Ficant differences in stent patency time involving two groups (p.). Although tumor ingrowth with recurrent obstruction was far more typical within the uSEMS group vs,acute cholecystitis vs . and acute pancreatitis vs . were far more typical inside the cSEMS group. Conclusion: Both PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/21046372 cSEMS and uSEMS are powerful and protected in attaining sturdy biliary drainage in patients with pancreatic cancer getting neoadjuvant therapy,regardless of unique patterns of late stent failure. Disclosure of Interest: None declaredContact E mail Address: malte.buchholzstaff.unimarburg.de Introduction: Plac is really a little protein with unknown molecular function which according to the cellular context shows unique subcellular localisation and could be involved inside a wide selection of physiological and pathophysiological processes. In normal pancreata,Plac is expressed neither inside the endocrine nor within the exocrine compartment. Here we demonstrate that the protein is strongly upregulated in human pancreatic neuroendocrine Peficitinib tumours (pNETs) and centrally regulates the growth of cultured cells derived from pNETs. Aims Strategies: Immunohistochemistry,RNAi,cell proliferation and viability assays,Western blots,apoptosis assays Outcomes: Plac is strongly overexpressed in primary human pNET tissues both on the mRNA level,as determined by quantitative RealTime PCR,at the same time as on the protein level,as determined by Western blot and immunohistochemistry. Furthermore,robust Plac expression is also retained in cultured cell lines from human and rat pNETs. siRNAmediated knockdown of Plac expression in these cells uniformly resulted in powerful inhibition of cell growth,as determined by BrdU incorporation and MTT assays,when apoptosis levels were not influenced. This development inhibition was linked with upregulation on the cell cycle inhibito pCDKNA also as downregulation of cyclin D. Conclusion: Overexpression of Plac protein in pancreatic neuroendocrine tumours is centrally significant for the upkeep in the proliferative phenotype on the tumour cells. Additional analyses to determine the involved molecular mechanisms and signalling pathways are ongoing. Disclosure of Interest: None declaredP CLINICAL MANAGEMENT OF Tiny PANCREATIC NEUROENDOCRINE TUMORS (PNETS): Results FROM A YEAR SINGLECENTER Prospective STUDYS. Massironi,R. E. Rossi,,A. Zilli,D. Conte,C. Ciafardini,M. Peracchi Gastroenterology and Endoscopy Unit,irccs ca` granda ospedale maggiore policlinico,Postgraduate College of Gastroenterology,Division of Pathophysiology and Transplantation,Universita` degli Studi di Milano,Milan,ItalyP SURVIVAL PROGNOSTIC Factors OF ENTEROPANCREATIC NEUROENDOCRINE TUMORS: A SINGLECENTER RETROSPECTIVE Evaluation OF Cases F. Foubert,M.F. Heymann,C. Dumars,H. Senellart,T. MatysiakBudnik,Y. Touchefeu Institut des Maladies de l’Appareil Digestif,Anatomopathology Division,Institut de Cance ologie de l’Ouest,Nantes,France Contact E-mail Address: marietilliehotmail Introduction: Enteropancreatic neuroendocrine tumors (EPNET) are uncommon and heterogeneous illnesses. The aim of our study was to determine clinical,histopathological and therapeutic elements impacting the survival of sufferers with EPNET. Aims Approaches: All patients with histopathological diagnosis of EPNET in our university hospital amongst October and October have been included. Information were retrospectively collected. When proliferative index (Ki and mitotic index) weren’t offered on our database,a potential critique of tumor tissue was performed. Prognostic elements had been de.