Transcription enhancer identified near the human C mu immunoglobulin heavy chain gene is unavailable to the translocated c-myc gene in a Burkitt lymphoma.
Rabbitts TH., Forster A., Baer R., Hamlyn PH.
In Burkitt lymphoma the c-myc gene, the cellular homologue of the viral oncogene v-myc, has been implicated in the aetiology of this human B-cell malignancy. Burkitt lymphoma cells possess specific chromosomal rearrangements involving the region proximal to the c-myc gene and one of the three human immunoglobulin loci. The nature of the effect exerted by the immunoglobulin loci on the translocated c-myc gene is controversial: whereas some reports have suggested c-myc transcription is elevated in Burkitt lymphoma cells, others have suggested the level of transcription is unaffected by the translation. Recently, transcription enhancer elements have been identified in the intron between the JH and C mu segments of the heavy-chain immunoglobulin gene in mice. If similar enhancers exist in humans they may lead to increased transcription of the translocated c-myc gene and thus contribute to oncogenesis in Burkitt lymphoma. We report here the identification of an enhancer element adjacent to the human C mu gene on normal chromosome 14, but this enhancer does not remain on the abnormal chromosome 14 to which the c-myc gene has been translocated in the Burkitt lymphoma cell line Raji. This element is, therefore, not available for control of the translocated c-myc gene in this case.