This phenotype is encountered only in B lymphocytes and induces their proliferation. It is usually referred to as Type III EBV expression or growth C188-9 chemical structure transformation program. Such cells are readily

recognized by the immune response. The presence of the EBV genome in lymphocytes with a restricted viral protein expression, as it occurs in Hodgkin’s and nasal NK lymphomas, that lacks the nuclear protein EBNA-2, does not induce proliferation. However it modifies the behaviour of the cell. Such 17DMAG purchase cells can avoid apoptosis, and induce an enrichment of inflammatory cells in the microenvironment environment. Intercellular contacts and /or cytokines induce their proliferation. We studied the details of IL21 imposed modification of EBV gene expression: We found that in Type III cells IL-21, enhanced the LMP-1 promoter and silenced the C click here promoter with the consequence that 5 of the 6 EBNAs disappeared. EBNA-1 that can be transcribed from its own specific promoter, Qp, was maintained. Thus the cells switched to the Type IIa (EBNA-1 and LMP-1) pattern with elevated expression

of the LMP-1 protein. Exposure of Type I (only EBNA-1 expressed) BL cells to IL-21, activatied the LMP-1p and thus resultsd also in a Type IIa pattern because the cells maintained the Qp deriven EBNA-1 expression. We could show that IL21 has a direct effect on the LMP-1p. We postulate that silencing of the Cp occurs through the activation of a suppressor protein O81 Adhesive Interactions Regulate Transcriptional Diversity in Malignant B-cells Ben-Zion Katz 1,4 , Liat Nadav1,2, Tal Shay3, Eytan Domany3, Elizabeth Naparstek1,4, Benjamin Geiger2 1 The Hematology

Institute, Tel Aviv Sourasky Medical Center, Tel-Aviv, Israel, 2 Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel, 3 Department of Physics of Complex Systems, Weizmann Institute of Science, Rehovot, Israel, 4 Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel The genetic profiling of B-cell malignancies is rapidly NADPH-cytochrome-c2 reductase expanding, providing important information on the tumorigenic potential, response to treatment, and clinical outcome of these diseases. However, the relative contributions of inherent gene expression vs. microenvironmental effects are poorly understood. The regulation of gene expression programs by means of adhesive interactions was studied in ARH-77 human malignant B-cell variants, derived from the same cell line by selective adhesion to a fibronectin matrix. The populations included cells that adhere to fibronectin and are highly tumorigenic (designated “Type-A” cells), and cells that fail to adhere to fibronectin, and fail to develop tumors in vivo (“Type-F” cells). To identify genes directly affected by cell adhesion to fibronectin, Type-A cells deprived of an adhesive substrate (designated “AF cells”) were also examined.