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Unwinding Fanconi Anemia

  August, 24 2005 9:05
your information resource in human molecular genetics
A series of five related papers published in the September issues of Nature Genetics and Nature Structural & Molecular Biology describe two new genes associated with Fanconi anemia, acting in the Fanconi anemia tumor suppressor pathway. Together, these studies provide insight into the mechanism underlying the chromosomal instability that characterizes the disease.

Fanconi anemia is an inherited anemia that predisposes to bone marrow failure and cancer, with many individuals developing acute myelogenous leukemia (AML) at an early age. Fanconi anemia is a rare pediatric disorder, typically diagnosed in children age 2 - 15 years, with varied expected survival ranging from 2 to 25 years.

Cells from individuals with Fanconi anemia have been characterized as highly sensitive to chromosomal breakage, suggesting that there may be a deficiency in repairing damaged DNA. The two new genes implicated in the Fanconi anemia pathway encode proteins that interact directly with DNA and are involved in DNA unwinding. This provides clues into the mechanism by which the complex of related Fanconi anemia genes recognize and processes damaged DNA.

Author contacts:

Arleen D. Auerbach (The Rockefeller University, New York, NY, USA)
E-mail: auerbac@rockefeller.edu
Abstract available online.

Hans Joenje (VU University Medical Center, Amsterdam, The Netherlands)
E-mail: h.joenje@vumc.nl
Abstract available online.

Weidong Wang (National Institute of Aging, Baltimore, MD, USA)
E-mail: wangw@grc.nia.nih.gov
Abstract available online.

Dr. Kevin Hiom (MRC Laboratory of Molecular Biology, Cambridge, UK)
E-mail: hiom@mrc-lmb.cam.ac.uk
Abstract available online.

Katen Patel (MRC Laboratory of Molecular Biology, Cambridge, UK)
E-mail: kjp@mrc-lmb.cam.ac.uk
Abstract available online.

Additional contact for comment on this research:

Larry H. Thompson (Lawrence Livermore National Laboratory, Livermore, CA, USA)
E-mail: thompson14@llnl.gov

(C) Nature press release.

Message posted by: Trevor M. D'Souza

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