© 1992 Oxford University Press
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Variable breakpoints in Burkitt lymphoma cells with chromosomal t(8; 14) translocation separate c-myc and the IgH locus up to several hundred kb
GSF-Forschungszentrum für Umwelt und Gesundheit GmbH, Institut für Klinische Molekularbiologie und Tumorgenetik Marchioninistraße 25, 8000 München 70 1Deutsches Krebsforschungszentrum, Angewandte Tumorvirologie 6900 Heidelberg, Germany 2Dana-Faber Cancer Institut Boston, MA 02115, USA 3Inserm U 75, Faculté de Médecine Necker-Enfants Malades 75730 Paris, Cedex 15 4Centre international de recherche sur le cancer 69003 Lyon, France
* Deutsches Krebsforschungszentrum, Angewandte Tumorvirologie, Im Neuenheimer Feld 280, 6900 Heidelberg, Germany
Received June 30, 1992; Revised September 4, 1992; Accepted September 4, 1992
In about 80% of Burkitt's lymphoma cases, the tumour cell harbours a reciprocal chromosomal translocation which invariably transposes the coding exons 2 and 3 of c-myc from chromosome 8 to the immunoglobulin heavy chain locus on chromosome 14. Those t(8;14) translocations which disrupt chromosome 8 within or close to the c-myc gene are well documented. In this study we have focussed on t(8; 14) translocations with the chromosomal breakpoint far upstream of c-myc. We analyzed the breakpoint position in 44 BL cell lines with t(8; 14) translocations of different geographical origin and identified 9 cell lines with the breakpoint more than 14 kb upstream of c-myc. In these cell lines the positions of the translocation junctions on the derivative chromosomes 8q– and 14q+ were mapped by pulsed field gel electrophoresis and multicolour fluorescence in situ hybridization. The breakpoints occur at distances between 55 and more than 340 kb upstream of c-myc with no preferential site on chromosome 8. On chromosome 14, however, the translocation breakpoints are clustered in a narrow region 5' of the intron enhancer of the immunoglobulin heavy chain gene. In 7 of 9 cases, the enhancer is fused to the c-myc bearing sequences of chromosome 8. In two cases, the translocation has occurred in switch µ and downstream of Cµ, respectively. The impact of these results with respect to the hypothesis, that cisregulatory sequences from the immunoglobulin heavy chain locus can deregulate c-myc expression in a manner sufficient for tumour formation, is discussed.
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