FUSION OF THE LAZ3 BCL6 AND BOB1/OBF1 GENES BY T(3-11) (Q27-Q23) CHROMOSOMAL TRANSLOCATION/

Citation
S. Galieguezouitina et al., FUSION OF THE LAZ3 BCL6 AND BOB1/OBF1 GENES BY T(3-11) (Q27-Q23) CHROMOSOMAL TRANSLOCATION/, Comptes rendus de l'Academie des sciences. Serie 3, Sciences de la vie, 318(11), 1995, pp. 1125-1131
Citations number
27
Categorie Soggetti
Multidisciplinary Sciences
ISSN journal
07644469
Volume
318
Issue
11
Year of publication
1995
Pages
1125 - 1131
Database
ISI
SICI code
0764-4469(1995)318:11<1125:FOTLBA>2.0.ZU;2-N
Abstract
The LAZ3/BCL6 gene on chromosome 3q27 is recurrently disrupted in B-ce ll 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 w as created by fusion, 5' to the LAZ3 exon 2, with a transcribed sequen ce identical to BOB1/OBF1, a B cell-specific coactivator of octamer-bi nding transcription factors, recently described. Nucleotidic sequence of a nearly full-length cDNA of the BOB1/OBF1 gene revealed particular features es in the 3' untranslated region of the gene, including pyri midine-rich sequence repeats, an Alu motif, and a polymorphic [CCTT] t etranucleotide microsatellite. Two A to G transition mutations were al so detected in the coding region of one allele of a lymphoma B-cell li ne, Raji, leading to 2 amino-arid changes in the C-terminal region. Du e to its cell-specificity and role as a coactivating transcription fac tor, chromosomal translocation and/or perhaps point mutation of BOB1/O BF1 may contribute to B cell tumorigenesis.