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Public release date: 19-Nov-2012[ | E-mail |
Share ] Contact: Jillian Hurst
press_releases@the-jci.org
Journal of Clinical Investigation
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.
TITLE:
C/EBP? deregulation results in differentiation arrest in acute myeloid leukemia
AUTHOR CONTACT:
Daniel Tenen
Beth Israel Deaconess Medical Center, Boston, MA, USA
Phone: 617-735-2235; Fax: 617-735-2222; E-mail: dtenen@bidmc.harvard.edu
View this article at: http://www.jci.org/articles/view/65102?key=2caafbb63e0b6ae08fa7
###
[ | E-mail | Share ] ?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Public release date: 19-Nov-2012[ | E-mail |
Share ] Contact: Jillian Hurst
press_releases@the-jci.org
Journal of Clinical Investigation
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.
TITLE:
C/EBP? deregulation results in differentiation arrest in acute myeloid leukemia
AUTHOR CONTACT:
Daniel Tenen
Beth Israel Deaconess Medical Center, Boston, MA, USA
Phone: 617-735-2235; Fax: 617-735-2222; E-mail: dtenen@bidmc.harvard.edu
View this article at: http://www.jci.org/articles/view/65102?key=2caafbb63e0b6ae08fa7
###
[ | E-mail | Share ] ?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Source: http://www.eurekalert.org/pub_releases/2012-11/joci-aco111412.php
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