Preliminary molecular and histological characterizations indicate
a 35% KRAS mutation rate on clinical samples, which is in accordance with the mutation learn more frequency described in the literature for CRC, and a high degree of histological similarity between early passages of xenografts and the original clinical tumor samples. All model characteristics are being compiled in a web-based database for efficient features search and interconnection. We will present the first characterized models and will discuss their usefulness and chance to bring benefit to patients via novel therapeutic strategies. Poster No. 70 Circulating Endothelial Cells and Microparticles as Potential Surrogate Biomarkers in Multiple Myeloma Management Hélène Duval 1 , Frédéric Dugay1, Mikael Roussel2, Karin Tarte3, Thierry Fest2, Benoît Guillet1 1 Pôle Cellules et Tissus, Service d’Hémostase Bioclinique, CHU Pontchaillou, Rennes, France, 2 Pôle Cellules et Tissus, Laboratoire d’Hématologie Biologique, CHU Pontchaillou, Rennes, France, 3 INSERM U917 – MICA, Faculté de Médecine de Rennes, Rennes, France New blood vessel development is an important process in tumor progression. In multiple myeloma (MM),
the growth of neoplastic plasma cells is directly regulated by neoangiogenesis. Evidence is emerging that angiogenesis not only relies on the sprouting of resident endothelial cells from preexisting vessels. Circulating endothelial progenitors (CEP) derived from Unoprostone the bone marrow and blood circulating endothelial cells detached from mature vessels (CEC) may also contribute to postnatal angiogenesis. Upon cell activation, procoagulant
SGC-CBP30 microparticles (MP) derived from platelets, leukocytes, endothelial cells or erythrocytes are also found in circulating blood. Besides their potential implication in cancer-associated thrombosis, MPs are able to trigger an angiogenic program. Interestingly, MM is characterized by an increased incidence of deep venous thrombosis. In this context, we aimed to test the potential usefulness of studying angiogenic markers (levels of CEP, CEC, VEGF, Endostatin) and MP in circulation but also directly in the bone marrow, as potential biomarkers for the prognostic and the follow-up of myeloma patients. DNA+CD45- CD31+ CD146+ CD34+ circulating endothelial cells were enumerated using a flow cytometer dedicated to the study of rare events (CyanTM ADP Analyser). Phenotypic specifications were shown to be partly shared with plasma cells. Endothelial cell phenotype was confirmed by immunocytochemistry using anti-von Willebrand Factor staining and UEA-1 lectin binding. In parallel, annexinV+CD41+ platelets-derived microparticles were mTOR inhibitor quantitated. Quantification and kinetics of occurrence of CEC, CEP and MP should reflect vascular injury or malignancy and would be therefore useful to optimize therapeutic options. This project aim to develop a less invasive method to improve the patient management. Poster No.