BCR/ABL stimulates WRN to promote survival and genomic instability

BCR/ABL-transformed chronic myeloid leukemia (CML) cells accumulate numerous DNA double-strand breaks (DSBs) induced by reactive oxygen species (ROS) and genotoxic agents. To repair these lesions BCR/ABL stimulate unfaithful DSB repair pathways, homologous recombination repair (HRR), non-homologous...

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Bibliografiske detaljer
Main Authors: Slupianek, Artur, Poplawski, Tomasz, Jozwiakowski, Stanislaw K., Cramer, Kimberly, Pytel, Dariusz, Stoczynska, Ewelina, Nowicki, Michal O., Blasiak, Janusz, Skorski, Tomasz
Format: Artigo
Sprog:Inglês
Udgivet: 2010
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Article
Online adgang:https://ncbi.nlm.nih.gov/pmc/articles/PMC3032814/
https://ncbi.nlm.nih.gov/pubmed/21123451
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1158/0008-5472.CAN-10-1066
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