The DOI matches its Crossref record; 80 of the 80 references it cites were found in a registry or an index.
BCR/ABL oncogenic kinase promotes unfaithful repair of the reactive oxygen species–dependent DNA double-strand breaks
Abstract
The oncogenic BCR/ABL tyrosine kinase induces constitutive DNA damage in Philadelphia chromosome (Ph)-positive leukemia cells. We find that BCR/ABL-induced reactive oxygen species (ROSs) cause chronic oxidative DNA damage resulting in double-strand breaks (DSBs) in S and G2/M cell cycle phases. These lesions are repaired by BCR/ABL-stimulated homologous recombination repair (HRR) and nonhomologous end-joining (NHEJ) mechanisms. A high mutation rate is detected in HRR products in BCR/ABL-positive cells, but not in the normal counterparts. In addition, large deletions are found in NHEJ products exclusively in BCR/ABL cells. We propose that the following series of events may contribute to genomic instability of Ph-positive leukemias: BCR/ABL → ROSs → oxidative DNA damage → DSBs in proliferating cells → unfaithful HRR and NHEJ repair.
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Metadata
- Authors
- Nowicki, M. O., Falinski, R., Koptyra, M., Slupianek, A., Stoklosa, T., Gloc, E., Nieborowska-Skorska, M., Blasiak, J., & Skorski, T.
- Affiliations
- University of Łódź (PL)
- From the Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA; and the Department of Molecular Genetics, University of Lodz, Poland.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2004-12-01
- Volume
- 104
- Issue
- 12
- Pages
- 3746-3753
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2047224624
- Semantic Scholar
- cf9bb4e46891074679e103c5136c82209addf4f9
- Cited by
- 278
- References
- 78
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 7 · 2023: 4 · 2022: 4 · 2021: 11 · 2020: 8 · 2019: 8 · 2018: 7 · 2017: 11 · 2016: 9 · 2015: 9 · 2014: 11 · 2013: 21 · 2012: 30
- FWCI
- 5.58
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Blood (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Hematology › Chronic Myeloid Leukemia Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
- Keywords
- BCR-ABL, tyrosine kinase, reactive oxygen species, oxidative DNA damage, DNA double-strand breaks, homologous recombination repair, non-homologous end joining, mutation rate, genomic instability, Philadelphia chromosome-positive leukemia, DNA repair fidelity
- MeSH terms
- Animals, DNA Damage, DNA Repair, Interphase, Leukemia, Mutation, Tumor Cells, Cultured, Fusion Proteins, bcr-abl, Reactive Oxygen Species, Comet Assay, Genomic Instability, Mice
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- CoChat. (2026). Citation check: BCR/ABL oncogenic kinase promotes unfaithful repair of the reactive oxygen species–dependent DNA double-strand breaks. https://app.cochat.ai/papers/10.1182/blood-2004-05-1941
- The paper
- Nowicki, M. O., Falinski, R., Koptyra, M., Slupianek, A., Stoklosa, T., Gloc, E., Nieborowska-Skorska, M., Blasiak, J., & Skorski, T. (2004). BCR/ABL oncogenic kinase promotes unfaithful repair of the reactive oxygen species–dependent DNA double-strand breaks. Blood. https://doi.org/10.1182/blood-2004-05-1941
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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