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Originally published in Science Express on 13 June 2002
Science 26 July 2002:
Vol. 297. no. 5581, pp. 606 - 609
DOI: 10.1126/science.1073834
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Reports

Biallelic Inactivation of BRCA2 in Fanconi Anemia

Niall G. Howlett,1 Toshiyasu Taniguchi,1 Susan Olson,2 Barbara Cox,2 Quinten Waisfisz,3 Christine de Die-Smulders,4 Nicole Persky,1 Markus Grompe,2 Hans Joenje,3 Gerard Pals,3 Hideyuki Ikeda,5 Edward A. Fox,1 Alan D. D'Andrea1*

Fanconi anemia (FA) is a rare autosomal recessive cancer susceptibility disorder characterized by cellular hypersensitivity to mitomycin C (MMC). Six FA genes have been cloned, but the gene or genes corresponding to FA subtypes B and D1 remain unidentified. Here we show that cell lines derived from FA-B and FA-D1 patients have biallelic mutations in BRCA2 and express truncated BRCA2 proteins. Functional complementation of FA-D1 fibroblasts with wild-type BRCA2 complementary DNA restores MMC resistance. Our results link the six cloned FA genes with BRCA1 and BRCA2 in a common pathway. Germ-line mutation of genes in this pathway may result in cancer risks similar to those observed in families with BRCA1 or BRCA2 mutations.

1 Department of Pediatric Oncology, Dana-Farber Cancer Institute and Department of Pediatrics, Children's Hospital, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA.
2 Department of Molecular and Medical Genetics and Department of Pediatrics, Oregon Health Sciences University, Portland, OR 97201, USA.
3 Department of Clinical Genetics and Human Genetics, Free University Medical Center, Van der Boechorststraat 7, NL-1081 BT Amsterdam, The Netherlands.
4 Department of Clinical Genetics, Academic Hospital Maastricht, Maastricht, Netherlands.
5 Department of Pathology, Sapporo Medical University School of Medicine, S-1, W-17, Chuo-ku, Sapporo 060-8557, Japan.
*   To whom correspondence should be addressed. E-mail: alan_dandrea{at}dfci.harvard.edu

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