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- W2276124751 abstract "Severe impairments in immune function — genetically determined, iatrogenic or acquired as a consequence of infection — are associated with increased frequencies of lymphomas, most often of B cell origin. The mechanisms responsible for development of these tumors are poorly understood although roles for EBV and alterations in the structure of the myc protooncogene have been suggested for human lymphomas appearing in the post-transplant setting or during the course of AIDS. We previously reported that mice with a retrovirus-induced immunodeficiency syndrome, termed mouse AIDS (MAIDS), develop B cell lineage lymphomas at a low frequency at 20 or more weeks after infection (1). These lymphomas appeared to pass through several stages during their evolution — an initial phase of polyclonal B cell activation and differentiation to Ig secretion (1, 2) followed by oligoclonal expansion of cells with preferred growth advantage and eventually, a monoclonal neoplastic population. We suggested previously (3) this progression might be attributed to chronic stimulation of B cells by T cells responding to the virus etiologic for MAIDS (4) but more recent studies (5) demonstrated that the tumors recovered in tissue culture contained multiple integrated copies of this virus." @default.
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- W2276124751 date "1992-01-01" @default.
- W2276124751 modified "2023-09-26" @default.
- W2276124751 title "Lymphomas in Mice with Retrovirus-lnduced Immunodeficiency" @default.
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- W2276124751 doi "https://doi.org/10.1007/978-3-642-77633-5_50" @default.
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