Abstract
The limited contribution of DNA methylation to PML-RARα induced leukemia
Highlights
Cellular transformation by oncogenes involves disturbance of multiple cellular systems
PML-RARα binding-sites remained non-methylated and appeared protected from the actual hypermethylation phenotype in acute promyelocytic leukemia (APL). In contrast to this protection from DNA methylation, PML-RARα target-genes are silenced via recruitment of histone deacetylases (HDACs) to PML-RARα binding-sites [4, 5]
The actual binding of PML-RARα takes place at accessible chromatin [6], which together with our data underscores that heterochromatin formation at PML-RARα targeted genes is not required for APL pathogenesis
Summary
Cellular transformation by oncogenes involves disturbance of multiple cellular systems. PML-RARα is an oncogene that induces acute promyelocytic leukemia (APL). PML-RARα binding-sites remained non-methylated and appeared protected from the actual hypermethylation phenotype in APL. In contrast to this protection from DNA methylation, PML-RARα target-genes are silenced via recruitment of histone deacetylases (HDACs) to PML-RARα binding-sites [4, 5].
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