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DNA Repair (Amst). 2006 Feb 3;5(2):243-50. Epub 2005 Nov 16.

BCR/ABL modifies the kinetics and fidelity of DNA double-strand breaks repair in hematopoietic cells.

Author information

1
Center for Biotechnology, College of Science and Technology, Temple University, Bio-Life Sciences Building, Room 419, 1900 N. 12th Street, Philadelphia, PA 19122, USA.

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.

PMID:
16297667
PMCID:
PMC2856314
DOI:
10.1016/j.dnarep.2005.10.005
[Indexed for MEDLINE]
Free PMC Article

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