Human Pathol 1997; 28: 801–808. 10 Boulanger E, Agbalika F, Maarek O et al. A clinical, molecular and cytogenetic study of 12 cases of human herpesvirus 8 associated primary effusion lymphoma in HIV-infected patients. Haematol J 2001; 2: 172–179. 11 Oksenhendler E, Clauvel JP, Jouveshomme S et al. Complete remission of a primary effusion lymphoma with antiretroviral therapy. Am J Hematol 1998; 57: 266. 12 Simonelli C, Spina M, ABT-737 cost Cinelli R et al. Clinical features and outcome of primary effusion lymphoma in HIV-infected patients: a single-institution

study. J Clin Oncol 2003; 21: 3948–3954. 13 Valencia ME, Martinez P, Moreno V et al. AIDS-related body cavity-based lymphomas, herpesvirus-8 and HIV infection: a study of seven cases. AIDS 1999; 13: 2603–2605. 14 Ascoli V, Signoretti S, Onetti-Muda A et al. Primary effusion lymphoma in HIV-infected patients

with multicentric Castleman’s disease. J Pathol 2001; 193: 200–209. 15 Toomey NL, Deyev VV, Wood C et al. Induction of a TRAIL-mediated Carfilzomib suicide program by interferon alpha in primary effusion lymphoma. Oncogene 2001; 20: 7029–7040. Plasmablastic lymphoma accounts for 2.6% of all HIV-related lymphomas [1]. In the original report, 15 of the 16 cases were HIV infected and had involvement of the oral cavity [2]. The disease can also occur in the non-HIV population, particularly in those with immunosuppression. There are three recognized subtypes of plasmablastic lymphoma. The first is the usually found in the oral mucosa and contains a monomorphic population of plasmablasts with minimal plasmacytic differentiation. The second type tends to have more plasmacytic differentiation Phospholipase D1 and is usually extraoral. The third type is plasmablastic lymphoma associated with Castleman’s disease and is typically nodal or splenic.

In the WHO classification [3], the tumour is a subtype of diffuse large B cell lymphoma (DLBCL). The majority of patients with PBL are men, particularly in the HIV population, with a mean age of presentation of 39 years. These tumours need to be distinguished from the immunoblastic variant of DLBCL and body and extracavity variants of primary effusion lymphoma (PEL), Burkitt lymphoma (BL) with plasmacytoid differentiation, and extramedullary plasmablastic secondary multiple myeloma. Advances in immunophenotyping have facilitated these distinctions based on the low or absent expression of leukocyte common antigen (CD45) or the B cell markers CD20, CD79a, and PAX5. The plasma cell markers VS38c, CD38, multiple myeloma oncogene-1 (mum-1) and CD138 (syndecan-1) are almost always expressed [4]. The tumour cells are nearly always Epstein–Barr virus positive and this may be demonstrated in their three latent forms by the use of fluorescent or chromogenic in situ hybridization and may be useful in distinguishing it from plasmablastic multiple myeloma.