ArticleOncogene2016
The oncofusion protein FUS-ERG targets key hematopoietic regulators and modulates the all-trans retinoic acid signaling pathway in t(16;21) acute myeloid leukemia.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 49 citations in OpenAlex.
- Targeting fusion proteins in solid tumors: from oncogenic mechanisms to clinical interventions.Acta pharmacologica Sinica · 2026Review
- Hypoplastic acute myeloid leukemia with aberrant lymphoid antigen expression andTherapeutic advances in hematology · 2026Article
- Allogeneic transplantation in adverse-risk acute myeloid leukemia: Challenges, strategies, and future directions.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2025Article
- EZH2-driven immune evasion at disease presentation defines a targetable high-risk subset of acute leukemia exemplified by t(16;21) FUS::ERG AML.bioRxiv : the preprint server for biology · 2025Article
- Novel classification system and high-risk categories of pediatric acute myeloid leukemia.Haematologica · 2025Review
- Acute myeloid leukemia with RAM immunophenotype: A report of three patients and comprehensive literature review.EJHaem · 2025Article
- ChromatinHD connects single-cell DNA accessibility and conformation to gene expression through scale-adaptive machine learning.Nature communications · 2025Article
- The RTK-RAS signaling pathway is enriched in patients with rare acute myeloid leukemia harboring t(16;21)(p11;q22)/Blood science (Baltimore, Md.) · 2024Article
- BloodChIP Xtra: an expanded database of comparative genome-wide transcription factor binding and gene-expression profiles in healthy human stem/progenitor subsets and leukemic cells.Nucleic acids research · 2024Article
- FUS-ERG induces late-onset azacitidine resistance in acute myeloid leukaemia cells.Scientific reports · 2023Article
- ETV6 Deficiency Unlocks ERG-Dependent Microsatellite Enhancers to Drive Aberrant Gene Activation in B-Lymphoblastic Leukemia.Blood cancer discovery · 2023Article
- Article
- Relapsed acute myeloid leukemia in children and adolescents: current treatment options and future strategies.Leukemia · 2022Review
- Homodimeric and Heterodimeric Interactions among Vertebrate Basic Helix-Loop-Helix Transcription Factors.International journal of molecular sciences · 2021Review
- Review
- Fusion Oncoproteins in Childhood Cancers: Potential Role in Targeted Therapy.The journal of pediatric pharmacology and therapeutics : JPPT : the official journal of PPAG · 2021Review
- Hyper-SUMOylation of ERG Is Essential for the Progression of Acute Myeloid Leukemia.Frontiers in molecular biosciences · 2021Article
- Targeting the ERG oncogene with splice-switching oligonucleotides as a novel therapeutic strategy in prostate cancer.British journal of cancer · 2020Article
- The role of the retinoids in schizophrenia: genomic and clinical perspectives.Molecular psychiatry · 2020Review
- The incidence, genetic characteristics, and prognosis of leukemia with concurrent pathogenic fusion genes: a series of 25 cases from a large cohort of leukemia patients.Cancer gene therapy · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ETS transcription factor ERG has been implicated as a major regulator of both normal and aberrant hematopoiesis. In acute myeloid leukemias harboring t(16;21), ERG function is deregulated due to a fusion with FUS/TLS resulting in the expression of a FUS-ERG oncofusion protein. How this oncofusion protein deregulates the normal ERG transcription program is unclear. Here, we show that FUS-ERG acts in the context of a heptad of proteins (ERG, FLI1, GATA2, LYL1, LMO2, RUNX1 and TAL1) central to proper expression of genes involved in maintaining a stem cell hematopoietic phenotype. Moreover, in t(16;21) FUS-ERG co-occupies genomic regions bound by the nuclear receptor heterodimer RXR:RARA inhibiting target gene expression and interfering with hematopoietic differentiation. All-trans retinoic acid treatment of t(16;21) cells as well as FUS-ERG knockdown alleviate the myeloid-differentiation block. Together, the results suggest that FUS-ERG acts as a transcriptional repressor of the retinoic acid signaling pathway.
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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.