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JCI table of contents: Aug. 9, 2007
Date:8/13/2007

Houston, Texas, USA.
Phone: (713) 798-0285; Fax: (713) 798-0270; E-mail: dmann@bcm.tmc.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=29134


ONCOLOGY: New SNP for acute myeloid leukemia

Tumor suppressor proteins are so called because their functions oppose the development of cancer. Studies in mice indicate that the protein PU.1 is a tumor suppressor. Mice lacking a specific portion of the DNA (known as the upstream regulatory element; URE) that controls the level of expression of the PU.1 gene develop acute myeloid leukemia (AML). When researchers from Harvard Medical School, Boston, analyzed the equivalent URE in humans they found that a subset of individuals with AML had a genetic mutation known as a SNP that decreased the ability of this region of DNA to enhance PU.1 gene expression.

In the study, which appears online on August 9 in advance of publication in the September print issue of the Journal of Clinical Investigation, Daniel Tenen and colleagues show that the SNP decreased the ability of a protein known as SATB1 to bind the URE and promote PU.1 gene expression. Expression of the PU.1 gene was therefore much decreased. This effect was observed specifically in the precursors of immune cells known as myeloid cells. This study raises the possibility that genetic mutations in UREs might have a critical role in the development of cancer.

TITLE: A distal single nucleotide polymorphism alters long-range regulation of the PU.1 gene in acute myeloid leukemia

AUTHOR CONTACT:
Daniel G. Tenen
Harvard Medical School, Boston, Massachusetts, USA.
Phone: (617) 667-5561; Fax: (617) 667-3299; E-mail: dtenen@bidmc.harvard.edu.

View the PDF of this article at: ht
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Contact: Karen Honey
press_releases@the-jci.org
215-573-1850
Journal of Clinical Investigation
Source:Eurekalert

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