ArticleOncotarget2012
STAT5 triggers BCR-ABL1 mutation by mediating ROS production in chronic myeloid leukaemia.
Article in Oncotarget, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
41 citing papers in PubMed, 69 citations in OpenAlex.
- Olverembatinib in accelerated-phase chronic myeloid leukemia: efficacy and safety evaluation.Haematologica · 2026Article
- Screening and Activity Evaluation of Novel BCR-ABL/T315I Tyrosine Kinase Inhibitors.Current medicinal chemistry · 2024Article
- The therapeutic and biomarker significance of ferroptosis in chronic myeloid leukemia.Frontiers in immunology · 2024Article
- Mechanisms underlying therapeutic resistance of tyrosine kinase inhibitors in chronic myeloid leukemia.International journal of biological sciences · 2024Review
- Genomic Mutations of the STAT5 Transcription Factor Are Associated with Human Cancer and Immune Diseases.International journal of molecular sciences · 2022Review
- Inflammation Promotes Oxidative and Nitrosative Stress in Chronic Myelogenous Leukemia.Biomolecules · 2022Article
- Review
- The Discovery of Novel BCR-ABL Tyrosine Kinase Inhibitors Using a Pharmacophore Modeling and Virtual Screening Approach.Frontiers in cell and developmental biology · 2021Article
- The multifaceted role of reactive oxygen species in tumorigenesis.Cellular and molecular life sciences : CMLS · 2020Review
- Signal-transducing adapter protein-1 is required for maintenance of leukemic stem cells in CML.Oncogene · 2020Article
- Novel HDAC inhibitor MAKV-8 and imatinib synergistically kill chronic myeloid leukemia cells via inhibition of BCR-ABL/MYC-signaling: effect on imatinib resistance and stem cells.Clinical epigenetics · 2020Article
- Pharmacological Inhibition of Oncogenic STAT3 and STAT5 Signaling in Hematopoietic Cancers.Cancers · 2020Review
- A Novel Inhibitor of STAT5 Signaling Overcomes Chemotherapy Resistance in Myeloid Leukemia Cells.Cancers · 2019Article
- Signal transducer and activator of transcription (STAT)-5: an opportunity for drug development in oncohematology.Oncogene · 2019Review
- Clonal Hematopoiesis with Oncogenic Potential (CHOP): Separation from CHIP and Roads to AML.International journal of molecular sciences · 2019Review
- Reduced expression but not deficiency of GFI1 causes a fatal myeloproliferative disease in mice.Leukemia · 2019Article
- The Cooperative Relationship between STAT5 and Reactive Oxygen Species in Leukemia: Mechanism and Therapeutic Potential.Cancers · 2018Review
- Reactive oxygen species in haematopoiesis: leukaemic cells take a walk on the wild side.Journal of experimental & clinical cancer research : CR · 2018Review
- Differential proteomic profile of leukemic CD34+ progenitor cells from chronic myeloid leukemia patients.Oncotarget · 2018Article
- Targeting Oncogenic Transcription Factors: Therapeutic Implications of Endogenous STAT Inhibitors.Trends in cancer · 2017Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
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 expression and the incidence of BCR-ABL1 mutations in primary CML. Forced expression of STAT5 in murine BCR-ABL1 transformed cells sufficed to enhance the production of reactive oxygen species (ROS) and to trigger DNA damage. STAT5-mediated ROS production is independent of JAK2 but requires concomitant BCR-ABL1 signalling as forced STAT5 expression in untransformed BCR-ABL1 negative cells has no impact on ROS levels. Only within the context of a BCR-ABL1 positive cell does STAT5 transcriptionally regulate a target gene or set of genes that causes the enhanced ROS production. Our study suggests the existence of a feed-forward loop accelerating disease progression, in which BCR-ABL1 enhances its own mutation rate in a STAT5-ROS dependent manner. This model explains the increased occurrence of inhibitor-resistant BCR-ABL1 mutations in advanced disease stages driven and characterized by high STAT5 expression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.