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Published Online June 13, 2002
Science DOI: 10.1126/science.1074482

Perspectives

Submitted on June 6, 2002
Accepted on June 11, 2002

D-Day for BRCA2

Emily Witt 1* Alan Ashworth 1

1 The Breakthrough Breast Cancer Research Centre, The Institute of Cancer Research, London SW3 6JB UK.

* To whom correspondence should be addressed. E-mail: ewitt{at}icr.ac.uk.

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


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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