HOST TUMOR INTERACTION IN BURKITTS LYMPHOMA

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Our recent work on the SJL mouse model of follicular center B cell lymphoma (RCS) has established a strong link between the transcription of a novel endogenous mouse mammary tumor virus (MMTV) that serves as an indirect oncogen, mediating the vigorous superantigen-like stimulation of syngeneic CD4+Vbeta16+ T cells upon which RCS depend for their growth. RCS lymphomas share a number of salient features with Burkitt's lymphomas (BL). Both lymphomas are germinal center derived (both express the germinal center specific antigen, CD77); and like RCS lymphomas, BL tumors have T cell infiltrations that could have a potential role in the lymphomagenesis. The overall aim of this proposal is to utilize the findings in the RCS model as a basis for dissection of the role of host T cells in the development of BL. In view of the heterogeneous nature of BL tumors, we will examine a number of African BL tumors from various patients in Ghana (where BL is prevalent) in an attempt to relate tumor phenotypes to their stimulation of particular host T cell subpopulations and to their sensitivity to apoptosis.