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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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Blood, 1 September 2003, Vol. 102, No. 5, pp. 1872-1876
NEOPLASIA
Brief report
Intronic BCL-6 mutations are preferentially targeted to the translocated allele in t(3;14)(q27;q32) non-Hodgkin B-cell lymphoma
Fabrice Jardin,
Christian Bastard,
Nathalie Contentin,
Françoise Parmentier,
Jean-Michel Picquenot,
Hervé Tilly,
Freda K. Stevenson, and
Surinder S. Sahota
From the Department of Haematology, Centre Henri Becquerel, Rouen,
France; EMI 9906-IRFMP no. 23, Centre Henri Becquerel, Rouen, France; and the
Molecular Immunology Group, Tenovus laboratory, Southampton University
Hospitals, Southampton, United Kingdom.
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 2 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
untranslocated BCL-6 alleles in 7 t(3;14)(q27;14q32) lymphomas. In 6
of 7 cases, the translocated allele revealed significantly higher mutations
(mean, 5.8 x 10–2
bp–1) than did the untranslocated allele (mean,
5.3 x 10–3 bp–1;
P < .01). The increase mapped to der(14q32), which retains the
BCL-6 promoter and is transcriptionally active, as revealed by fusion
transcripts and ongoing 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 elements or
gain of IgH enhancer elements. Junctional sequences indicate
translocation origins from earlier BCL-6 mutations and switch
recombinase events.
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