| Abstract: |
In Burkitt's lymphoma, which carries the t(8;14) chromosome translocation, the c-myc oncogene normally located on band q24 of human chromosome 8 (refs 1-3) translocates to the heavy-chain locus on chromosome 14 (refs 1,4,5); this results in transcriptional deregulation of the translocated c-myc oncogene, which is transcribed constitutively at elevated levels5-9, while the normal c-myc oncogene on the uninvolved chromosome 8 is either silent 6-11 or expressed at very low levels (A.ar-R. and C.M.C., unpublished results). We have now introduced the active c-myc oncogene of proliferating mouse spleen cells into human lymphoma cells carrying the t(8;14) chromosome translocation by hydridization, and have examined the hybrids for expression of the human and murine c-myc oncogene. The results of this analysis, reported here, indicate that the active mouse myc gene is shut off at the transcriptional level in the human lymphoma cells, implying that human B cells at the stage of differentiation of lymphoma cells used in this study are nonpermissive for normal c-myc transcription. © 1985 Nature Publishing Group. |
| Keywords: |
human cell; mouse; animals; mice; heredity; cell line; transcription, genetic; in vitro study; oncogenes; gene expression regulation; oncogene; dna; lymphoma cell; gene repression; murinae; translocation, genetic; oncogene c myc; burkitt lymphoma; hybrid cells; chromosomes, human, 6-12 and x; suppression, genetic; humans; human; priority journal; chromosomes, human, 13-15
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