ABSTRACT Epstein-Barr Virus (EBV) is the etiological agent of several hematopoietic malignancies including multiple types of non-Hodgkin lymphoma (NHL). These EBV-positive NHL subtypes are comprised of post-transplant lymphoproliferative disease (PTLD), diffuse large B cell lymphomas (DLBCL), T cell lymphomas, Natural killer (NK)/T cell lymphoma (NKTL), and Burkitt's lymphoma (BL). Our studies have found that FAM72A is highly expressed in EBV-positive lymphomas and contributes to EBV-mediated lymphomagenesis, which gives rise to EBV-positive NHL. In response to PAR-21-348, we propose to address how EBV’s upregulation of FAM72A contributes to the development of EBV-driven NHL.

NARRATIVE Epstein-Barr Virus (EBV) is the etiological agent of several malignancies including Hodgkin lymphoma (HL) and multiple types of non-Hodgkin lymphoma (NHL) such as post-transplant lymphoproliferative disease (PTLD), diffuse large B cell lymphomas (DLBCL), T cell lymphomas, NK/T cell lymphoma (NKTL), and Burkitt's lymphoma (BL). We propose to determine the mechanism by which EBV drives lymphomagenesis and identify new therapeutics for EBV-associated lymphomas.