DNA double-strand break repair pathway choice and cancer |
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| Affiliation: | 1. Institute for Cancer Genetics & Department of Genetics and Development, Columbia University Medical Center, New York, NY, USA;2. Institute for Cancer Genetics & Department of Pathology and Cell Biology, Columbia University Medical Center, New York, NY, USA;1. Department of Oncology, Wayne State University, 110 East Warren Avenue, Detroit, MI 48201, United States;2. Karmanos Cancer Institute, Wayne State University, 110 East Warren Avenue, Detroit, MI 48201, United States;3. Department of Pathology, Wayne State University, 110 East Warren Avenue, Detroit, MI 48201, United States;1. Division of Immunology, Boston Children''s Hospital, Harvard Medical School, Boston, Mass;9. Department of Transfusion Medicine, Boston Children''s Hospital, Harvard Medical School, Boston, Mass;2. Department of Immunology, Erasmus Medical Center, Rotterdam, The Netherlands;3. Angelo Nocivelli Institute for Molecular Medicine, Department of Pediatrics, University of Brescia, Brescia, Italy;4. Immunology Department, Ihsan Dogramaci Children''s Hospital, Hacettepe University Medical School, Sıhhiye, Ankara, Turkey;5. Department of Pediatric Immunology and Allergy, Necmettin Erbakan University, Meram Medical Faculty, Konya, Turkey;6. CLIP-Childhood Leukemia Investigation Prague, Department of Pediatric Hematology and Oncology, 2nd Faculty of Medicine and University Hospital Motol, Charles University, Prague, Czech Republic;7. Laboratory of “Genome Dynamics in the Immune System”, INSERM UMR1163, Université Paris Descartes Sorbonne Paris Cité, Institut Imagine, Paris, France;8. Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Mo;10. Harvard Stem Cell Institute, Harvard University, Boston, Mass |
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| Abstract: | Since DNA double-strand breaks (DSBs) contribute to the genomic instability that drives cancer development, DSB repair pathways serve as important mechanisms for tumor suppression. Thus, genetic lesions, such as BRCA1 and BRCA2 mutations, that disrupt DSB repair are often associated with cancer susceptibility. In addition, recent evidence suggests that DSB “mis-repair”, in which DSBs are resolved by an inappropriate repair pathway, can also promote genomic instability and presumably tumorigenesis. This notion has gained currency from recent cancer genome sequencing studies which have uncovered numerous chromosomal rearrangements harboring pathological DNA repair signatures. In this perspective, we discuss the factors that regulate DSB repair pathway choice and their consequences for genome stability and cancer. |
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| Keywords: | DNA double strand break Repair pathway choice Microhomology-mediated end joining DNA ends Resection 53BP1–BRCA1 |
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