We have determined the frequency with which each of the breakpoint areas of bcl-2 are involved in translocation and are currently investigating whether the specific breakpoints might influence the clinical behavior of lymphoma. In the process, we are fine mapping the sites of these breakpoint regions. To adapt PCR technology to the diagnosis of t(14;18) translocated lymphomas, we have developed sets of oligonucleotide primers specific for each of four reported breakpoint clusters so that the majority of t(14;18) translocated lymphomas can be identified. we are continuing to study the feasibility of using PCR to follow response to therapy and predict relapse using peripheral blood and other tissue samples. we are continuing retrospective studies using fixed tissues. We have shown the bcl-l major breakpoint region is associated with malignant lymphoma of intermediate differentiation. we have examined several additional breakpoint regions and are currently initiating studies to investigate the role of the candidate bcl-l gene, PRAD1. We have identified and sequenced a T-cell receptor delta gene rearrangement occurring in over a third of precursor B ALL. This common rearrangement can be used to aid in the diagnosis of primary and particularly recurrent disease. We have performed a molecular study of small non-cleaved cell lymphomas and have shown that molecular differences exist between the Burkitt's subgroup and the non-Burkitt's subgroup. The separation of these two entities has been controversial, and these results suggest the two subgroups have a different molecular pathogenesis, supporting the uniqueness of these entities. We have initiated studies into possible viral involvement in several lymphoproliferative diseases. These include the involvement of HTLV-like viruses in T cell diseases and the involvement of herpes viruses in angiocentric lymphomas, AILD, and Kikuchi's disease.
