BCR-ABL1 kinase inhibits uracil DNA glycosylase UNG2 to enhance oxidative DNA damage and stimulate genomic instability

Tyrosine kinase inhibitors (TKIs) revolutionized the treatment of CML-CP. Unfortunately, 25% of TKI-naive patients and 50–90% of TKI-responding patients carry CML clones expressing TKI resistant BCR-ABL1 kinase mutants. We reported that CML-CP leukemia stem and progenitor cell populations accumulate...

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Main Authors: Slupianek, Artur, Falinski, Rafal, Znojek, Pawel, Stoklosa, Tomasz, Flis, Sylwia, Doneddu, Valentina, Pytel, Dariusz, Synowiec, Ewelina, Blasiak, Janusz, Bellacosa, Alfonso, Skorski, Tomasz
Formato: Artigo
Idioma:Inglês
Publicado: 2012
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Article
Acceso en liña:https://ncbi.nlm.nih.gov/pmc/articles/PMC3598941/
https://ncbi.nlm.nih.gov/pubmed/23047475
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1038/leu.2012.294
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