MLL is fused to CBP, a histone acetyltransferase, in therapy-related acute myeloid leukemia with a t(11;16)(q23;p13.3)

摘要: The recurring translocation t(11;16)(q23;p13.3) has been documented only in cases of acute leukemia or myelodysplasia secondary to therapy with drugs targeting DNA topoisomerase II. We show that the MLL gene is fused codes for CBP (CREB-binding protein), protein binds specifically DNA-binding CREB (cAMP response element-binding protein) this translocation. in-frame a different exon two patients producing chimeric proteins containing AT-hooks, methyltransferase homology domain, and transcriptional repression domain binding bromodomain CBP. Both fusion products retain histone acetyltransferase may lead by promoting acetylation genomic regions targeted leading deregulation via aberrant chromatin organization. first partner well defined structural functional motifs provide unique insights into potential mechanisms which these translocations contribute leukemogenesis.