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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Fusion of the LAZ3/BCL6 and BOB1/OBF1 genes by t(3; 11) (q27; q23) chromosomal translocation.

The LAZ3/BCL6 gene on chromosome 3q27 is recurrently disrupted in B-cell non Hodgkin's lymphomas by translocations involving immunoglobulin genes or other chromosome regions. We have studied the t(3; 11) (q27; q23) translocation, present in a B-cell leukemia cell line (Karpas 231). As a consequence of this translocation, a LAZ3 chimeric transcript was created by fusion, 5' to the LAZ3 exon 2, with a transcribed sequence identical to BOB1/OBF1, a B cell-specific coactivator of octamer-binding transcription factors, recently described. Nucleotidic sequence of a nearly full-length cDNA of the BOB1/OBF1 gene revealed particular features in the 3' untranslated region of the gene, including pyrimidine-rich sequence repeats, an Alu motif, and a polymorphic [CCTT] tetranucleotide microsatellite. Two A to G transition mutations were also detected in the coding region of one allele of a lymphoma B-cell line, Raji, leading to 2 amino-acid changes in the C-terminal region. Due to its cell-specificity and role as a coactivating transcription factor, chromosomal translocation and/or perhaps point mutation of BOB1/OBF1 may contribute to B cell tumorigenesis.[1]


  1. Fusion of the LAZ3/BCL6 and BOB1/OBF1 genes by t(3; 11) (q27; q23) chromosomal translocation. Galiègue-Zouitina, S., Quief, S., Hildebrand, M.P., Denis, C., Lecocq, G., Collyn-d'Hooghe, M., Bastard, C., Yuille, M., Dyer, M.J., Kerckaert, J.P. C. R. Acad. Sci. III, Sci. Vie (1995) [Pubmed]
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