STAT5 triggers BCR-ABL1 mutation by mediating ROS production in chronic myeloid leukaemia

We recently reported that chronic myeloid leukaemia (CML) patients harbour high levels of STAT5 when they progress to advanced phases of disease. Advanced disease is characterized by an increased incidence of BCR-ABL1 mutations. We now describe a highly significant correlation between STAT5 expressi...

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Veröffentlicht in:	Oncotarget 2012-12, Vol.3 (12), p.1669-1687
Hauptverfasser:	Warsch, Wolfgang, Grundschober, Eva, Berger, Angelika, Gille, Lars, Cerny-Reiterer, Sabine, Tigan, Anca-Sarmiza, Hoelbl-Kovacic, Andrea, Valent, Peter, Moriggl, Richard, Sexl, Veronika
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Disease Progression DNA Breaks, Double-Stranded Feedback, Physiological Fusion Proteins, bcr-abl - genetics Gene Expression Regulation, Neoplastic Humans Janus Kinase 2 - metabolism K562 Cells Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology Mice Mice, Inbred NOD Mice, SCID Mutation Oxidative Stress Protein-Tyrosine Kinases - genetics Reactive Oxygen Species - metabolism Research Papers RNA Interference RNA, Messenger - metabolism Signal Transduction STAT5 Transcription Factor - genetics STAT5 Transcription Factor - metabolism Transcription, Genetic Transfection Tumor Suppressor Proteins - genetics Tumor Suppressor Proteins - metabolism
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