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Burkitt lymphoma cells seem to have abnormal c-myc gene activity resulting from chromosomal translocation. We have examined the consequences of translocation on putative control sequences near to the c-myc gene by DNase I hypersensitivity mapping of chromatin. There is no detectable difference in the pattern of hypersensitivity (compared with the actively transcribed c-myc gene of lymphoblastoid cells) in Burkitt lymphoma cells where the translocation point occurs at a considerable distance upstream or downstream of c-myc. When the translocation occurs near the 5' end of the c-myc gene, resulting in loss of hypersensitive sites, those that remain show the same sensitivity as in lymphoblastoid cell lines. We conclude that translocation has little general effect on the usual pattern of hypersensitive sites near to the c-myc gene but new sites can be observed in some cases in the immunoglobulin region near to the breakpoint. These may be sites normally involved in immunoglobulin gene transcription and may exert a subtle effect on the translocated c-myc gene.

Original publication




Journal article


Proc Natl Acad Sci U S A

Publication Date





1984 - 1988


Base Sequence, Burkitt Lymphoma, Chromatin, Deoxyribonucleases, Humans, Immunoglobulins, Oncogenes, Translocation, Genetic