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Reply to “Involvement of oxidative stress in Fanconi's anaemia: from phenotype to FA protein functions”

Nature Reviews Cancer volume 3, page 78 (2003)Cite this article

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The letter by Drs Pagano and Rutherford criticizes our recent review 'The Fanconi anaemia/BRCA pathway' (Nature Rev Cancer 3, 23–34) for failing to give due coverage to those reports connecting Fanconi anaemia (FA) to oxidative damage and oxygen metabolism. We are aware of the papers cited here to support the oxidative stress hypothesis for FA, but chose to focus on those parts of the FA literature that have stood the test of time and are likely to contribute to the final understanding of this important disease. This reflects our personal bias that the published work on oxidative damage and FA describes only secondary phenotypes (epiphenomena) rather than the primary defect in FA.

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Authors and Affiliations

  1. the Department of Molecular and Medical Genetics, Oregon Health Sciences University, 3181 SW Sam Jackson Park Road L103, Portland, 97201, Oregon, USA

    Markus Grompe

  2. the Department of Pediatric Oncology, Dana–Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, 02115, Massachusetts, USA

    Alan D'Andrea

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  1. Markus Grompe
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Correspondence to Markus Grompe.

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Grompe, M., D'Andrea, A. Reply to “Involvement of oxidative stress in Fanconi's anaemia: from phenotype to FA protein functions”. Nat Rev Cancer 3, 78 (2003). https://doi.org/10.1038/nrc970-c2

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