Crosstalk between the nucleotide excision repair and Fanconi anemia/BRCA pathways |
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| Affiliation: | 1. Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, United States;2. Harvard Radiation Oncology Program, Boston, MA, United States;1. Department of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, MO 63110, USA;2. Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA;1. Department of Therapeutic Radiology and Oncology, Innsbruck Medical University, Innsbruck, Austria;2. Department of Anatomy, Histology and Embryology, Innsbruck Medical University, Innsbruck, Austria;1. Massachusetts General Hospital Cancer Center, Harvard Medical School, Charlestown, MA 02129, USA;2. Department of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02115, USA;3. Laboratory of Genome Maintenance, Rockefeller University, New York, NY 10065, USA;4. Department of Developmental, Molecular, and Chemical Biology, Tufts University School of Medicine, Boston, MA 02111, USA;1. Department of Pharmacology & Cancer Biology, Duke University School of Medicine, DUMC Box 3813, Durham, NC 27710, USA;1. Centre for Therapeutics Discovery, MRC Technology, 1-3 Burtonhole Lane, Mill Hill, London NW7 1AD, UK;2. MRC Institute of Genetics and Molecular Medicine, University of Edinburgh, MRC Human Genetics Unit, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, UK |
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| Abstract: | Cells have evolved multiple distinct DNA repair pathways to efficiently correct a variety of genotoxic lesions, and decades of study have led to an improved understanding of the mechanisms and regulation of these individual pathways. However, there is now an increasing appreciation that extensive crosstalk exists among DNA repair pathways and that this crosstalk serves to increase the efficiency and diversity of response to damage. The Fanconi anemia (FA)/BRCA and nucleotide excision repair (NER) pathways have been shown to share common factors, and often work in concert to repair damage. Genomic studies are now revealing that many tumors harbor somatic mutations in FA/BRCA or NER genes, which may provide a growth advantage, but which could also be exploited therapeutically. |
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| Keywords: | Fanconi anemia Nucleotide excision repair Crosslink repair BRCA PARP inhibitor |
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