Abstract Submission Submission navigation links for EBV-Associated Lymphoma Consortium Annual Meeting (Abstracts) ‹ Previous submission Next submission › Submission information Submission Number: 3 Submission ID: 150046 Submission UUID: 0573b5ec-04a8-458e-bf34-00f0b8ab1387 Submission URI: /nci/ealv/venue/abstract Submission Update: /nci/ealv/venue/abstract?token=wg-U3YtY3ei5pmyiR0L0Jr-_SCUs39ywuiS1LGZb1lE Created: Wed, 08/27/2025 - 16:49 Completed: Wed, 08/27/2025 - 16:49 Changed: Wed, 08/27/2025 - 16:49 Remote IP address: 10.208.28.150 Submitted by: Anonymous Language: English Is draft: No Webform: EBV-Associated Lymphoma Consortium Annual Meeting (Abstracts) Submitted to: EBV-Associated Lymphoma Consortium Annual Meeting (Abstract) OMB No.: 0925-0740 Expiration Date: 9/30/2025 Public reporting burden for this collection of information is estimated to average 60 minutes per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing the collection of information. An agency may not conduct or sponsor, and a person is not required to respond to, a collection of information unless it displays a currently valid OMB control number. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to: NIH, Project Clearance Branch, 6705 Rockledge Drive, MSC 7974, Bethesda, MD 20892-7974, ATTN: PRA (0925-0740). Do not return the completed form to this address. Presenter Information Please enter information for the person who will be the primary presenter/speaker/author. First Name Middle Initial Last Name Degree(s) Please use the following formatting for these degrees: M.D. Ph.D. MPH Position/Title/Career Status Organization Organization Address Organization City/Town Email Please provide a contact email for conference organizers to reach you. Abstract Information Abstract Keywords Up to five keywords of your choice Abstract Title Abstract Summary EBV causes human B-cell lymphomas, including Burkitt lymphomas (BLs), diffuse large B cell lymphomas (DLBCLs), Hodgkin lymphomas (HLs) and Plasmablastic lymphomas (PLs). EBV+ lymphomas in immunocompetent humans are usually derived from germinal center (GC)-experienced B cells and have stringent latency forms that do not express the viral transforming protein, EBNA2. EBV+ lymphomas with “Type II” latency (the most common latency type in DLBCLs and HLs) are driven by the LMP1 and LMP2A EBV proteins, which activate NF-KB and B-cell receptor-like signaling, respectively. However, there is currently no model system for studying how type II latency transforms normal human GC-derived B cells into lymphomas in vivo. Here we show that tonsil GC B cells (GCBs) infected with an EBNA2-deleted EBV mutant (ΔEBNA2) proliferate indefinitely on a CD40L/IL21-expressing feeder layer and form lymphomas in NSG mice that resemble human DLBCLs and PLs. ΔEBNA2-infected tumors that have high-level LMP2A expression (with type II latency) form lymphomas that express plasmablast markers, while tumors with LMP2A-negative “Wp-restricted” latency (a latency type found in some EBV+ human BLs) have a GCB DLBCL-like phenotype. Using this novel model system, we show that LMP2A activates expression of cellular proteins required for plasmablast differentiation and decreases expression of cellular proteins required for GCB and B-cell identity. Furthermore, LMP2A increases expression of genes involved in lymphocyte mobility and trafficking and enhances tumor invasiveness in vivo. This new model system can thus be used to define roles of viral and cellular proteins in EBV-induced human GCB-derived lymphomas that lack EBNA2 expression Save Leave this field blank
