ArticleLeukemia2015
NFATc1 as a therapeutic target in FLT3-ITD-positive AML.
Article in Leukemia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 52 citations in OpenAlex.
- Article
- NFAT2 Induces Tumor Cell Proliferation and Metastasis by Acting as a Transcriptional Co-activator of the TGF-β1/SMAD Signaling Pathway and Inducing the Epithelial-Mesenchymal Transition in Liver Cancer.Digestive diseases and sciences · 2025Article
- The MYC-NFATC2 axis maintains the cell cycle and mitochondrial function in acute myeloid leukaemia cells.Molecular oncology · 2024Article
- CD37 is a safe chimeric antigen receptor target to treat acute myeloid leukemia.Cell reports. Medicine · 2024Article
- Genetic associations with ratios between protein levels detect new pQTLs and reveal protein-protein interactions.Cell genomics · 2024Article
- Combined GLUT1 and OXPHOS inhibition eliminates acute myeloid leukemia cells by restraining their metabolic plasticity.Blood advances · 2023Article
- In Vivo Screening Unveils Pervasive RNA-Binding Protein Dependencies in Leukemic Stem Cells and Identifies ELAVL1 as a Therapeutic Target.Blood cancer discovery · 2023Article
- Involvement of ORAI1/SOCE in Human AML Cell Lines and Primary Cells According to ABCB1 Activity, LSC Compartment and Potential Resistance to Ara-C Exposure.International journal of molecular sciences · 2022Article
- Put in a "CaCells · 2022Review
- CNST is Characteristic of Leukemia Stem Cells and is Associated With Poor Prognosis in AML.Frontiers in pharmacology · 2022Article
- Article
- Decreased PRC2 activity supports the survival of basal-like breast cancer cells to cytotoxic treatments.Cell death & disease · 2021Article
- Isoform-Selective NFAT Inhibitor: Potential Usefulness and Development.International journal of molecular sciences · 2021Review
- Maintenance therapy forHaematologica · 2021Review
- Somatic Mutations Drive Specific, but Reversible, Epigenetic Heterogeneity States in AML.Cancer discovery · 2020Article
- Outcome of Relapsed or RefractoryCancers · 2020Article
- Aberrant expression of NKL homeobox genes HMX2 and HMX3 interferes with cell differentiation in acute myeloid leukemia.PloS one · 2020Article
- Activation of the Peroxisome Proliferator-Activated Receptor γ Coactivator 1β/NFATc1 Pathway in Circulating Osteoclast Precursors Associated With Bone Destruction in Rheumatoid Arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2019Article
- Nuclear factor of activated T-cells, NFATC1, governs FLT3Journal of hematology & oncology · 2019Article
- Targeting the RNA mCell stem cell · 2019Article
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Internal tandem duplications (ITD) in the Fms-related tyrosine kinase 3 receptor (FLT3) are associated with a dismal prognosis in acute myeloid leukemia (AML). FLT3 inhibitors such as sorafenib may improve outcome, but only few patients display long-term responses, prompting the search for underlying resistance mechanisms and therapeutic strategies to overcome them. Here we identified that the nuclear factor of activated T cells, NFATc1, is frequently overexpressed in FLT3-ITD-positive (FLT3-ITD+) AML. NFATc1 knockdown using inducible short hairpin RNA or pharmacological NFAT inhibition with cyclosporine A (CsA) or VIVIT significantly augmented sorafenib-induced apoptosis of FLT3-ITD+ cells. CsA also potently overcame sorafenib resistance in FLT3-ITD+ cell lines and primary AML. Vice versa, de novo expression of a constitutively nuclear NFATc1-mutant mediated instant and robust sorafenib resistance in vitro. Intriguingly, FLT3-ITD+ AML patients (n=26) who received CsA as part of their rescue chemotherapy displayed a superior outcome when compared with wild-type FLT3 (FLT3-WT) AML patients. Our data unveil NFATc1 as a novel mediator of sorafenib resistance in FLT3-ITD+ AML. CsA counteracts sorafenib resistance and may improve treatment outcome in AML by means of inhibiting NFAT.
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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.