Translocated c-myc oncogene of Burkitt lymphoma is transcribed in plasma cells and repressed in lymphoblastoid cells.

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Abstract
Somatic cell hybrids between Burkitt lymphoma cells and either human lymphoblastoid cells or mouse plasmacytoma cells were examined for the expression of the translocated c-myc oncogene. The translocated c-myc oncogene is transcribed in plasma cells but is repressed in lymphoblastoid cells. The factors necessary for translocated c-myc transcription are present in plasma cells and Burkitt lymphoma cells but are absent or inactive in lymphoblastoid cells. Since the distance between the rearranged Ig loci and the c-myc oncogene can even exceed 30-50 kilobases, the translocated c-myc oncogene may be under the transcription control of enhancer-like elements capable of acting over long distances. The activity of this long-range enhancer may depend on the interaction with transacting factors that are active in plasma cells and in Burkitt lymphoma cells but are not active in lymphoblastoid cells. The transcription of the 1st exon of the c-myc oncogene was examined, which becomes separated from the 2nd and 3rd exon because of the chromosomal break involving the 1st intron. This exon is transcribed at high levels in ST486 Burkitt lymphoma cells with the t(8;14) chromosome translocation. Hybrids between lymphoblastoid and ST486 cells expressed high levels of transcripts of the 1st exon, whereas hybrids between plasma cells and ST486 cells did not. Transcription of the separated 1st exon can be enhanced in lymphoblastoid and Burkitt lymphoma cells because of its close proximity to the H chain enhancer that is normally located between the joining and the switch region of the C.mu. gene. Such enhancement does not occur in plasma cells, possibly because these cells are able to suppress completely the c-myc oncogene, unless it was placed in the proximity of a rearranged Ig constant region gene.