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Access through your institution Buy or subscribe BCR/ABL kinase-positive CD34+ stem/progenitor cells from chronic myeloid leukemia (CML) display elevated levels of DNA double-strand breaks
(DSBs) induced by reactive oxygen species (ROS) and various genotoxic agents, including γ-radiation.1 To survive, CML cells repair these numerous DSBs, which generate chromosomal aberrations
because BCR/ABL kinase affects the fidelity of repair mechanisms.1 Thus, CML cells can accumulate additional chromosomal aberrations during the course of disease (ROS dependent) and also in
cells surviving bone marrow transplantation (genotoxic agent dependent). The latter statement is supported by the reports that CD34+ CML stem and progenitor cells are resistant to genotoxic
agents.2 Our earlier studies showed that BCR/ABL kinase interacts with RAD51 resulting in its phosphorylation on Y315, which stimulates repair of DNA lesions by the homologous recombination
repair (HRR).3 HRR is responsible for the repair of about 43% of DSBs in BCR/ABL-transformed cells.4 RAD51 protein promotes homology search and strand invasion during HRR, which uses an
undamaged copy of broken DNA as a template for the repair process.5 This is a preview of subscription content, access via your institution ACCESS OPTIONS Access through your institution
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Contact customer support REFERENCES * Skorski T . BCR/ABL, DNA damage and DNA repair: implications for new treatment concepts. _Leuk Lymphoma_ 2008; 49: 610–614. Article CAS Google Scholar
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Download references ACKNOWLEDGEMENTS This work was supported by CA89052 and the Scholarship of the Leukemia and Lymphoma Society to T Skorski, and by the Leukemia Research Foundation New
Investigator Grant and the Lauri Strauss Leukemia Foundation Research Grant to A Slupianek. AUTHOR INFORMATION AUTHORS AND AFFILIATIONS * Department of Microbiology and Immunology, School of
Medicine, Temple University, Philadelphia, PA, USA A Slupianek & T Skorski * Department of Biology, College of Science and Technology, Temple University, Philadelphia, PA, USA S K
Jozwiakowski & E Gurdek * Institute for Cell and Molecular Biosciences, The University of Newcastle, Newcastle upon Tyne, UK S K Jozwiakowski Authors * A Slupianek View author
publications You can also search for this author inPubMed Google Scholar * S K Jozwiakowski View author publications You can also search for this author inPubMed Google Scholar * E Gurdek
View author publications You can also search for this author inPubMed Google Scholar * T Skorski View author publications You can also search for this author inPubMed Google Scholar
CORRESPONDING AUTHOR Correspondence to T Skorski. RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Slupianek, A., Jozwiakowski, S., Gurdek, E. _et al._
BCR/ABL kinase interacts with and phosphorylates the RAD51 paralog, RAD51B. _Leukemia_ 23, 2308–2310 (2009). https://doi.org/10.1038/leu.2009.164 Download citation * Published: 06 August
2009 * Issue Date: December 2009 * DOI: https://doi.org/10.1038/leu.2009.164 SHARE THIS ARTICLE Anyone you share the following link with will be able to read this content: Get shareable link
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