ArticleBlood2022
Mutated SETBP1 activates transcription of Myc programs to accelerate CSF3R-driven myeloproliferative neoplasms.
Article in Blood, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Colony-Stimulating Factor 3 Receptor Mutations and Variants in Hematological Malignancies.Cancers · 2025Review
- Research progress of additional pathogenic mutations in chronic neutrophilic leukemia.Annals of hematology · 2024Review
- The landscape of SETBP1 gene expression and transcription factor activity across human tissues.PloS one · 2024Article
- Case report: Safety and efficacy of synergistic treatment using selinexor and azacitidine in patients with atypical chronic myeloid leukemia with resistance to decitabine.Frontiers in oncology · 2024Article
- The landscape ofbioRxiv : the preprint server for biology · 2023Article
- Article
- The impact of SETBP1 mutations in neurological diseases and cancer.Genes to cells : devoted to molecular & cellular mechanisms · 2023Review
- SETBP1 mutation determines sensitivity to immune checkpoint inhibitors in melanoma and NSCLC.Aging · 2023Article
- A novel colony stimulating factor 3 receptor activating mutation identified in a patient with chronic neutrophilic leukemia.Haematologica · 2023Article
- Circulating tumor DNA determining hyperprogressive disease after CAR-T therapy alarms in DLBCL: a case report and literature review.Frontiers in oncology · 2023Article
- CSF3R and SETBP1 getting high on LSD1.Blood · 2022Article
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11 authors at 1 institution in 1 country.
Funding
Abstract
Colony stimulating factor 3 receptor (CSF3R) mutations lead to JAK pathway activation and are the molecular hallmark of chronic neutrophilic leukemia (CNL). Approximately half of patients with CNL also have mutations in SET binding protein 1 (SETBP1). In this study, we developed models of SETBP1-mutated leukemia to understand the role that SETBP1 plays in CNL. SETBP1 mutations promote self-renewal of CSF3R-mutated hematopoietic progenitors in vitro and prevent cells from undergoing terminal differentiation. In vivo, SETBP1 mutations accelerate leukemia progression, leading to the rapid development of hepatosplenomegaly and granulocytosis. Through transcriptomic and epigenomic profiling, we found that SETBP1 enhances progenitor-associated programs, most strongly upregulating Myc and Myc target genes. This upregulation of Myc can be reversed by LSD1 inhibitors. In summary, we found that SETBP1 mutations promote aggressive hematopoietic cell expansion when expressed with mutated CSF3R through the upregulation of Myc-associated gene expression programs.
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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.