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Nowicki, Michal O.; Falinski, Rafal; Koptyra, Mateusz; Slupianek, Artur; Stoklosa, Tomasz; Gloc, Ewa; Nieborowska-Skorska, Margaret; Blasiak, Janusz; Skorski, Tomasz
Blood, 12/2004, Letnik: 104, Številka: 12Journal Article
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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in: SICRIS
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