Activation of a translocated human c-myc gene by an enhancer in the immunoglobulin heavy-chain locus

Deregulation of the proto-oncogene c-myc through t(8;22) translocation in Burkitt's lymphoma

“…In the case of t(8;14) translocations, which link the c-myc gene to the immunoglobulin heavy chain locus, it has been shown that the m intron enhancer, the 3' Ca enhancer and the Ca¯anking matrix attachment region are required for c-myc deregulation (Hayday et al, 1984;Madisen et al, 1994). For the immunoglobulin k locus it has also been demonstrated that three elements are necessary for the BL cell speci®c deregulation: only the interplay of the k intron enhancer (Ei), 3'-enhancer (E3') and the matrix attachment region (MAR) causes c-myc overexpression, promoter shift and the absence of the RNA elongation block (HoÈ rtnagel et al, 1995;Polack et al, 1993).…”

microRNA 28 controls cell proliferation and is down-regulated in B-cell lymphomas

“…The involvement of MYC in the regulation of miR-28 is an intriguing observation given that ectopic/deregulated MYC expression represents the hallmark of BL and is also frequently found in other GC-derived lymphomas (33,34). MYC is known to directly induce the expression of the prooncogenic miR-17-92 cluster (3), but it is also involved in a widespread down-regulation of miRNA expression (35).…”

An active chromatin structure acquired by translocated c-myc genes.

“…This demonstrates a requirement for B-cell-specific factors and suggests that B-cell factors normally involved in immunoglobulin gene transcription may also activate the cryptic c-myc promoters translocated adjacent to immunoglobulin genes. With few exceptions (7,11,16,22,39), the known immunoglobulin heavy-chain enhancer (3,19,29,30) does not remain on the same chromosome as the translocated c-myc gene and thus is not responsible for this activation (18,24,29,35). Since DNase I-sensitive structure is associated with active genes (23,44 46), we reasoned that an analysis of c-myc gene chromatin in plasmacytomas might provide insight into mechanisms responsible for activation of the cryptic promoters.…”