The development of acute myeloid leukemia (AML) is associated with a variety of genetic changes. Some of these alterations are epigenetic, wherein the sequence of the genes is unchanged, but chemical modifications to the DNA alter gene expression. In a study published in the Journal of Clinical Investigation, researchers led by Daniel Tenen at Beth Israel Deaconess Medical Center found that a transcriptional regulator known as C/EBPG was highly expressed in a subset of AML samples that had an epigenetically silenced C/EBPA gene. By blocking the epigenetic modification of C/EBPA, Tenen and colleagues found that they could reduce C/EBPG and restore normal myeloid blood cells. This study suggests that targeting the balance of C/EBPG and C/EBPA could represent a new therapeutic approach in the treatment of AML.
C/EBPγ deregulation results in differentiation arrest in acute myeloid leukemia
Beth Israel Deaconess Medical Center, Boston, MA, USA
Phone: 617-735-2235; Fax: 617-735-2222; E-mail: email@example.com
View this article at: http://www.jci.org/articles/view/65102?key=2caafbb63e0b6ae08fa7
|Contact: Jillian Hurst|
Journal of Clinical Investigation