ArticleNature communications2022
Epigenetic activation of the FLT3 gene by ZNF384 fusion confers a therapeutic susceptibility in acute lymphoblastic leukemia.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- Advances in targeted therapies for pediatric tumors.Acta pharmacologica Sinica · 2026Article
- Interplay between cohesin and RNA polymerase II in regulating chromatin interactions and gene transcription.Nature structural & molecular biology · 2026Article
- Article
- Case Report: Acute myeloid leukemia with mixed immunophenotypic features and TCF3::ZNF384 fusion in a pediatric patient with CNS involvement: a diagnostic and therapeutic challenge.Frontiers in pediatrics · 2026Article
- Article
- Novel molecular mechanisms of FLT3 deregulation: from the acute myeloid leukemia experience to therapeutic insights in acute lymphoblastic leukemia.Molecular cancer · 2025Review
- Current Therapeutic Strategies for FLT3-Mutated Acute Myeloid Leukemia: A Narrative Review.Cureus · 2025Review
- Integrated Network Analysis Decipher ZNF384-Related miR-20b-5p and miR-424-5p in Colon Adenocarcinoma.Cancer reports (Hoboken, N.J.) · 2025Article
- Targeting LMO2-induced autocrine FLT3 signaling to overcome chemoresistance in early T-cell precursor acute lymphoblastic leukemia.Leukemia · 2025Article
- RGS1 and CREB5 are direct and common transcriptional targets of ZNF384-fusion proteins.Cancer medicine · 2024Article
- EP300-ZNF384 transactivates IL3RA to promote the progression of B-cell acute lymphoblastic leukemia.Cell communication and signaling : CCS · 2024Article
- Characterisation of FLT3 alterations in childhood acute lymphoblastic leukaemia.British journal of cancer · 2024Article
- Children's Oncology Group blueprint for research: Acute lymphoblastic leukemia.Pediatric blood & cancer · 2023Article
- Clinical significance and biofunction of ZNF384 in renal cell carcinoma discovered by data mining and experimentation.Human cell · 2023Article
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Authors and funding
20 authors at 4 institutions in 2 countries.
Funding
Abstract
FLT3 is an attractive therapeutic target in acute lymphoblastic leukemia (ALL) but the mechanism for its activation in this cancer is incompletely understood. Profiling global gene expression in large ALL cohorts, we identify over-expression of FLT3 in ZNF384-rearranged ALL, consistently across cases harboring different fusion partners with ZNF384. Mechanistically, we discover an intergenic enhancer element at the FLT3 locus that is exclusively activated in ZNF384-rearranged ALL, with the enhancer-promoter looping directly mediated by the fusion protein. There is also a global enrichment of active enhancers within ZNF384 binding sites across the genome in ZNF384-rearranged ALL cells. Downregulation of ZNF384 blunts FLT3 activation and decreases ALL cell sensitivity to FLT3 inhibitor gilteritinib in vitro. In patient-derived xenograft models of ZNF384-rearranged ALL, gilteritinib exhibits significant anti-leukemia efficacy as a monotherapy in vivo. Collectively, our results provide insights into FLT3 regulation in ALL and point to potential genomics-guided targeted therapy for this patient population.
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