ArticleOncogene2003
Constitutive and specific activation of STAT3 by BCR-ABL in embryonic stem cells.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 57 citations in OpenAlex.
- Cancer-Associated STAT3 Mutations Maintain ES Cell Self-Renewal Through Phosphorylation-Independent Mechanisms.Genes to cells : devoted to molecular & cellular mechanisms · 2026Article
- STAT3-mediated osteogenesis and osteoclastogenesis in osteoporosis.Cell communication and signaling : CCS · 2022Review
- Genome-Wide ChIP-seq and RNA-seq Analyses of STAT3 Target Genes in TLRs Activated Human Peripheral Blood B Cells.Frontiers in immunology · 2022Article
- STAT3 Interactors as Potential Therapeutic Targets for Cancer Treatment.International journal of molecular sciences · 2018Review
- Stat3 and CCAAT enhancer-binding protein β (C/ebpβ) activate Fanconi C gene transcription during emergency granulopoiesis.The Journal of biological chemistry · 2018Article
- Role of STAT3 in Genesis and Progression of Human Malignant Gliomas.Molecular neurobiology · 2017Review
- Combined targeting of STAT3 and STAT5: a novel approach to overcome drug resistance in chronic myeloid leukemia.Haematologica · 2017Article
- Tyrosine kinase c-Abl regulates the survival of plasma cells.Scientific reports · 2017Article
- Article
- Withacnistin inhibits recruitment of STAT3 and STAT5 to growth factor and cytokine receptors and induces regression of breast tumours.British journal of cancer · 2014Article
- Kinase-independent mechanisms of resistance of leukemia stem cells to tyrosine kinase inhibitors.Stem cells translational medicine · 2014Review
- Salmonella modulation of host cell gene expression promotes its intracellular growth.PLoS pathogens · 2013Article
- Article
- Gene Expression upon Proliferation and Differentiation of Hematopoietic Cells with Ph Chromosome ex vivo.Acta naturae · 2012Article
- Dampened ERK signaling in hematopoietic progenitor cells in rheumatoid arthritis.Clinical immunology (Orlando, Fla.) · 2012Article
- Role of STAT3 in Transformation and Drug Resistance in CML.Frontiers in oncology · 2012Article
- Article
- Stat5 is indispensable for the maintenance of bcr/abl-positive leukaemia.EMBO molecular medicine · 2010Article
- Cell Regulation of Proliferation and Differentiation ex vivo for Cells Containing Ph Chromosome in Chronic Myeloid Leukemia.Acta naturae · 2009Article
- Engagement of the B-cell antigen receptor activates STAT through Lyn in a Jak-independent pathway.Oncogene · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BCR-ABL oncogene, the molecular hallmark of chronic myelogenous leukemia (CML) arises in a primitive hematopoietic stem cell with both differentiation and self-renewal ability. To study the phenotypic effects of BCR-ABL in a clonal in vitro self-renewal and differentiation model, we have introduced BCR-ABL in the ES cell line CCE. The major effect of BCR-ABL expression was the persistence of primitive morphology of ES cells despite LIF deprivation, correlated with a constitutive activation of STAT3, the major self-renewal factor of ES cells, but no evidence of activation of STAT5. The enforced expression of BCR-ABL in an ES cell line, engineered to express a tetracycline-inducible dominant-negative form of a STAT3, triggered ES cell differentiation with an increased generation of hematopoietic cells expressing erythroid and megakaryocytic phenotypes. RT-PCR analysis for Oct4, Brachyury and beta-globin expression confirmed a delay of differentiation in BCR-ABL expressing clones, which could be entirely reversed upon activation of the dominant-negative form of STAT3. To study the possible relevance of STAT3 activation by BCR-ABL in human CML, Western blot analyses performed on the CD34+ cells, purified from CML patients at different stages of their disease, also demonstrated increased levels of STAT3 proteins phosphorylated both on tyrosine and serine residues. These results represent to our knowledge the first functional link between BCR-ABL oncogene and a self-renewal in the context of ES cells through constitutive activation of STAT3. Thus, the BCR-ABL embryonic stem cell model that we developed as well as the results obtained in human CML samples suggests a role for STAT3 in the pathogenesis of human CML.
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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.