Missteps in 'tango' for epigenome targeting.

摘要

Deregulated epigeneticmarks, represented by methylation of clusters of CpG dinucleotides in the promoter DNA along with histone methylation and deacety-lation, result in silencing of tumor suppressor genes (TSGs), which play a significant role in the pathogenesis and biology of my-elodysplastic syndrome (MDS) and acute myeloid leukemia. Sequential treatment with DNA methyltransferase 1 (DNMT1) followed by a histone deacetylase (HDAC) inhibitor derepressed TSGs, as well as induced cell-cyclin dependent kinase inhibitors, growth arrest, differentiation, and apo-ptosis of transformed cells.