Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0026764 (multiple myeloma)
36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aleutian disease of mink is a viral illness characterized by systemic plasmocytosis and hypergammaglobulinemia. Some affected mink develop a monoclonal gammaglobulin spike and Bence-Jones proteinuria. A case of multiple myeloma in a mink handler with a 15-year history of exposure to Aleutian mink is presented. Previously reported cases of possible Aleutian disease (AD) in man are discussed and the pathogenesis of AD reviewed. Aleutian disease virus (ADV) may produce asymptomatic infection in exposed individuals. Available data suggest symptomatic disease in humans is extremely rare.
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PMID:Multiple myeloma in a mink handler following exposure to Aleutian disease. 22 31

368 1- to 5-year-old mink of wild-type or black genetic background were infected with Aleutian disease virus (ADV) naturally or using virus-containing immune complexes or purified virus. Thirty of the mink were immunized with dinitrophenol-conjugated ovalbumin (DNP-OA) before and during infection. Blood samples were taken at monthly intervals. We found that weak (and transient) monoclonal or oligoclonal immunoglobulin components were present in the plasma or serum approximately 1 month after infection, as judged by zone electrophoresis. In a few cases, we found quite stable myeloma-like hypergammaglobulinemia, which usually occurs much later in the infection. All sera with monoclonal immunoglobulin components and most of the sera with immunoglobulins of restricted heterogeneity were analysed by crossed serum line immunoelectrophoresis. In all cases, the distinct immunoglobulins were found to have antibody activity to ADV proteins. In the few sera from DNP-OA-immunized mink showing restricted immunoglobulin heterogeneity, this was also the case. The findings from the study imply that ADV-specific B lymphocytes are probably the primary targets for ADV. The resulting ADV replication introduces a "pseudo-transformation" stage, so that the infected B lymphocytes proliferate and differentiate to an extreme degree. The mechanism behind this B-cell pseudotransformation ability of ADV is a puzzle. It may, however, be important, that the p75/85 structural polypeptides of ADV contain an amino acid sequence almost identical to the GTP-binding pocket of the Ras oncogene.
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PMID:Virus-specific B-lymphocytes are probably the primary targets for Aleutian disease virus. 165 Oct 29