BCR/ABL modifies the kinetics and fidelity of DNA double-strand breaks repair in hematopoietic cells |
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Authors: | Slupianek Artur Nowicki Michal O Koptyra Mateusz Skorski Tomasz |
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Affiliation: | Center for Biotechnology, College of Science and Technology, Temple University, Bio-Life Sciences Building, Room 419, 1900 N. 12th Street, Philadelphia, PA 19122, USA. |
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Abstract: | The oncogenic BCR/ABL tyrosine kinase facilitates the repair of DNA double-strand breaks (DSBs). We find that after gamma-irradiation BCR/ABL-positive leukemia cells accumulate more DSBs in comparison to normal cells. These lesions are efficiently repaired in a time-dependent fashion by BCR/ABL-stimulated non-homologous end-joining (NHEJ) followed by homologous recombination repair (HRR) mechanisms. However, mutations and large deletions were detected in HRR and NHEJ products, respectively, in BCR/ABL-positive leukemia cells. We propose that unfaithful repair of DSBs may contribute to genomic instability in the Philadelphia chromosome-positive leukemias. |
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