ArticleOncotarget2016
Myb expression is critical for myeloid leukemia development induced by Setbp1 activation.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
- SETBP1 variants outside the degron disrupt DNA-binding, transcription and neuronal differentiation capacity to cause a heterogeneous neurodevelopmental disorder.Nature communications · 2025Article
- Reciprocal and non-reciprocal effects of clinically relevant SETBP1 protein dosage changes.Human molecular genetics · 2025Article
- The mLeukemia · 2024Article
- Article
- The landscape of SETBP1 gene expression and transcription factor activity across human tissues.PloS one · 2024Article
- MYB as a Critical Transcription Factor and Potential Therapeutic Target in AML.Advances in experimental medicine and biology · 2024Review
- Article
- Identification of a novel de novo mutation of SETBP1 and new findings of SETBP1 in tumorgenesis.Orphanet journal of rare diseases · 2023Article
- Article
- Recruitment of MLL1 complex is essential for SETBP1 to induce myeloid transformation.iScience · 2022Article
- Putative Roles of SETBP1 Dosage on the SET Oncogene to Affect Brain Development.Frontiers in neuroscience · 2022Article
- Selective Requirement of MYB for Oncogenic Hyperactivation of a Translocated Enhancer in Leukemia.Cancer discovery · 2021Article
- SETBP1 accumulation induces P53 inhibition and genotoxic stress in neural progenitors underlying neurodegeneration in Schinzel-Giedion syndrome.Nature communications · 2021Article
- SETBP1 overexpression acts in the place of class-defining mutations to drive FLT3-ITD-mutant AML.Blood advances · 2021Article
- Regulation of MYB by distal enhancer elements in human myeloid leukemia.Cell death & disease · 2021Article
- F-Box Proteins and Cancer.Cancers · 2020Review
- Identification of a Splenic Marginal Zone Lymphoma Signature: Preliminary Findings With Diagnostic Potential.Frontiers in oncology · 2020Article
- Article
- Insertional mutagenesis identifies cooperation between Setbp1 and Mllt3 in inducing myeloid leukemia development.Leukemia · 2019Article
- SETBP1 induces transcription of a network of development genes by acting as an epigenetic hub.Nature communications · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
SETBP1 missense mutations have been frequently identified in multiple myeloid neoplasms; however, their oncogenic potential remains unclear. Here we show that expression of Setbp1 mutants carrying two such mutations in mouse bone marrow progenitors efficiently induced development of acute myeloid leukemias (AMLs) in irradiated recipient mice with significantly shorter latencies and greater penetrance than expression of wild-type Setbp1, suggesting that these mutations are highly oncogenic. The increased oncogenicity of Setbp1 missense mutants could be due in part to their capability to drive significantly higher target gene transcription. We further identify Myb as a critical mediator of Setbp1-induced self-renewal as its knockdown caused efficient differentiation of myeloid progenitors immortalized by wild-type Setbp1 and Setbp1 missense mutants. Interestingly, Myb is also a direct transcriptional target of Setbp1 and Setbp1 missense mutants as they directly bind to the Myb locus in immortalized cells and dramatically activate a critical enhancer/promoter region of Myb in luciferase reporter assays. Furthermore, Myb knockdown in Setbp1 and Setbp1 missense mutations-induced AML cells also efficiently induced their differentiation in culture and significantly prolonged the survival of their secondary recipient mice, suggesting that targeting MYB pathway could be a promising strategy for treating human myeloid neoplasms with SETBP1 activation.
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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.