ArticleCancer research2013
STAT5 is crucial to maintain leukemic stem cells in acute myelogenous leukemias induced by MOZ-TIF2.
Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- p160 nuclear receptor coactivator family members and their role in rare fusion‑driven neoplasms (Review).Oncology letters · 2024Review
- MK256 is a novel CDK8 inhibitor with potent antitumor activity in AML through downregulation of the STAT pathway.Oncotarget · 2022Article
- Molecular mechanisms for stemness maintenance of acute myeloid leukemia stem cells.Blood science (Baltimore, Md.) · 2019Article
- Twins with different personalities: STAT5B-but not STAT5A-has a key role in BCR/ABL-induced leukemia.Leukemia · 2019Article
- A novel, dual pan-PIM/FLT3 inhibitor SEL24 exhibits broad therapeutic potential in acute myeloid leukemia.Oncotarget · 2018Article
- Cancer Stem Cells (CSCs) in Drug Resistance and their Therapeutic Implications in Cancer Treatment.Stem cells international · 2018Review
- Acetylation and deacetylation in cancer stem-like cells.Oncotarget · 2017Review
- Oncogenic STAT5 signaling promotes oxidative stress in chronic myeloid leukemia cells by repressing antioxidant defenses.Oncotarget · 2017Article
- SEL120-34A is a novel CDK8 inhibitor active in AML cells with high levels of serine phosphorylation of STAT1 and STAT5 transactivation domains.Oncotarget · 2017Article
- Hematopoietic Differentiation Is Required for Initiation of Acute Myeloid Leukemia.Cell stem cell · 2015Article
- Tetraspanin Family Member, CD82, Regulates Expression of EZH2 via Inactivation of p38 MAPK Signaling in Leukemia Cells.PloS one · 2015Article
- The Role of Histone Acetyltransferases in Normal and Malignant Hematopoiesis.Frontiers in oncology · 2015Review
- STAT activation status differentiates leukemogenic from non-leukemogenic stem cells in AML and is suppressed by arsenic in t(6;9)-positive AML.Genes & cancer · 2014Article
- Potent co-operation between the NUP98-NSD1 fusion and the FLT3-ITD mutation in acute myeloid leukemia induction.Haematologica · 2014Article
- Emerging therapeutic paradigms to target the dysregulated Janus kinase/signal transducer and activator of transcription pathway in hematological malignancies.Leukemia & lymphoma · 2014Review
- Reactive oxygen species in eradicating acute myeloid leukemic stem cells.Stem cell investigation · 2014Review
- Cooperation between RUNX1-ETO9a and novel transcriptional partner KLF6 in upregulation of Alox5 in acute myeloid leukemia.PLoS genetics · 2013Article
- The Impact of FLT3 Mutations on the Development of Acute Myeloid Leukemias.Leukemia research and treatment · 2013Article
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Authors and funding
17 authors at 4 institutions in 2 countries.
Funding
Abstract
MOZ-TIF2 is a leukemogenic fusion oncoprotein that confers self-renewal capability to hematopoietic progenitor cells and induces acute myelogenous leukemia (AML) with long latency in bone marrow transplantation assays. Here, we report that FLT3-ITD transforms hematopoietic cells in cooperation with MOZ-TIF2 in vitro and in vivo. Coexpression of FLT3-ITD confers growth factor independent survival/proliferation, shortens disease latency, and results in an increase in the number of leukemic stem cells (LSC). We show that STAT5, a major effector of aberrant FLT3-ITD signal transduction, is both necessary and sufficient for this cooperative effect. In addition, STAT5 signaling is essential for MOZ-TIF2-induced leukemic transformation itself. Lack of STAT5 in fetal liver cells caused rapid differentiation and loss of replating capacity of MOZ-TIF2-transduced cells enriched for LSCs. Furthermore, mice serially transplanted with Stat5(-/-) MOZ-TIF2 leukemic cells develop AML with longer disease latency and finally incomplete penetrance when compared with mice transplanted with Stat5(+/+) MOZ-TIF2 leukemic cells. These data suggest that STAT5AB is required for the self-renewal of LSCs and represents a combined signaling node of FLT3-ITD and MOZ-TIF2 driven leukemogenesis. Therefore, targeting aberrantly activated STAT5 or rewired downstream signaling pathways may be a promising therapeutic option.
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