A Repressor of c-myc Transcription Is Found Specifically in Plasmacytomas
Since the discovery that translocation of c-myc genes results in altered c-myc gene expression (for review see Cory 1986), a great deal of effort has been directed toward understanding how regulation of c-myc occurs under both normal and altered conditions. Work by many groups has shown that translocated c-myc is activated in plasmacytomas, but little insight has been gained into the mechanism of this activation (Cory 1986, Kakkis, Mercola and Calame 1988). Another interesting finding is that c-myc genes in their normal chromosomal context are not transcribed at detectable levels in plasmacytomas (Fahrlander et al 1985, Kakkis, Mercola and Calame 1988). Although many interpretations of this result are possible, we considered it likely that the c-myc gene could be normally repressed at the terminal stage of B-cell differentiation and that translocation could release c-myc from repression and activate its transcription. The repression of c-myc in plasmacytomas may represent the cell’s attempt to turn off cell division. Studies on a number of in vitro differentiation systems suggest that c-myc expression correlates with proliferation and c-myc repression reflects the cessation of cell division (e.g. Bentley and Groudine 1986, Lachman and Skoultchi 1984, Resnitsky et al 1986). The mechanism for this repression in plasmacytomas is thus of considerable importance.
KeywordsLymphoma DMSO Titration Chloramphenicol Plasmacytomas
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