OFP-16-009 EpCAM -A marker for Tufting enteropathy (TE) and a useful tool in the differential diagnosis of congenital enteropathies C. Thoeni * * Division of Cell Biology, Medical University Innsbruck, Austria Objective: Congenital enteropathies (CE) are characterized by villous atrophy and disruption of apical microvilli in duodenal enterocytes. TE is characterized by focal eptithelial tufts and mutations in the EpCAM gene, coding for epithelial cell adhesion molecule, important for cell-cell contacts. Microvillus inclusion disease (MVID), shows loss of apical microvilli and formation of intracytoplasmatic microvillus inclusions. MVID is caused by mutations in the MYO5B gene, important for intracellular transport and organization of epithelial cell polarity. In this study, we identified a new EpCAM mutation in a patient with TE and used anti-EpCAM antibody as a marker for the diagnosis of TE and distinction from MVID. Method: We used Immunohistochemistry (IHC) with monoclonal EpCAM antibody (mouse monoclonal AB for EpCAM, NCL ESA/Leica Microsystems) on routinely processed duodenal biopsies from patients with TE, MVID and age matched controls. Immunostaining for E-Cadherin served as reference. Results: EpCAM expression was completely absent in the biopsy from TE patient homozygous for a novel EpCAM mutation (c227 C>G, Ser 76X). E-Cadherin showed normal expression and distribution pattern in the enterocytes. In MVID, expression and distribution pattern was comparable to controls for both EpCAM and E-Cadherin. Conclusion: Loss of EpCAM is specific and a sensitive marker for confirmation of TE. EpCAM antibody is useful in the differential diagnosis of CE. Objective: In pulmonary adenocarcinoma EGFR mutation analysis has become an important part of the diagnostic work-up. Frequently the tissue of bronchoscopies is of limited diagnostic value. The aim of the present study was to evaluate the impact of ROSE on brochoscopy specimens with regard to EGFR mutation. Method: ROSE was used for adequacy of the specimen and for separating adenocarcinomas and carcinomas NOS from other neoplasms in the lung. If it was not possible to retrieve material for histology, cytology and cellblock were made. If adenocarcinoma or carcinoma NOS was suspected in ROSE, further two biopsies or two cell blocks were obtained. EGFR mutation analysis was performed by PCR (Light Cycler 480; EGFR RGQ PCR Kit; Qiagen). Results: Malignancy was diagnosed in 93 of 354 cases by histology or on cytology with and without cell blocks. Adenocarcinomas (n=30) and carcinomas NOS (n=9), SCC (n =26), SCLC (n = 13), and rare tumors (n=15) were diagnosed, respectively. Among the group of adenocarcinomas and carcinomas NOS (n = 39), EGFR mutation analysis was performed in 29 (74,3 %) cases and showed mutations in 3 (10,3 %) and "wild type" in 26 (89,7 %) tumors. No material was left in 10 (25,6 %) cases. Conclusion: ROSE supports bronchoscopic procedures to retrieve adequate specimens for tumor diagnosis and subsequent EGFR mutation analysis. Objective: Patients with Fibroblast growth factor receptor 1 (FGFR1) amplified squamous cell lung cancers (L-SCC) are treated in phase I clinical trials using small molecule inhibitors (SMI). SCC of the lung share common molecular alterations with squamous cell head and neck cancers (HN-SCC). Aim of our study is to assess if HN-SCCs also harbor FGFR1 amplifications. Furthermore, we aim to inhibit cell proliferation of FGFR1 amplified HN-SCC cell lines using a SMI. Method: The cohort consists of 227 patients suffering from HN-SCC, 97 of these suffering from metastatic disease. Primary tumors and metastatic tumors were assessed for FGFR1 copy number status using fluorescence in-situ hybridization (FISH). We tested cell lines for FGFR1 amplification status and inhibited these with SMIs. Objective: The pulp of pequi has high levels of antioxidants properties. Method: Eighteen male BALB/c mice divided: 14 animals received by gavage 0,5 μL/mg/day of pequi oil (Control + CBCoil=4) during 75 days. After 15 days, 10 of these mices received two doses of 1,5 g/kg intraperitoneal of urethane (Urethane + CBC oil=10). The other 4 animals were only submitted to two doses of 1,5 g/kg intraperitoneal of urethane (Urethane group=4). After 75 days, groups were sacrificed. Antioxidant activity was evaluated in the lung tissues by TBARS (Thiobarbituric acid-reactive substances), CAT (catalase) and SOD (superoxido dismutase) test. DNA damage was estimated by comet test. Results: The lung parenchyma from Urethane groups without oil and with oil showed neoplasic formations induced by the chemical carcinogenesis in contrast with Control + CBC oil group. The results of TBARS test showed a significant decrease of lipid peroxidation in the Urethane + CBC oil, than Urethane group. The CAT and SOD test didn't show a significant difference. Comet assay showed a significant decrease of DNA damage in Urethane + CBC oil when compared with Urethane group. Conclusion: The antioxidant components in the pequi oil diminish the oxidative stress status and DNA damage in chemical carcinogenesis, suggesting that this type of strategies may have a greater impact in lung cancer treatment. Financial Support: FAPESP.