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Background AIDS-related lymphomas (ARLs), which include Burkitt lymphoma and diffuse large B cell lymphoma (DLBCL), are a heterogeneous group of lymphoproliferative disorders that occur in the setting of HIV-mediated immune suppression. A subset of cases are associated with EpsteinBarr virus (EBV) infection. EBV expresses latent viral oncoproteins that constitutively activate the transcription factor NFB, a potent inducer of genes involved in promoting B cell survival and proliferation [1]. In immunocompetent individuals, lymphomas that are not associated with EBV can also display increased NFB activity, and recent reports have described mutations in regulators of NFB. One of the frequently mutated regulatory genes is TNFAIP3, which encodes A20, a ubiquitin modifying enzyme involved in the termination of NFB signaling. Mutations resulting in the inactivation of A20 have been found in a significant proportion of marginal zone lymphomas [2], classical Hodgkin’s lymphomas and primary mediastinal B cell lymphomas [3], and DLBCLs [4]. In ARL the role of NFB activation and the incidence of mutations in A20 have not been described.

TNFAIP3(A20) genetic alterations in AIDS-related lymphomas