References Abou-Merhi, R., Khoriaty, R., Arnoult, D., El Hajj, H., Dbouk, H., Munier, S., El-Sabban, M.E., Hermine, O., Gessain, A., de The, H., Mahieux, R. & Bazarbachi, A. (2007) PS-341 or a combination of arsenic trioxide and interferon-alpha inhibit growth and induce caspase-dependent apoptosis in KSHV/HHV-8-infected primary effusion lymphoma cells. Leukemia, 21, 1792–1801. An, J., Sun, Y., Fisher, M. & Rettig, M.B. (2004) Antitumor effects of bortezomib (PS-341) on primary effusion lymphomas. Leukemia, 18, 1699–1704. Boulanger, E., Gerard, L., Gabarre, J., Molina, J.M., Rapp, C., Abino, J.F., Cadranel, J., Chevret, S. & Oksenhendler, E. (2005) Prognostic factors and outcome of human herpesvirus 8-associated primary effusion lymphoma in patients with AIDS. Journal of Clinical Oncology, 23, 4372–4380. Keller, S.A., Schattner, E.J. & Cesarman, E. (2000) Inhibition of NF-kappaB induces apoptosis of KSHV-infected primary effusion lymphoma cells. Blood, 96, 2537–2542. Lee, R.K., Cai, J.P., Deyev, V., Gill, P.S., Cabral, L., Wood, C., Agarwal, R.P., Xia, W., Boise, L.H., Podack, E. & Harrington, Jr, W.J. (1999) Azidothymidine and interferon-alpha induce apoptosis in herpesvirus-associated lymphomas. Cancer Research, 59, 5514– 5520. Luppi, M., Trovato, R., Barozzi, P., Vallisa, D., Rossi, G., Re, A., Ravazzini, L., Potenza, L., Riva, G., Morselli, M., Longo, G., Cav- anna, L., Roncaglia, R. & Torelli, G. (2005) Treatment of herpesvirus associated primary effusion lymphoma with intracavity cidofovir. Leukemia, 19, 473–476. Matta, H. & Chaudhary, P.M. (2005) The proteasome inhibitor bortezomib (PS-341) inhibits growth and induces apoptosis in primary effusion lymphoma cells. Cancer Biol Ther, 4, 77–82. Sin, S.H., Roy, D., Wang, L., Staudt, M.R., Fakhari, F.D., Patel, D.D., Henry, D., Harrington, Jr, W.J., Damania, B.A. & Dittmer, D.P. (2007) Rapamycin is efficacious against primary effusion lymphoma (PEL) cell lines in vivo by inhibiting autocrine signaling. Blood, 109, 2165–2173. Keywords: human herpesvirus 8, non-Hodgkin lymphoma, primary effusion lymphoma, bortezomib, human immunode- ficiency virus type-1. First published online 13 March 2008 doi:10.1111/j.1365-2141.2008.07057.x t(14;19)(q32;q13) incidence and significance in B-cell lymphoproliferative disorders We read with interest the paper by Huh et al (2007) detail- ing the clinicopathological assessment of seven cases of t(14;19)(q32;q13) positive small B-cell leukaemias. Their study comprised of five men and two women with a median age of 48 years. All seven patients had an absolute lymphocytosis, six patients had lymphadenopathy, and one splenomegaly. Large cell transformation was documented in two cases. Immuno- phenotypic analysis showed that all seven cases expressed CD5, six were negative for CD23 and five were positive for CD38 and FMC7. There was no expression of cyclin D1 or evidence of the t(11;14)(q32;q13) but trisomy 12 was detected in five of the seven cases. The underlying pathological diagnosis was considered to be atypical chronic lymphocytic leukaemia (CLL). We would like to report a further six patients with lymphoproliferative disorders characterised by an under- lying t(14;19)(q32;q13), as detailed in Table I. The t(14;19)(q13;q32) deregulates BCL3 as a consequence of its juxtaposition to the IGH locus. Cases were therefore evaluated by interphase fluorescent in situ hybridisation (FISH) with IGH and BCL3 dual colour gene rearrangement probe sets (Abbott Molecular Inc, Des Plaines, IL, USA and Dako, Glostrup, Denmark respectively) and cases with rearrangements of both IGH and BCL3 were considered to have a t(14;19)(q32;q13), although a combined assay was not performed. This FISH strategy was evaluated in the following groups: CD5 + CD23 ) atypical CLL (n = 76), diffuse large B-cell lymphoma (DLBCL, n = 97), extranodal marginal zone lymphoma (ENMZL) (n = 47) and CD5-B-cell lymphoproliferative disorders (LPD) (n = 136). Cases of mantle cell lymphoma and follicular lymphoma were excluded from this analysis as they have disease-defining IGH translocations. The t(14;19)(q32;q13) was demonstrated in two of 76 cases (2Æ6%) of CD5 + D23 ) atypical CLL. All cases assessed lacked the t(11;14). Both cases with the translocation were characterised by clinical lymphadenopathy and bone marrow infiltration but lymphocytosis was demonstrated in only one patient. Both remain alive with 14 and 19 months follow-up with no evidence of large cell trans- formation. Of the 97 cases with DLBCL, two (2Æ1%) were shown to have a t(14;19)(q32;q13). Interestingly, both cases had a preceding history of CLL. In case 3, the CLL was characterised Correspondence ª 2008 The Authors Journal Compilation ª 2008 Blackwell Publishing Ltd, British Journal of Haematology, 141, 557–563 561