Journal Thoracic Oncology

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Abstracts Journal of Thoracic Oncology • Volume 12 Issue S1 January 2017 Conclusion: The anti-proliferative effect of MFN2 deficiency and its risk in lung adenocarcinoma were found by transcriptional profiling. Keywords: microarray, The Cancer Genome Atlas, MFN2, lung adenocarcinoma POSTER SESSION 2 – P2.01: BIOLOGY/PATHOLOGY MARKER FOR PROGNOSIS, PREDICTION – TUESDAY, DECEMBER 6, 2016 POSTER SESSION 2 – P2.01: BIOLOGY/PATHOLOGY MARKER FOR PROGNOSIS, PREDICTION – TUESDAY, DECEMBER 6, 2016 P2.01-083 PROGNOSTIC FACTORS OF OVERALL SURVIVAL IN 150 RESECTED LUNG ADENOCARCINOMA PATIENTS Yue Cheng 1 , Ping Zhou 1 , Zhixin Qiu 2 , Dan Liu 2 , Weimin Li 2 1 West China School of Medicine,west China Hospital,sichuan University, Chengdu,sichuan/China, 2 West China Hospital,sichuan University, Chengdu,sichuan/China Background: The 2011 IASLC/ATS/ERS pathological calssification of pulmonary adenocarcinoma(ADC) gives new direction to clinical individualised treatment strategies and prognostic evaluation.We analyzed the prognostic effect of invasive ADC sub-types according to the new classification system. Methods: 150 invasive lung ADCs resected in West China Hospital from 2008 to 2013 was analyzed in 5% increments, and classified and graded according to their predominant patterns, as proposed by the IASLC/ATS/ERS. Clinical data,including smoking status, chemotherapy/ radiotherapy after surgery and patient outcomes were collected.Overall survival was evaluated. Results: Tumor necrosis (p=0.033), poor differentiation (p=0.027), lymph node metastasis (p
Abstracts Journal of Thoracic Oncology • Volume 12 Issue S1 January 2017 1 Thoracic Oncology and Translational Research Unit, Instituto Angel H Roffo, Caba/Argentina, 2 Molecular Pathology Department, Instituto Angel H Roffo, Caba/Argentina, 3 Medical Oncology, Cemic, Buenos Aires/Argentina, 4 Molecular Pathology Section, Cemic, Buenos Aires/Argentina Background: Lung cancer is the worldwide leading cause of death from cancer. Epigenetic silencing of tumor suppressor genes (TSG) contributes to the development and progression of lung cancer. In this prospective study we assess the methylation profile of locally advanced and oligometastatic versus widespread metastatic Non-Small Cell Lung Cancer (NSCLC). We will determine the ability of a panel of tumor suppressor genes (TSG) to discriminate these clinical phenotypes Methods: Patients (≥18 years) were eligible for inclusion if they had histologically confirmed unresectable non-pretreated stage III/ IV NSCLC. Paraffin-embedded blocks from patients from this study cohort were macro-dissected based on hematoxylin-eosin evaluations to ensure a minimum of 75% of tumor cells. DNA was extracted. Promoter methylation status of TSG (SFRP5, TIMP3, HLTF, RUNX3, ID4) will be evaluated by EpiTect Methyl II Signature PCR (Qiagen). Data analysis was done using integrated Excel-based templates, which provide gene methylation status as percentage unmethylated (UM) and percentage methylated (M) fraction of input DNA. Methylation levels were described as: ³1-19%: low methylation level, 20-59%: moderate methylation level and ³60%: high methylation level. Presence of intrathoracic disease and limited extrathoracic disease, (M1b, proposed 8th TNM edition) vs multiple metastatic disease (M1c) was described for clinical and molecular analysis. Results: From March 2015 to June 2016, 40 out of 60 sixty patients had enough tissue to be included. Intrathoracic disease was present in 19 patients (47.5%), M1b disease in 8(20%) and 13 patients (32.5%) had multiple extrathoracic disease. The methylation profile for intrathoracic disease was: SFRP5 was found in 4/19 patients (21.1%), ID4 7/19 (36.6%), HLTF 12/19 (63.2%), RUNX3 19/19 (100%) and TIMP3 10/19 (52.6%); for M1b disease: SFRP5 was found in 4/8 patients (50%), ID4 3/8 (37.5%), HLTF 6/8 (75%), RUNX3 6/8 (75%) and TIMP3 7/8 (87.5%); for M1c disease: SFRP5 6/13 patients (46.2%), ID4 9/13 (69.2%), HLTF 11/13 (84.6%), RUNX3 13/13 (100%) and TIMP3 8/13 (61.5%). Overall survival was shortened for the group of patients with methylation of ID4³20% (14.5 vs 19 months, p=0.010 Log Rank Test). In the subgroup analysis this difference was sustained for patients with oligoprogressive disease (Intrathoracic plus IVb) vs IVc (9.5 vs 17.5 months, p=0.05 Log Rank Test vs 14 vs 19 months, p=0.51, respectively) Conclusion: Although no definitive conclusions can be done because of the sample size, it seems that patients with methylation of ID4 of 20% or more have worse prognosis. ID4 could also help to differentiate oligometastatic vs widespread NSCLC Keywords: methylation, lung cancer, tumor supressor gene POSTER SESSION 2 – P2.01: BIOLOGY/PATHOLOGY Targets for Treatment Prediction – TUESDAY, DECEMBER 6, 2016 Keywords: chemoresistance, NSCLC, Luteolin, Axl POSTER SESSION 2 – P2.01: BIOLOGY/PATHOLOGY TARGETS FOR TREATMENT PREDICTION – TUESDAY, DECEMBER 6, 2016 P2.01-087 PROGNOSTIC SIGNIFICANCE OF CA IX OVEREXPRESSION IN STAGE III NSCLC PATIENTS RECEIVED NEOADJUVANT TREATMENT Sezer Saglam 1 , Kamuran Ibis 2 , Esra Kaytan Saglam 2 , Pınar Fırat 3 , Dilek Yilmazbayhan 3 , Alper Toker 4 , Berker Ozkan 4 , Veysel Hancer 5 , Murat Buyukdogan 5 , Rian Disci 6 1 Medical Oncology, Istanbul Bilim University, Istanbul/Turkey, 2 Radiation Oncology, Istanbul University Oncology Institute, Istanbul/Turkey, 3 Pathology, Istanbul University Medical Faculty, Istanbul/Turkey, 4 Department of Thoracic Surgery, Istanbul University, Istanbul/Turkey, 5 Genetic Diseases, Goztepe Medical Park Hospital, Istanbul/Turkey, 6 Statistics, Istanbul University Medical Faculty, Istanbul/Turkey Background: The aim of study to investigate prognostic significance of carbonic anhydrase IX gene (CA IX) mRNA expression in stage III NSCLC patients received neoadjuvant treatment Methods: We have studied Carbonic Anhydrase IX (CA IX) mRNA expression at biopsy or surgical pathology tissues of 77 patient with Stage III A/B NSCLC received neoadjuvan treatment. CA IX mRNA expression were evaluated with 50 control .Total RNA were isolated from FFPE tissue from patients while the controls were isolated from the peripheral blood. Results: Median age is 56.Patients histology is 47 pts(61%)squamous cell carcinoma (SCC),30 pts(39%) adenocarcinoma (AC). Neoadjuvan Chemotherapy (NeoAdj CT) was given 45 pts (58,4%); Neoadjuvant chemoradiotherapy (neoAdjCT/RT) was given 32pts (41,6%). Median Neoadjuvan chemotherapy cycles is 3(2-6). Radiotherapy median dose was 60 Gy(45-66).Surgery outcomes is Lobectomy 38pts (49,4%);sleeve lobectomy 11 pts (14,3%), Bilobectomy 6pts (7,8%) Left pnemonectomy (18.2%), right pnemonectomy 8pts (10,4%). Recurrence rate was 39 pts (50,6%). Two year disease free (DFS) and overall survival (OS) was 59,6% and 71,4%. There was OS and DFS difference in favor of Neoadj CT 4-6 cycles versus 2-4 cycles (p=0.009 and p=0.034). There is no statistical difference (p=0,344) for CA IX mRNA expression between SCC and AC. There is no statictical difference for CA IX mRNA expression in Neoadj CT and NeoadjCT/RT groups (p=0.199). There is no statistical difference for OS between ≤Median CA IX versus ≥median groups (20 events/39 versus 20/38 events p=0,799) There is no statistical difference for DFS between ≤median CA IX versus median groups ≥ (19 events/39 versus 20events/38) Conclusion: There is no any prognostic significance of Carbonic Anhydrase IX expression on DFS and OS in Stage III A/B NSCLC patients received neoadjuvat treatments. Keywords: neoadjuvant, stage III, Carbonic Anhydrase IX, NSCLC P2.01-086 LUTEOLIN IS A NOVEL TARGET OF AXL RECEPTOR TYROSINE KINASE TO INHIBIT CELL PROLIFERATION AND CIRCUMVENT CHEMORESISTANCE IN LUNG CANCER CELLS Kyungchan Kim Pulmonology Department, Catholic University of Daegu Hospital, Daegu City/ Korea, Republic of Background: Axl receptor tyrosine kinase (RTK) plays a critical role in cell growth, proliferation, and anti-apoptosis. In this study, we demonstrated the effect of luteolin, a non-toxic flavonoid widely found in various plants, on expression and activation of Axl RTK in NSCLC, H460, and its cisplatin-resistant cell, H460/CisR. Methods: 1. Cell viability measurement & Clonogenic assay. 2. Western blot analysis. 3. Promoter activity test. 4. Ectopic expression of Axl. 5.siRNA trasnfection for Axl knockdown. Results: Luteolin treatment of H460 and H460/CisR cells was found to cause a dosedependent decline of Axl protein as well as mRNA levels. Axl promoter activity was also reduced by luteolin, suggesting the transcriptional down-regulation of Axl expression by luteolin. Axl phosphorylation upon its ligand, Gas6, was inhibited by luteolin, indicating that luteolin also abrogates Gas6-induced Axl phosphorylation. Next, it was found that treatment of both H460 and H460/CisR cells with luteolin decreased the cell viability and clonogenic ability in dosedependent manner. We further observed the synergistic anti-proliferative effect of luteolin in cells transfected with Axl specific siRNA, while the reduction of its cytotoxic effect in Axl RTK overexpressing cells, confirming that luteolin exerts its anticancer potential via interference of Axl expression. In addition, luteolin was found to result in the increase of p21, a cyclin-dependent kinase inhibitor, in H460 and H460/CisR cells. Conclusion: In summary, our data demonstrate that luteolin inhibits Axl expression and the activation which are associated with its anti-proliferative activity in both parental and cisplatin-resistant NSCLC cells. Thus, Axl seems to be a potent therapeutic target of luteolin to inhibit cell proliferation and to overcome chemoresistance of NSCLC cells. POSTER SESSION 2 – P2.01: BIOLOGY/PATHOLOGY TARGETS FOR TREATMENT PREDICTION – TUESDAY, DECEMBER 6, 2016 P2.01-088 PRENYLATION INHIBITORS IN LUNG ADENOCARCINOMA: COMPARISON OF ZOLEDRONIC ACID AND A NOVEL LIPOPHILIC BISPHOSPHONATE Eszter Molnar 1 , Tamas Garay 2 , Dominika Rittler 1 , Marcell Baranyi 1 , Clemens Aigner 3 , Zoltan Lohinai 4 , Balazs Dome 5 , József Tímár 2 , Balazs Hegedus 5 1 2nd Department of Pathology, Semmelweis University, Budapest/Hungary, 2 Has-Se Molecular Oncology Research Group, Budapest/Hungary, 3 Department of Thoracic Surgery, University Clinic Essen, Essen/Germany, 4 National Korányi Institute of TB and Pulmonology, Budapest/Hungary, 5 Departement of Thoracic Surgery, Medical University of Vienna, Vienna/Austria Background: The prenylation inhibitor zoledronic acid is a standard-ofcare therapeutic option in bone metastasis. Recent studies suggest that prenylation inhibition using novel lipophilic bisphosphonates might be active against various malignancies outside the bone metastatic setting. Since prenylation is an important posttranslational modification in RAS protein function we explored the sensitivity of a panel of lung adenocarcinoma cells representing various oncogenic driver mutations. Methods: 8 human lung adenocarcinoma cell lines were investigated in vitro to assess the short-term viability and long-term clonogenic potential following zoledronic acid and BPH- 1222 treatments. The eight lung cancer cell lines represented wild type (HCC78, CALU3), EGFR- (H1650, H1975) KRAS- (A549, H358), BRAF- (CRL5885) and BRAF + NRAS double mutant (CRL5922) molecular subtypes. Effect on short and long term proliferation were measured with a SRB based photometric assay. Results: Neither short-term nor long-term treatment showed significant differences between the proliferation inhibitory effect of the hydrophilic zoledronic acid and novel lipophilic bisphosphonate BPH-1222. Interestingly, we found that the two KRAS mutant lung adenocarcinoma cell lines were more Copyright © 2016 by the International Association for the Study of Lung Cancer S439
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LILLY ONCOLOGY IS DEDICATED TO ADVA
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