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Originally published in Science Express on 13 June 2002
Science 26 July 2002:
Vol. 297. no. 5581, p. 534
DOI: 10.1126/science.1074482

Perspectives

BIOMEDICINE:
D-Day for BRCA2

Emily Witt and Alan Ashworth*

Individuals with certain mutations in the gene BRCA2 are at a very high risk for developing breast cancer because a DNA repair pathway cannot properly repair ongoing wear and tear to the DNA. In their Perspective, Witt and Ashworth discuss new findings (Howlett et al.) showing that other mutations in this same BRCA2 gene are one cause of another disease, Fanconi anemia, also thought to be a result of defective DNA repair. This unexpected result identifies BRCA2 as a central control point in the DNA repair mechanism of cells, which maintains the stability of the genome.


The authors are at The Breakthrough Breast Cancer Research Centre, The Institute of Cancer Research, London SW3 6JB, UK. E-mail: elisa{at}icr.ac.uk

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THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Oxidative Stress/Damage Induces Multimerization and Interaction of Fanconi Anemia Proteins.
S.-J. Park, S. L. M. Ciccone, B. D. Beck, B. Hwang, B. Freie, D. W. Clapp, and S.-H. Lee (2004)
J. Biol. Chem. 279, 30053-30059
   Abstract »    Full Text »    PDF »
Phenotypic effects of heterozygosity for a BRCA2 mutation.
M. Warren, C. J. Lord, J. Masabanda, D. Griffin, and A. Ashworth (2003)
Hum. Mol. Genet. 12, 2645-2656
   Abstract »    Full Text »    PDF »
Breast-Cancer Genomics.
B. Friedenson, M. S. Piver, B. L. Weber, and R. Wooster (2003)
N. Engl. J. Med. 349, 910-911
   Full Text »    PDF »
Fanconi anaemia.
M D Tischkowitz and S V Hodgson (2003)
J. Med. Genet. 40, 1-10
   Abstract »    Full Text »
A DNA Double Strand Break Repair Defect in Fanconi Anemia Fibroblasts.
S. L. Donahue and C. Campbell (2002)
J. Biol. Chem. 277, 46243-46247
   Abstract »    Full Text »    PDF »



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Science. ISSN 0036-8075 (print), 1095-9203 (online)