Genetics All types of<unk>  are characterized by dysregulation of the c-myc gene by one of three chromosomal translocations. This gene is found at 8q24. * The most common variant is t(8;14)(q24;q32), which accounts for about 85% of cases. This involves c-myc and IGH@. A variant of this, a three-way translocation, t(8;14;18), has also been identified. * A rare variant is at t(2;8)(p12;q24). This involves IGK@ and c-myc. * Another rare variant is t(8;22)(q24;q11). This involves IGL@ and c-myc. Combined, the two less-common translocations, t(2;8)(p12;q24) and t(8;22)(q24;q11), account for the remaining 15% of cases not due to the t(8;14)(q24;q32) translocation. The c-myc gene found on chromosome 8 is part of the Myc family of genes that serve as regulators of cellular transcription and is associated with<unk> . Expression of the c-myc gene results in the synthesis of transcriptional factors that increase the expression of other genes involved in aerobic glycolysis. Ultimately, an increase in aerobic glycolysis plays a role in providing the necessary energy for cellular growth to occur. The translocation of the c-myc gene to the IGH, IGK, or IGL region moves the gene to a location in the genome near immunoglobulin enhancers which increases the expression of the c-myc gene. Overall, this translocation leads to increased cellular proliferation that is found in<unk> . Point mutations can also be present in the translocated c-myc gene resulting in the expressed c-myc protein being overactive. Other mutations found include the TCF transcription factor mutation, which increases cellular proliferation via the increased expression of other genes. Along with mutations that support cell proliferation,<unk>  has been found to also harbor mutations in the TP53 gene that is a tumor suppressor and would normally function to limit cellular growth. Virology The complete role of EBV in the pathogenesis of endemic<unk>  is not completely elucidated, but it has been shown to cause DNA damage, dysfunction of telomeres, and genome instability. B cell infection with EBV is latent, and the virus does not undergo replication. These latently infected B cells can then go on to produce proteins that function to promote cellular growth through modification of normal signaling pathways. EBV promotes the development of malignant B cells via proteins that limit apoptosis in cells that had the c-myc translocation. Apoptosis is limited by EBV through various means such as the EBNA1 protein, BHF1 protein, EBER transcripts, vIL-10, BZLF1, and LMP1. Malaria has been found to cause genomic instability in endemic<unk> . Malaria can lead to the reactivation of latent EBV and also MYC translocations via activation of the toll-like receptor 9. Malaria also promotes B-cell proliferation by altering the regular immune response. The immune system targets antigens (e.g., EBNA2 and LMP-1) and eliminates most B cells infected with EBV. Downregulation of antigens targeted by the immune system leads to the development of persistent B cells. These B cells can then undergo further mutations (e.g., c-myc translocation) that promote cancer development. Immunology<unk>  cells express HLA class I molecules normally, as well as some HLA class II complexes; however, CD4+ T cells are not properly activated.<unk>  cells only express EBNA 1, a poorly antigenic EBV-associated antigen, that is able to escape HLA class I presentation, thus evades an immune response. EBNA 1 can be presented via HLA class II molecules, however HLA Class II pathway is unable to activate the CD4+ T cells.
Burkitt lymphoma
Hodgkin lymphoma
AIDS-related lymphoma
Thymic carcinoma
B-cell lymphoma
Thymoma with immunodeficiency
Diffuse large B-cell lymphoma
Mantle cell lymphoma