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JCI early table of contents for Nov. 19, 2012
Date:11/19/2012

A code of silence in acute myeloid leukemia

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 alters 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/EBPγ 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

Immune cells fail to migrate in Huntington's disease

Huntington disease (HD) is an incurable neurodegenerative disease caused by a mutation in the huntingtin gene (htt). Though most of the symptoms of HD are neurological, the mutant HTT protein is expressed in non-neural cells as well. In this issue of the Journal of Clinical Investigation, researchers led by Paul Muchowski at the J. David Gladstone Institutes in San Franscisco examined the role of immune cells in HD. Immune cells known as microglia, which were isolated from the brains of HD mice, as well a
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Contact: Jillian Hurst
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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