35-16.15 SESSION III: IMMUNOTHERAPY (II) Chairs: S. Baka (GR), G. Oikonomopoulos (GR)

15.35-15.55 Patients relapsing after 1st line chemo-IO: and now what? F. Koinis (GR) 15.55-16.15 Resistance mechanism of immunotherapy: the role of T cells P. Verginis (GR)

16.15-17.00 Oral Presentations (3)

16.15-16.30 Resistance to immune checkpoint inhibitors. Is methylation D. Papadatos-Pastos (UK) the answer? 03-1 16.30-16.45 Delineating the complexity, heterogeneity and functional diversification M. Tsoumakidou (GR) of lung cancer antigen presenting cells to uncover novel immunotherapeutic targets 03-2 16.45-17.00 Efficacy of an hTERT vaccine in NSCLC with immunologically K. Kosmatopoulos (FR) cold tumors

17.00-17.30 C o f f e e B r e a k

17.30-18.45 SESSION IV: NEWS FROM THE KINOME (I) Chairs: P. Kosmidis (GR), I. Mountzios (GR)

17.30-17.55 EGFR mutant lung cancer: Treatment strategies after failure of N. Karachaliou (DE) 3rd generation EGFR-TKIs 17.55-18.20 ALK positive lung cancer: choosing the optimal sequence P. Christopoulos (DE) 18.20-18.45 KRAS mutant lung cancer: light at the end of the tunnel? F. Skoulidis (US)


O4-1, 2 18.45-19.00 Defining molecular risk in ALK+ and EGFR+ NSCLC P. Christopoulos (DE) O4-3 19.00-19.15 NF-κB & NSCLC: clinical perspectives F.I. Dimitrakopoulos (GR) O4-4 19.15-19.30 CD200/CD200R Immune Checkpoint in Lung Cancer I. Vathiotis (GR) 19.30-19.45 General Discussion

19.45-20.15 Invited Lecture Chairs: V. Georgoulias (GR), K. Syrigos (GR)

19.45-20.15 Mechanisms of resistance to checkpoint inhibitors and V. Papadimitrakopoulou (UΚ) targeting alternative pathways


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SATURDAY, OCTOBER 2409.00-10.00 SESSION V: NEWS FROM THE KINOME (II) Chair: J. Remon (ES), F.Ι. Dimitrakopoulos (GR)

09.00-09.20 Upcoming new targets M. Rovithi (GR) 09.20-09.40 Kinase signaling networks in SCLC A. Agbarya (ISR) 09.40-10.00 When EGFR is not alone P. Tsantoulis (CH)


O5-1 10.00-10.15 Phosphoproteomics and functional genomics to investigate resistance A. Georgiou (UK) mechanisms to targeted therapies O5-2 10.15-10.30 Inhibition of SHP2 increases response to MET inhibitors in tumors with L. Pudelko (DE) MET amplification or MET exon 14 skipping mutations O5-3 10.30-10.45 The role of YAP signaling in KRAS driven non-small cell lung cancer M. Keil (DE) O5-4 10.45-11.00 Gene expression profile of size-based enriched circulating tumor cells A. Ntzifa (GR) reveals a dynamic role of EMT and PD-L1 during osimertinib treatment in EGFR-mutant NSCLC patients 11.00-11.15 Panel Discussion

11.15-11.45 C o f f e e B r e a k

11.45-12.35 Special Lectures (I) Chairs: V. Georgoulias (GR), N. Karachaliou (DE)

11.45-12.10 Overview of early phase clinical research with a focus on A. Patrikidou (UK) thoracic oncology 12.10-12.35 Lung cancer evolution and its clinical implications Μ. Jamal-Hanjani (UK)

12.35-13.50 Special Lectures (II) Chairs: P. Christopoulos (DE), D. Papadatos-Pastos (UK)

12.35-12.55 Impact of COVID-19 crisis in UK lung cancer services: G. Geropoulos (UK) The UCLH experience 12.55-13.15 Robotic assisted thoracic surgery (RATS) - The UCLH experience G. Panagiotopoulos (UK) 13.15-13.35 Segmentectomy for the indeterminate lung lesion G. Sotiropoulos (UK) 13.35-13.50 General Discussion

13.50-15.10 Satellite Lectures Chairs: A. Kotsakis (GR), A. Patrikidou (UK)

13.50-14.10 The clinical development of the MET inhibitor Tepotinib Ν. Κarachaliou (DE) 14.10-14.30 Synergies and collaboration are essential to the battle against Α. Somarakis (GR) Lung Cancer. The «Lung Ambition Alliance» project 14.30-14.50 The dual inhibition of checkpoint inhibitors in 1st line NSCLC I. Mountzios (GR) *Satellite lecture by


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14.50-15.10 Mobocertinib (TAK-788): covering the unmet needs of NSCLC patients E. Mantouvalou (GR) with EGFR Exon 20 insertion mutations

15.10-16.00 L i g h t L u n c h

16.00-18.00 SESSION VΙ: Small Cell lung Cancer and other Thoracic Malignancies Chairs: I. Mountzios (GR), Α. Christopoulou (GR)

16.00-16.20 Immunotherapy in SCLC: Future strategies to improve outcome Η. Linardou (GR) 16.20-16.40 Implementation of targeted therapies and immunotherapy in J. Remon (ES) the treatment of thymic malignancies 16.40-17.00 Inherited genetic mutations and polymorphisms in D. Oluf Roe (NO) malignant mesothelioma: comprehensive review 17.00-17.20 Pathogenesis of Malignant Pleural Effusion I. Kalomenidis (GR) 17.20-17.40 Therapeutic advances in the treatment of mesothelioma I. Metaxas (CH) 17.40-18.00 Panel Discussion

18.00-18.20 General Discussion for Future Perspectives and Closing Remarks

ABSTRACTSΟ1-1 PRELIMINARY RESULTS OF EARLY STAGE NON-SMALL CELL LUNG CANCER HETEROGENEITY BASED ON THE TUMORAL GENETIC PROFILING

Α. Voutsina1, P. Makrythanasis1, I. Vamvakaris2, K. Potaris3, I.S. Pateras4, E. Patsea5, Z. Kanaki1, A. Klinakis1, V. Georgoulias6, A. Kotsakis7

1Biomedical Research Foundation of the Academy of Athens, Athens, Greece; 2Department of Pathology and 3Department of Thoracic Surgery, Athens Chest Hospital “Sotiria”, Athens, Greece; 4Department of Histology and Embryology, Medical School, National and Kapodistrian University of Athens, Athens, Greece; 5Department of Pathology, Metropolitan General Hospital of Athens, Cholargos, Greece; 6Hellenic Oncology Research Group (HORG), Athens, Greece, 7Department of Medical Oncology, University General Hospital of Larisa, Greece.

Early-stage Non-Small Cell Lung Cancer (NSCLC) has been found to harbor extensive genetic Intra-Tumor Heterogeneity (gITH) for somatic mutations which underlie the evolution and adaptation of cancer cells.

Accordingly, treatment decisions based on the analysis of single tumor region often meet drug resistance and limited thera-peutic benefit.

The assessment gITH involves the accurate detection of somatic Single Nucleotide Variants (SNVs) unmasking a more ac-curate genomic landscape of the tumor.

In this study we aimed to investigate the gITH among different subtypes of early-stage NSCLC, including 24 adenocarcinomas, 28 squamous cell carcinomas and 8 other less common histologies.

We performed two-region sampling (periphery and core) per surgically excised tumor and analyzed somatic mutations in 58 cancer driver genes across 60 treatment naïve patients. We used hybrid capture-based next generation deep sequencing (2000× on average) to identify somatic mutations in each sector and compared the identified variants. Τhe preliminary results of the analysis will be presented during the meeting.

O1-2 PRELIMINARY RESULTS OF LIQUID BIOPSY IN EARLY STAGE NSCLC PATIENTS

A. Markou1, D. Stergiopoulou1, D. Londra1, Α. Voutsina2, ΑP. Makrythanasis2, K. Potaris3, I. Vamvakaris3, V. Georgoulias4, A. Kotsakis5, E. Lianidou1

1Analysis of Circulating Tumor Cells, Lab of Analytical Chemistry, Department of Chemistry, University of Athens, 15771 Athens, Greece 2Biomedical Re-search Foundation of the Academy of Athens, Athens, Greece 3Department of Thoracic Surgery and Department of Pathology, “Sotiria” General Hospital, Athens, Greece 4First Department of Medical Oncology, IASO General Hospital of Athens, Greece 5Department of Medical Oncology, University General Hospital of Larissa, Thessaly, Greece

Lung cancer is the most common cause of cancer-related mortality worldwide. Definitive treatment of NSCLC is possible only in early stages where surgical excision of the tumor can be oncologically radical. However, even after complete primary tumor resection, about 45% of early stage NSCLC patients develop local or distant recurrence within 8-18 months. These distant metastases arise from single migratory tumor cells that, detached from the primary tumor, survive in the circulation and, finally, colonize distant target tissue.

In the present study by analysing consecutive peripheral blood samples from 56 operated early stage NSCLC patients, we aim to stratify patients in high and low risk to develop metastasis. Tumour samples were analyzed by Next Generation Sequencing (NGS) using a panel of genes in order to define differences of the molecular profile of tumor cells. We further monitored the presence of KRAS and PIK3CA mutations detected in the primary tumor, in ctDNA (at pre-defined time points both before the


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surgical excision of the primary tumor, during the post-op follow-up period and at the time of disease progression) using ARMS-HRMA tests and Droplet Digital PCR (ddPCR) technology. Finally we compared the results of liquid biopsy with the results of NGS in tissue biopsy in order to identify the blood-based marker combination with the highest sensitivity and specificity for detection high-risk NSCLC patients. Here we report the preliminary data regarding the detection of ctDNA in association with the probability of disease recurrence and the patients’ survival.

O1-3 PHENOTYPIC CHARACTERIZATION AND CLINICAL RELEVANCE OF CIRCULATING TUMOR CELLS IN NSCLC

Spyridoula D. Katsarou1, Ippokratis Messaritakis2, Anastasia Voumvouraki1, Α. Κotsaki3,4, Saad Alkahtani1, , Christos. Stouraras1, Stuart S. Martin6, Vassilis Georgoulias4, Galatea Kallergi1,7

1Department of Biochemistry, Medical School, University of Crete Heraklion, Greece 2Laboratory of Tumor Cell Biology, Medical School, University of Crete, Heraklion, Greece 3Department of Medical Oncology, University General Hospital ofLarisa, Mertzoulo Larisa, Greec 4Hellenic Oncology Research Group (HORG) 5Department of Zoology, Science College, King Saud University, Riyadh, Saudi Arabia 6Marlene and Stewart Greenebaum Comprehensive Cancer Center, University of Maryland, School of Medicine, Department of Physiology, 655 W. Baltimore Street, Baltimore, Maryland. USA 7Division of Genetics, Cell and Developmental Biology, Department of Biology, University of Patras, Patras, Greece

Introduction: Vimentin (VIM) expression in CTCs is a poor prognostic factor for breast cancer patients. Furthermore, upregu-lation of alpha-Tubulin (TUB) and Detyrosinated tubulin (GLU) in CTCs is related to patients’ outcome. In the current study, we evaluated TUB, GLU and VIM in NSCLC cell lines and patients’ CTCs.

Methods: Four NSCLC cell lines (H460, H1299, HCC827, SKMES) were used for the evaluation of our method. In addition, 60 patients with metastatic NSCLC before the initiation of any line of treatment (33 treatment-naïve and 27 pre-treated patients) were enrolled in this study. CTCs were isolated using ISET platform and stained with pancytokeratin (CK)/CD45/TUB and CK/GLU/VIM combination of antibodies. Samples were analyzed using confocal laser scanning microscopy and Image J software.

Results: In patients’ samples, (CK +/CD45-) cells were observed in 86.7% (52 out of 60) patients. CTCs with TUB expression were detected in 65.4% (34/52) of the patients. Among the total isolated CTCs, 30.6 % belonged to the (CK+/TUB+/CD45-)-phenotype.The rest of the CTCs detected with either low (31.2%) or no expression (24.8%) of TUB. Interestingly the phenotype [(CK-/TUB+/CD45-) (4.79% of the total CTCs)] was present only in advanced disease. The proportion of TUB-low or negative CTCs was statistically higher in treatment-naïve compared to pre-treated patients (p=0.002 and p=0.004, respectively), im-plying that TUB expression increases after treatment and during disease evolution. Moreover, patients harboring TUB-positive CTCs experienced shorter OS compared to patients with CTCs with low or no TUB expression (4.4 vs 7.9 months, respectively; p=0.027). GLU and VIM were also evaluated in the same cohort of patients. The frequency of the observed phenotypes was as follow: (CK-/GLU-/VIM-): 35.2% (19 out of 54 CK-positive patients), (CK+/GLU+/VIM+): 63.0% (34/54), (CK+/GLU+/VIM-): 16.7% (9/54) and (CK+/GLU-/VIM+): 72.2%. The last one was the most abundant subpopulation in treatment-naïve patients (81.3%; 26/32). Furthermore, the most abundant phenotypes in advanced stage of the disease were the (CK+/GLU-/VIM-):59.1% (13/22), (CK+/GLU-/VIM+): 59.1%, (13/22) and (CK+/GLU+/VIM+) (54.6%): (12/22). The OS was significantly decreased in patients with high GLU (3.8 vs 7.9 months; p=0.018) and/or high VIM (3.2 vs 7.1 months; p=0.029) expression in their CTCs.

Conclusions: In agreement to our previous results in breast cancer patients, the current study revealed that alpha-Tubulin, GLU and Vimentin are overexpressed in CTCs from NSCLC patients. In addition, the presence of TUB, GLU and/or VIM-positive CTCs is potentially related to poor patients’ outcome.

O1-4 SMALL EXTRACELLULAR VESICLES IN PRE-THERAPY PLASMA PREDICTCLINICAL OUTCOME IN NON-

SMALL CELL LUNG CANCER PATIENTS

Eleni-Kyriaki Vetsika1,2, Priyanka Sharma2, Constantinos N. Baxevanis3, Vassilis Georgoulias1, Theresa L. Whiteside2, Athanasios Kotsakis4

1School of Medicine, University of Crete, Heraklion, Greece 2Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece 3De-partment of Pathology, University of Pittsburgh School of Medicine and UPMC Hillman Cancer Center, Pittsburgh, PA, USA 4Cancer Immunology and Im-munotherapy Center, Saint Savas Cancer Hospital, Athens, Greece 5Department of Medical Oncology, General University Hospital of Larissa, Larisa, Greece

Background: Small extracellular vesicles (sEV) mediate inter-cellular communication in the tumor-microenvironment and emerge as promising components of liquidtumorbiopsy in cancer. The aim of this study was to explore the potential use of plas-ma-derived sEV as predictors of response to therapy and clinical outcome in patients with non-small cell lung cancer (NSCLC).

Methods: sEVwere isolated by size-exclusion chromatography from pre-cleared plasma of 23 patients with stage IIIa/IIIb and 56 patients with stage IV chemotherapy-naïve NSCLC. Twelve healthy donors (HD) served as controls. sEV were characterized for particle size and counts by qNano, morphology by transmission electron microscopy, morphology, protein content and molecular profiles by western blots. Flow cytometry was performed to quantify PD-1 and PD-L1 expression on circulating anti-tumour immune cells. The pre-treatment levels of total sEV protein were correlated with overall (OS) and progression-free survival (PFS).

Results: The sEV numbers and sEV protein levels per mL of plasma were significantly elevated in chemotherapy-naïve stage IIIa/IIIb and IV NSCLC patients compared to HD (p=0.009 and 0.0001, respectively). At baseline, levels of total sEV protein (TEP) were higher in stage III and IV patients who developed progressive disease compared to patients with stable disease (p=0.007 and 0.001, respectively). Patients’-derivedsEV were enriched in immunosuppressive proteins CD39, CD73, PD-1, PD-L1, CTLA-4, TGFβ, Fas, FasL, COX-2 and TRAIL and had lower levels of immunostimulatory proteins such as OX40L compared to proteins carried by sEV from plasma of exosomal cargo from HD. The protein levels of patients’-derived sEV were correlated with the percentages of CD8+PD-1+ and CD8+PD-L1+ circulating T cells and were found to be positively and independently associated with poorer PFS (HR = 2.852; p=


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data. The analysis of the inflammatory infiltrate was further associated with the mutational profile of the tumors in the TC and the IF.

Results: Although preliminary our data reveal a unique spatial immune profile, opening a new dimension not only from a mechanistic point of view but also for cancer prognosis and treatment.

O2-2 PROTEOMIC SCREENING OF BRONCHOSCOPIC BIOPSIES-ON-CHIP FOR IMPROVED PREDICTION OF ANTI-PD-1RESPONSES IN REAL-TIME.

*Maria Tsoumakidou *Institute of Bioinnovation, BSRC Alexander Fleming, Athens, Greece

Anti-PD-1 monotherapy first-line is indicated for selected patients with advanced non-small-cell lung cancer (NSCLC). Still more than half of patients do not respond or become resistant after initial response. Identifying patients who will benefit from anti-PD-1 monotherapy is an unmet need. We aim to interrogate the applicability of an innovative 3D microfluidic device, i.e. organ-on-chip, in predicting real-time response to PD1-blockade in NSCLC patients. We will conduct a prospective multicen-tric exploratory co-clinical trial by studying in parallel clinical responses to a-PD1 monotherapy in treatment-naive advanced NSCLC patients matched to their bronchoscopic biopsies-on-chip (bronchoBOCs). We will profile proteome responses to a-PD1 using mass spectrometry (LC-MS/MS) andcytometric bead arrays. Artificial intelligence/machine learning approaches will be allied to bronchoBOC profiles and clinical data, to identify the best predictive biomarker patterns.

O2-3 ASSOCIATION OF THE ADVANCED LUNG CANCER INFLAMMATION INDEX (ALI SCORE) WITH IMMUNE CHECKPOINT INHIBITOR OUTCOMES IN PATIENTS WITH ADVANCED NON-SMALL CELL LUNG CANCER

Mountzios Giannis (1), Samantas Epameinontas (2), Bartzi Dimitra (3), Gountas Ilias (4), Zervas Eleftherios (5), Tzanos Dimitrios (1), Samitas Konstantinos (5), Angelaki Sofia (6), Kyriakidis Gerasimos (2), Makrakis Dimitrios (6), Ardavanis Gerasimos (2), Rounis Konstantinos (6), Giannakakou Maria (2), Baka Sofia (7), Georgakoudi Eleni (7), Nikolaidi Adamantia (8), Athanasiadis Ilias (8), Eleni Kokkotou (9), Christopoulou Athina (10), Pentheroudakis Georgios (11), Lianos Evangelos (12), Dellas Panagiotis (11), Mavroidis Leonidas (11), Linardou Elena (13), Sgourou Stevi (13), Kosmidis Paris (14), Economopoulou Panagiota (15), Psyrri Amanda (15), Andreadis Charalampos (16), Fountzila Elena (17), Emmanouilidis Christos (18), Touroutoglou Nikolaos (18), Oikonomopoulos Georgios (19), Saridaki Zaxarenia (20), Lainakis Georgios (21), Rigakos Georgios (22), Razi Evangelia (22), Michailidis Prodromos (23), Rigas Georgios (23), Perdikouri Eleni-Isidora (23), Tsoukalas Nikolaos (24), Boukovinas Ioannis (25) and Syrigos Konstantinos (9).

1. 2nd Oncology Department and Clinical Trials Unit, Henry Dunant Hospital Center, Athens, Greece 2. 3rd Oncology Department, “Agioi Anargyroi” Cancer Hospital, Athens, Greece 3. Faculty of Medicine, National and Kapodistrian University of Athens, Athens, Greece 4. Laboratoty of Hygiene, Epidemiology and Medical Statistics, Faculty of Medicine, National and Kapodistrian University of Athens, Athens, Greece 5. 7th Pneumonology Clinic , “Sotiria” Hospital, Athens, Greece 6. Oncology Department , University of Irakleion School of Medicine, Crete, Greece 7. Oncology Department, Interbalkan Medical Center, Thessaloniki, Greece 8. Oncology Department, “Mitera” Hospital, Athens, Greece 9. 3rd Department of Internal Medicine, “Sotiria” hospital, University of Athens School of Medicine, Athens, Greece 10. Oncology Unit, General Hospital of Patras “Agios Andreas”, Patras. Greece 11. Oncology Department, University of Ioannina School of Medicine, Ioannina, Greece 12. 2nd Oncology Department, “Metaxa” Cancer Hospital, Pireaus, Greece 13. 4th Oncology Department, Metropolitan Hospital, Pireaus, Greece 14. 2nd Oncology Department, “Ygeia” Hospital, Athens, Greece 15. Oncology Department, “Attikon” University Hospital, Athens, Greece

16. 3rd Oncology Department, “Theageneion” Cancer Hospital, Thessaloniki, Greece 17. 2nd Oncology Department, “Euromedica” Clinic, Thessaloniki, Greece 18. 2nd Oncology Department, Interbalkan Medical Center, Thessaloniki, Greece 19. 2nd Oncology Department, Metropolitan Hospital, Pireaus, Greece 20. Oncology Department “Asclepius” Clinic, Irakleion, Crete, Greece 21. 1st Oncology Department, Henry Dunant Hospital Center, Athens, Greece 22. 3rd Oncology Department, “Ygeia” Hospital, Athens, Greece 23. Oncology Department, “Achilopouleio” General Hospital of Volos, Volos, Greece 24. Oncology Department, 401 General Army Hospital, Athens, Greece 25. Oncology Department, “Bioclinica”, Thessaloniki, Greece

Introduction To date, there is no optimal surrogate of immunotherapy efficacy in advanced non-small-cell lung cancer (NSCLC). Advanced Lung Cancer Inflammation Index (ALI score: body mass index X serum albumine/blood neutrophil-to-lymphocyte ratio) reflects the systemic inflammation of the host and is easily reproducible in routine clinical practice.

Μethods We retrospectively analyzed patients with stage III or IV NSCLC who received PD1/PD-L1 inhibitors alone or in combination with chemotherapy in any line of treatment in 25 cancer centers in Greece. For every patient we recorded demo-graphic, somatometric and clinicopathological characteristics, as well as clinical outcomes of immunotherapy. ALI score was evaluated as a marker of efficacy through appropriate statistical tests.

Results Seven hundred and three (703) patients were included in final analysis, of whom 71.7% were men, 67.2% had tumors of adenocarcinoma histology, 88.4% had stage IV disease at diagnosis, 39.4% received immunotherapy as 1st-line treatment and 74.9% as monotherapy. Median age at diagnosis was 68 years, median BMI was 25.1 kg/m2, median albumin level was 3.9 g/dl and 35.4% of the patients had PD-L1 expression>50%. Using the bibliographic cut-off value of 18 for ALI, patients with ALI>18 had significantly longer PFS (12 vs 5.6 months, p


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there is an urgent need to establish novel predictive biomarkers that will help us to select patients that are more likely to benefit from treatment with ICIs.

We have previously reported that patients with metastatic NSCLC have pre-immunity (PreI), CD8+ T-cells which specifically recognize hTERT572peptide. We have shown that the administration of ICIs in patients with PreI against hTERT572, resulted in significantly higher OS compared to patients without PreI, suggesting that immunosuppressive mechanisms, prevailing at the tumor microenvironment (TME) and inhibit the cytotoxic activity of CD8+ T-cells. Since ICIsact on cancer cells that rec-ognized by specific CD8+ T-cells, it is reasonable to hypothesize that both the TCR repertoire,through the variable β-chain of their receptor (TCR-Vβ), and the tumor mutation burden in the plasma (bTMB) would be changed during treatment with ICIs. Therefore, both TCR repertoire and bTMB could represent more reliable, real-time and complementary predictive biomarkers for patient selection.

With the B-PREIMMUNE project we will evaluate, for the first time, a combination of both molecular and immune biomarkers in blood, of stage III NSCLC patientsduring treatment with ICI drug Darvalumab. The dynamics of PreI, TCR clonality and bTMB as well as their combination willbe evaluated in sequential blood samples during ICIs therapy, to develop novel predictive platforms for selection of candidates that will benefit by ICIs treatment.

02-5 DISCOVERY AND QUANTITATIVE MEASUREMENT OF BIOMARKERS IN TUMOR MICROENVIRONMENT

Maria Toki MD, MSc Internal Medicine Resident, National and Kapodistrian University of Athens, Greece Research Associate, Department of Pathology, Yale University, New Haven, CT, USA

Background: Protein expression in formalin-fixed, paraffin embedded tissue is routinely measured by IHC or quantitative fluorescence (QIF) on a handful of markers on a single section. Digital spatial profiling (DSP) allows spatially informed simultaneous assessment of multiple biomarkers. In this study, we used the DSP technology using a 44-plex immune mar-kerantibody cocktail and tested it as anew method for high-plex measurement of immune markers inmultiple compartments.

Experimental Design: The NanoStringGeoMx DSP technology is compared with automated QIF (AQUA) for immune marker compartment-specific measurement and prognostic value in non–small cell lung cancer (NSCLC).

Results: We used the AQUA method of QIF, a method thoroughly used and previously compared with mass spectrometry for validation of the DSP technology. We found that there is a high correlation between measurements by the two assays in a large number of patient cases with multiple markers (CD3, CD4, CD8, CD20, and PD-L1) measured in tumor and stroma compartments. In addition, CD3 measurement by DSP reproduced the prognostic value similar to that seen using AQUA.

Conclusions: DSP technology shows high concordance with QIF and validates based on both regression and outcome as-sessment. We can utilize its high-plex capacity to find protein expression signatures that could potentially be used to predict response to immunotherapy.

O3-1 DELINEATING THE COMPLEXITY, HETEROGENEITY AND FUNCTIONAL DIVERSIFICATION OF LUNG CAN-CERANTIGEN PRESENTING CELLS TO UNCOVER NOVEL IMMUNOTHERAPEUTIC TARGETS

*Maria Tsoumakidou *Institute of Bioinnovation, BSRC Alexander Fleming, Athens, Greece

Anti-cancer immunity depends on efficient presentation of tumor antigens and co-stimulatory signals by antigen-presenting cells to anti-tumor T cells. The overarching goal of our lab is to decipher the landscape of antigen-presenting cells in cancer patients with the ultimate aim to develop more effective and precise immunotherapies. The laboratory has strong clinical links and works simultaneously with the mouse and human system. By using state of the art omic technologies, cancer mouse models, patient-derived xenografts and advanced culture systems, such as cancer organ chips, we study cell subtypes, signaling pathways, genes, regulatory modules and interactions that control antigen presenting cells in cancer. Among the pioneering questions, we are interested in are: How do dendritic cells change as they transition from homeostasis to tumor and tumor draining lymph node microenvironments? How do non-hematopoietic cells, such as fibroblasts, evolve and acquire their exclusive antigen presenting signatures in the tumor microenvironment? Which are the cardinal interactions that signal for T cell priming in tumor-draining lymph nodes and tumor tissues?

O3-2 EFFICACY OF AN HTERT VACCINE (VX-001) IN NSCLC PATIENTS WITH IMMUNOLOGICALLY COLD TU-MORS

K. Kosmatopoulos1, A. Kotsakis2, I.S. Pateras2, E. Baliou2, E. Patsea2, P. Kouroupakis2, V. Georgoulias2

1Vaxon Biotech, Paris, France; 2Helenic Oncology Research Group, Athens, Greece

Background: Vx-001-201 was a randomized phase 2 clinical study aiming to test the clinical efficacy of the TERT-targeting Vx-001 vaccine in NSCLC. Vx-001 did prolong neither OS nor TTF in Vx-001 -treated over placebo treated patients. We hypoth-esized that Vx-001 could not work in the immunosuppressive environment of patients with PD-L1+ and/or TIL+ tumors. In this paper we analyzed the correlation between PD-L1 expression/TIL infiltration and clinical efficacy of Vx-001.

Methods: Vx-001-201 study was run in 70 investigation sites across eight European countries. Patients with metastatic TERT expressing NSCLC, positive for HLA-A*0201 and experiencing disease control after four cycles of platinum-based che-motherapy were randomized (1:1) to receive Vx-001 and placebo until disease progression. The primary endpoint was overall survival (OS). Secondary endpoint was Time to Treatment Failure (TTF).

Findings: To investigate if there is a correlation between clinical activity of Vx-001 and tumor immunogenicity 136 patients with available tumor biopsies were analyzed for tumor PD-L1 expression (TPS and CPS) and TIL infiltration, two param-eters that define hotimmunogenic/cold-nonimmunogenic tumor status. Vx-001 significantly prolonged OS in patients with TPS1% and/or TIL+ tumors (16.3 vs 14.3 months, HR=1.40 [0.84-2.32], p=0.188). Moreover, TTF was significantly longer in Vx-001 treated than in placebo treated patients with TPS1% and/or TIL+ (2.8 vs 2.3 months, HR=1.12 [0.69-1.80], p=0.629) tumors.

Interpretation: Vx-001 is clinically efficient in patients with PD-L1-/TIL- non-immunogenic “cold” tumors but not in PD-L1+ and/or TIL+ immunogenic “hot” tumors.


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O4-1 DEFINING MOLECULAR RISK IN ALK+ AND EGFR+ NSCLC

Petros Christopoulos1,4,*, Martina Kirchner2,*, Albrecht Stenzinger2,4,*, and Michael Thomas1,4,*

on behalf of all authors of the original publication (Lung Cancer 2020 Oct;148:105-112) * equal contribution

1 Department of Thoracic Oncology, Thoraxklinik and National Center for Tumor Diseases at Heidelberg University Hospital, Baden Württemberg, Heidel-berg, Germany 2 Institute of Pathology, Heidelberg University Hospital, Baden Württemberg, Heidelberg, Germany 3 Division of Cancer Genome Research, German Cancer Research Center and National Center for Tumor Diseases, Baden Württemberg, Heidelberg, Germany 4 Translational Lung Research Center Heidelberg, Member of the German Center for Lung Research, Baden Württemberg, Heidelberg, Germany

Objective: Panel-based next-generation sequencing (NGS) is increasingly used for the diagnosis of EGFR-mutated non-small-cell lung cancer (NSCLC) and could improve risk assessment in combination with clinical parameters.

Materials and methods: To this end, we retrospectively analyzed the outcome of 400 tyrosine kinase inhibitor (TKI)-treated EGFR+ NSCLC patients with validation of results in an independent cohort (n=130).

Results: EGFR alterations other than exon 19 deletions (non-del19), TP53 co-mutations, and brain metastases at baseline showed independent associations of similar strengths with progression-free (PFS hazard ratios [HR] 2.1–2.3) and overall survival (OS HR 1.7–2.2), in combination defining patient subgroups with distinct outcome (EGFR+ NSCLC risk Score, “ENS”, p


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O4-4 QUANTITATIVE ASSESSMENT OF CD200 AND CD200R EXPRESSION IN LUNG CANCER

Ioannis A. Vathiotis1,2, Tyler MacNeil1,2, Jon Zugazagoitia1,2, Sandra Martinez-Morilla1,2, Fahad Ahmed1,2, Konstantinos N. Syrigos3, Aaron M. Gruver4, Kyla Driscoll4 and David L. Rimm1,2

1Department of Pathology, Yale School of Medicine, New Haven, CT, USA; 2Yale Cancer Center, Yale School of Medicine, New Haven, CT, USA; 3Department of Medicine, National and Kapodistrian University of Athens School of Medicine, Athens, Greece; 4Eli Lilly and Company, Indianapolis, IN.

Background: CD200 is a membrane-bound glycoprotein expressed on normal tissue, tumor and immune cells. The interac-tion of CD200 with its receptor leads to attenuation of the inflammatory process, resulting in tumor cell mediated immune suppression. CD200 has been characterized in hematologic malignancies and consists of an independent negative prognostic factor for chronic lymphocytic leukemia, acute myeloid leukemia and multiple myeloma patients. Here we assess both CD200 and CD200R expression in lung cancer and evaluate its association with clinicopathologic characteristics, mutation status, outcome and PD-L1 expression.

Methods: We used quantitative multiplexed immunofluorescence (QIF) to measure the expression of CD200 and CD200R in 287 non-small cell lung cancer (NSCLC) patients and 30 patients with large cell neuroendocrine carcinomas (LCNEC) of the lung. We performed target measurement with tyramide-based QIF panels and analyzed the data using the PM2000 microscope and AQUA software. Targets were measured in cytokeratin-positive (CK+) tumor compartment and cytokeratin-negative (CK-) stromal compartment.

Results: CD200 tumor positivity was found in 29.7% of NSCLC patients and 33.3% of LCNEC patients. CD200 demonstrated notable intratumoral heterogeneity (R2=0.09-0.31 between different TMA blocks versus 0.46-0.60 for CD200R). CD200R was expressed in immune cells in 25% of NSCLC and 41.3% of LCNEC patients. While CD200R is predominantly expressed in immune cells, rare tumor cell staining was seen in a highly heterogeneous pattern. CD200R expression in the stromal com-partment was significantly higher in patients with squamous differentiation (p


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O5-3 THE ROLE OF YAP SIGNALING IN KRAS DRIVEN NON-SMALL CELL LUNG CANCER

Marina Keil1, Linda Pudelko1, Dirk Wienke1, Niki Karachaliou1

1 Merck KGaA, Darmstadt, Germany

Oncogenic KRAS mutant non-small cell lung cancer (NSCLC) remains treatment refractory. Even with the novel KRAS-G12C inhibitors in clinical development, caution should be taken because tumors will likely develop resistance. Subgroups of KRAS mutant NSCLC, defined by co-occurring genetic alterations in STK11/LKB1 (KL) and TP53 (KP) tumor suppressor genes, have distinct biology and therapeutic vulnerabilities. The Hippo pathway effector YAP1 has been shown to substitute oncogenic KRAS in promoting the growth of lung adenocarcinomas and confer resistance to MAPK pathway inhibitors and immunotherapy. Here we have examined the role of YAP1 in KL, KP and K-only (intact STK11/LKB1 and TP53) NSCLC cells. We found YAP1, TAZ and activated YAP1 (Y357) expressed in almost all KRAS mutant NSCLC cell lines, which was in line with nuclear YAP1 localization. Comparing the three subgroups we detected highest levels of YAP1 S127 phosphorylation and PD-L1 in KP cells. KL cell lines showed the lowest PD-L1 expression. Upon siRNA knockdown of YAP and/or TAZ cell viability was decreased, hereby the double knockdown of YAP1 and TAZ was more effective than each single knockdown. In addition, this effect was more evident in KRAS mutant cells with loss of STK11 compared to the other KRAS mutant subtypes. Overall, we found that the YAP/TAZ pathway is present and may contribute to the survival of KRAS mutant NSCLC. Further, our initial combination experiments corroborate the combination potential of YAP/TAZ and MEK inhibitionas a promising strategy to enhance treatment response and patient survival.

O5-4 GENE EXPRESSION PROFILE OF SIZE-BASED ENRICHED CIRCULATING TUMOR CELLS REVEALS A DYNAMIC ROLE OF EMT AND PD-L1 DURING OSIMERTINIB TREATMENT IN EGFR-MUTANT NSCLC PATIENTS

Aliki Ntzifa1, Areti Strati1, Nuria Jordana2, Galatea Kallergi3, Niki Karachaliou2, Vassilis Georgoulias4, Rafael Rosell2, Athanasios Kotsakis5, Evi Lianidou1

1Analysis of Circulating Tumor Cells Lab, Lab of Analytical Chemistry, Department of Chemistry, National and Kapodistrian University of Athens, 15771, Athens, Greece 2Pangaea Oncology, Laboratory of Molecular Biology, Quirón-Dexeus University Institute, Barcelona, Spain 3Division of Genetics, Cell and Developmental Biology, Department of Biology, University of Patras, Patras, Greece 4Hellenic Oncology Research Group (HORG), Athens, Greece 5Department of Medical Oncology, University General Hospital of Larisa, Larisa, Greece

Background: Liquid biopsy is a useful tool to unveil resistance mechanisms in NSCLC. Serial monitoring of EGFR-mutant NSCLC patients based on CTC and ctDNA analysis revealed molecular changes during osimertinib treatment.

Methods: Peripheral blood (PB) from 30 NSCLC patientsbefore, after 1 cycle of osimertinib and at progression of disease (PD) was analyzed by size-based CTC enrichment combined with RT-qPCR for gene expression of epithelial,mesenchymal/EMT, stem cell markers, AXL, PD-L1 and PIM-1. CTC isolation from 31PB samples was processed using ISET® technology. In parallel, analysis of EGFR mutations was carried out in the same subgroup for the matched plasma ctDNA samples.

Results: There was a strong positive correlation of VIMmRNA expression with PIM-1mRNA expression at baseline and increased PD-L1mRNA expression levels at PD. AXLmRNA overexpression varied among patients and high levels of PIM-1 transcripts were detected. PD-L1mRNA expression was significantly increased at PD compared to baseline (p=0.016). Patients positive for EGFR mutations in plasma and concurrentlypositive for the presence of CTCs exhibited prognostic significance in terms of PFS and OS.

Conclusions: The high prevalenceof VIM mRNApositive CTCs suggest a dynamic role of EMT during osimertinib treatment, while increased expression of PD-L1mRNA at PD suggests a theoretical background for immunotherapy in EGFR-mutant NSCLC patients resistant to osimertinib. Parallel assessment of CTCs and ctDNA was revealed as a valuable prognostic and predictive factor.

FACULTYA. Agbarya Head of Oncology, Bnai Zion MC, Haifa. Israel

S. Baka MD, MSc, PhD, Medical Oncologist, Interbalkan Medical Center, Thessaloniki, Greece

P. Christopoulos MD, PhD, Hematologist - Medical Oncologist, Thoraxklinik and National Center for Tumor Diseases, Heidelberg University Hospital, Germany

A. Christopoulou MD, PhD, Medical Oncologist, Director in the Oncology Unit, Saint Andrews General Hospital of Patras, Greece

F.I. Dimitrakopoulos MD, PhD, Medical Oncologist, Division of Oncology & Molecular Oncology Laboratory, Department of Medicine, University of Patras, Greece

A. Georgiou Guy’s Cancer centre, Guy’s and ST Thomas’ NHS Foundation Trust London, UK

V. Georgoulias MD, Emeritus Professor of Medical Oncology, School of Medicine, University of Crete, Greece

G. Geropoulos Thoracic Surgery Department, University College London Hospitals, UK

M. Jamal-Hanjani Senior Clinical Lecturer and Honorary Consultant in Translational Lung, Oncology, Research Department of Oncology, UCL Cancer Institute, UCL Hospital, London, UK

G. Kallergi Assistant Professor of Biochemistry, Department of Biology, University of Patras, Greece

I. Kalomenidis MD, PhD, Associate Prοfessor of Pulmonary Medicine 1st Department of Critical Care and Pulmonary Med-icine, University of Athens, School of Medicine, Evangelismos Hospital, Associate Editor of Respirology, Athens, Greece

N. Karachaliou MD, PhD, Medical Director, Global Clinical Development, Merck Healthcare KGaA, Darmstadt, Germany

M. Keil PhD, Postdoctoral Researcher, Merck KGaA, Darmstadt, Germany

A. Klinakis PhD, Director of Research - Professor level, Biomedical Research Foundation of the Academy of Athens, Greece

F. Koinis MD, PhD, Assistant Professor of Medical Oncology, Faculty of Medicine, School of Health Sciences, University of Thessaly, Larissa, Greece

K. Kosmatopoulos Chief Executive Officer, Vaxon Biotech, Paris, France

P. Kosmidis MD, Director, 2nd Department of Medical Oncology, Hygeia Hospital, Athens, Greece

A. Kotsakis MD, PhD, Associate Professor of Medical Oncology, School of Medicine, University of Thessaly, Director of the Department of Medical Oncology, General University Hospital of Larissa, Greece

G. Lazaridis MD, PhD, Medical Oncologist, Consultant, Papageorgiou General Hospital, Medical Oncology Department, Aristotle University of Thessaloniki, Greece

E. Lianidou PhD, Professor of Analytical Chemistry - Clinical Chemistry, Analysis of Circulating Tumor Cells Lab, Department of Chemistry, University of Athens, Greece

H. Linardou PhD, Director, 4th Oncology Department and Clinical Trials Unit, Metropolitan Hospital, Athens, Greece

P. Makrythanasis MD, PhD, FMH, PD, Investigator B’, Biomedical Research Foundation of the Academy of Athens (BRFAA), Systems Biology Research Center, Athens, Greece

E. Mantouvalou PhD, Molecular Biologist, Medical Lead Oncology, Takeda Hellas S.A., Athens, Greece


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A. Markou PhD, Postdoctoral Researcher, Lab of Analysis Circulating Tumor Cells (ACTC), Lab of Analytical Chemistry, Depart-ment of Chemistry, University of Athens, Greece

I. Metaxas Consultant Medical Oncologist, Department of Oncology - Hematology, Kantonsspital Graubünden, Chur, Switzerland

G. Mountzios ΜD, MSc, PhD, Medical Oncologist, 2nd Oncology Department and Clinical Trials Unit, Henry Dunant Hospital Center, Athens, Greece

A. Ntzifa MSc, PhD student, Laboratory of Analytical Chemistry, Analysis of Circulating Tumor Cells (ACTC) Lab, Department of Chemistry, University of Athens, Greece

G. Oikonomopoulos MSc, Consultant Medical Oncology, 2nd Oncology Department, Metropolitan Hospital, Athens, Greece

D. Oluf Roe MD, PhD, Professor, Department of Clinical and Molecular Medicine, Norwegian University of Science and Tech-nology (NTNU), Trondheim, Norway

G. Panagiotopoulos MD, PhD, Consultant Thoracic Surgeon, Honorary Clinical Associate Professor UCL, Thoracic Surgery Department, University College London Hospitals (UCLH), London, UK

D. Papadatos-Pastos MRCP (UK) PhD, Consultant in Medical Oncology, Lung Cancer and Acute Oncology, University College London Hospitals and The Princess Alexandra Hospital, London, UK

V. Papadimitrakopoulou MD, VP, Clinical Development Leader, Global Product Development, Oncology, Pfizer Inc, UK

F. Papageorgiou PhD, Molecular Biologist, Diagnostic Manager Oncology, AstraZeneca, Athens, Greece

I. Pateras BSc, MD, PhD, Assistant Professor, Department of Histology and Embryology Medical School, National and Kapodistrian University of Athens, Greece

A. Patrikidou MD, PhD, DDS, BSc(HumGen)(UCL) MSc(OMFS)(UCL) FDSRCS(Eng) DU, Carcinologie Cervico-faciale (Paris), DU Carcinologie Clinique (Paris), Consultant Medical Oncologist, Associate Medical Director SCRI UK, Honorary Consultant Medical Oncologist, UCLH & Senior Clinical Lecturer, UCL Cancer Institute, Drug Development Unit, Sarah Cannon Research Institute, London, UK

N. Pistamaltzian MD, PhD, Medical Oncologist, Oncology Department, Mitera Hospital, Athens, Greece

I. Pudelko PhD, Postdoctoral Researcher, Merck KGaA, Darmstadt, Germany

J. Remon Centro Integral Oncología Clara Campal Barcelona - HM Delfos Barcelona, Spain

M. Rovithi Medical Oncologist, Agios Nikolaos General Hospital, Crete, Greece

F. Skoulidis MD, PhD, Assistant Professor, Department of Thoracic and Head and Neck Medical Oncology, The University of Texas, MD Anderson Cancer Center, USA

A. Somarakis MSc, Biologist, Medical Manager Oncology, AstraZeneca, Athens, Greece

G. Sotiropoulos Barts Thorax Centre, St. Bartholomew’s Hospital, London, UK

K. Syrigos MD, PhD, FCCP, Adj. Professor of Medicine, Pittsburgh School of Medicine, USA, Vis. Professor of Thoracic Oncology, Yale School of Medicine, USA, Professor of Medicine & Medical Oncology, Head, 3rd Department of Medicine, Sotiria General Hospital, Athens School of Medicine, National & Kapodistrian University, Athens, Greece

M. Toki MD, MSc, Research Associate, Department of Pathology, Yale University, New Haven, CT, USA, Internal Medicine Resident, 3rd Department of Medicine, National and Kapodistrian University of Athens, Greece

P. Tsantoulis Department of Oncology, University Hospital of Geneva, Center for Translational Oncohematology, University of Geneva, Swiss Cancer Center Leman, Geneva, Switzerland

M. Tsiatas MD, PhD, BSc (Biol), Director Medical Oncologist, Department of Oncology and Cancer Clinical Trials Unit, Athens Medical Center, Athens, Greece

M. Tsoumakidou MD, PhD, Group Leader - Institute of Bioinnovation, BSRC Alexander Fleming, Athens, Greece

I. Vathiotis MD, MSc, Postdoctoral Associate, Department of Pathology, BML-112, Yale University School of Medicine, USA

P. Verginis Associate Professor Biochemistry and Immunology, School of Medicine, University of Crete, Greece

E.K. Vetsika MPhil, PhD, Head of Mass Cytometry Unit, Centre of New Biotechnologies and Precision Medicine, Department of Medicine, School of Health Sciences, National and Kapodistrian University of Athens, Greece

A. Voutsina Postdoctoral Researcher, Greek Genome Center, Biomedical Research Foundation Academy of Athens (BRFAA), Athens, Greece

A. Xagara PhD, Molecular Biologist, Laboratory of Oncology, School of Medicine, University of Thessaly, Larissa, Greece


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SponsorsInfoOrganized by

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Date23-24 October, 2020

Venue Divani Palace Acropolis19-25 Parthenonos str., 11742 Athens - GreeceTel.: +30 210 92 80 100 Fax: +30 210 92 14 993E-mail: [email protected]

Official LanguageThe official language of the Meeting is English.

Τhere will be a live streaming connection through a special platform.You can watch the Conference online through the Link www.nowcongress.gr and ask written questions throughout the presentations.

Certificate of AttendanceThe certificate of attendance will be given to the participants at the end of the event.Based on the latest circular of the National Drug Organization the Event is required to use an attendance tracking system. By the end of the event a certificate will be given to those who have attended at least 60% of the total hours of the scientific Program. The number of credits of Continuing Medical Education (CME-CPD) to be administered to the participants will be calculated on the basis of monitoring time.

The event will be awardedBy Hellenic Medical Association (Ph. M.A.) with 12 CME - CPD credits.

Secretariat

Congress & Event Planning 2-4, Kastriotou Str., Athens - Greece P.C.11476 Τ +30 210 7294559 E [email protected]

Congress & Event Planning2-4, Kastriotou str.

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Documents

International Meeting onLung Cancer · International Meeting on Lung Cancer International Meeting on Lung Cancer 11 SATURDAY, OCTOBER 24 09.00-10.00 SESSION V: NEWS FROM THE KINOME