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JCI table of contents: Dec. 22, 2010
Date:12/22/2010

because DNA damage causes cells to stop dividing, getting stuck at a point in cell division known as G2. The team found that in some individuals with Fanconi anemia, a few cells develop the ability to overcome the cell division arrest in G2. These cells prevented the dramatic loss of bone marrow cells and enabled the patients to reach adulthood. However, the cost of this improved clinical outcome was increased risk of developing leukemia. The authors therefore suggest that better understanding of disease in this unusual subset of patients might enable the development of strategies that can predict a patient's clinical course and guide treatment choices.

In an accompanying commentary, Monica Bessler and Philip Mason, at Children's Hospital of Philadelphia, Philadelphia, discuss the importance of this work and how it fits with other recent papers on cell division defects in Fanconi anemia cells.

TITLE: Spontaneous abrogation of the G2 DNA damage checkpoint has clinical benefits but promotes leukemogenesis in Fanconi anemia patients

AUTHOR CONTACT:
Jean Soulier
INSERM U944 and CNRS UMR7212, Institute of Hematology, Saint-Louis Hospital, Paris, France.
Phone: 33.1.4249.9891; Fax: 33.1.4249.4027; E-mail: jean.soulier@sls.aphp.fr.

View this article at: http://www.jci.org/articles/view/43836?key=431c96bdf2f3b6a7c786

ACCOMPANYING COMMENTARY
TITLE: Cytokinesis failure and attenuation: new findings in Fanconi anemia

AUTHOR CONTACT:
Philip J. Mason
The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA.
Phone: 267.426.9327; Fax: 215.590.4834; E-mail: masonp@email.chop.edu.

View this article at: http://www.jci.org/articles/view
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Contact: Karen Honey
press_releases@the-jci.org
734-546-5242
Journal of Clinical Investigation
Source:Eurekalert

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