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 Prepublished online as a Blood First Edition Paper on May 29, 2003; DOI 10.1182/blood-2002-12-3630.

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Submitted December 3, 2002
Accepted April 23, 2003

Intronic BCL-6 mutations are preferentially targeted to the translocated allele in t(3;14)(q27;q32) non Hodgkin's B-cell lymphoma

Fabrice Jardin*, Christian Bastard, Nathalie Contentin, Francoise Parmentier, Jean-Michel Picquenot, Herve Tilly, Freda K Stevenson, and Surinder S Sahota

Department of Haematology, Centre Henri Becquerel, Rouen, France; EMI 9906-IRFMP n 23, Centre Henri Becquerel, Rouen, France; Molecular Immunology Group, Tenovus Laboratory, Southampton, United Kingdom

* Corresponding author; email: fab.jardin{at}wanadoo.fr.

Translocations and somatic mutations are common genetic alterations of the BCL-6 gene on chromosome 3q27 in B-cell lymphoma, with implications for lymphomagenesis. The two events may have linked origins, and can influence juxtaposed loci. To evaluate this further, we compared mutations occurring within the major mutation cluster region of the translocated and the untranslocated BCL-6 alleles in 7 t(3;14)(q27;14q32) lymphomas. In 6/7 cases, the translocated allele revealed significantly higher mutations (mean 5.8x10-2 bp-1) when compared to the untranslocated allele (mean 5.3x10-3 bp-1) (p<0.01). The increase mapped to der(14q32) which retains the BCL-6 promoter, and is transcriptionally active as revealed by fusion transcripts and on-going somatic mutations, absent in the der(3q27) region. These results indicate that enhanced mutational activity at the translocated allele may be a consequence of loss of cis regulatory or gain of IgHenhancer elements. Junctional sequences indicate translocation origins from earlier BCL-6 mutations and switch recombinase events.


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