ArticleLeukemia2014
GATA1s induces hyperproliferation of eosinophil precursors in Down syndrome transient leukemia.
Article in Leukemia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 43 citations in OpenAlex.
- DLK1 is a GATA1s-driven dependency and therapeutic target in Down syndrome-associated myeloid leukemia.Blood advances · 2026Article
- Single-cell transcriptomics reveal individual and cooperative effects of trisomy 21 and GATA1s on hematopoiesis.Stem cell reports · 2025Article
- Synergistic roles of DYRK1A and GATA1 in trisomy 21 megakaryopoiesis.JCI insight · 2023Article
- RUN(X) out of blood: emerging RUNX1 functions beyond hematopoiesis and links to Down syndrome.Human genomics · 2023Review
- Article
- Leukemogenesis in infants and young children with trisomy 21.Hematology. American Society of Hematology. Education Program · 2022Article
- Mechanism of KIT gene regulation by GATA1 lacking the N-terminal domain in Down syndrome-related myeloid disorders.Scientific reports · 2022Article
- Article
- Increased risk of leukaemia in children with Down syndrome: a somatic evolutionary view.Expert reviews in molecular medicine · 2021Article
- Article
- Molecular Mechanisms of the Genetic Predisposition to Acute Megakaryoblastic Leukemia in Infants With Down Syndrome.Frontiers in oncology · 2021Review
- Modeling Transient Abnormal Myelopoiesis Using Induced Pluripotent Stem Cells and CRISPR/Cas9 Technology.Molecular therapy. Methods & clinical development · 2020Article
- RNA-Binding Proteins in Acute Leukemias.International journal of molecular sciences · 2020Review
- Acute Megakaryocytic Leukemia.Cold Spring Harbor perspectives in medicine · 2020Review
- Mechanisms of Progression of Myeloid Preleukemia to Transformed Myeloid Leukemia in Children with Down Syndrome.Cancer cell · 2019Article
- Changes in the peripheral blood cell count in pediatric patients with Down syndrome.The Journal of international medical research · 2019Article
- Article
- GATA factor mutations in hematologic disease.Blood · 2017Review
- Global transcriptome and chromatin occupancy analysis reveal the short isoform of GATA1 is deficient for erythroid specification and gene expression.Haematologica · 2015Article
- Stem and progenitor cell dysfunction in human trisomies.EMBO reports · 2015Review
Corrections and comments
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Authors and funding
18 authors at 6 institutions in 4 countries.
Funding
Abstract
Transient leukemia (TL) is evident in 5-10% of all neonates with Down syndrome (DS) and associated with N-terminal truncating GATA1 mutations (GATA1s). Here we report that TL-cell clones generate abundant eosinophils in a substantial fraction of patients. Sorted eosinophils from patients with TL and eosinophilia carried the same GATA1s mutations as sorted TL blasts, consistent with their clonal origin. TL blasts exhibited a genetic program characteristic of eosinophils and differentiated along the eosinophil lineage in vitro. Similarly, ectopic expression of Gata1s, but not Gata1, in wild-type CD34(+)-hematopoietic stem and progenitor cells induced hyperproliferation of eosinophil promyelocytes in vitro. Although GATA1s retained the function of GATA1 to induce eosinophil genes by occupying their promoter regions, GATA1s was impaired in its ability to repress oncogenic MYC and the pro-proliferative E2F transcription network. Chromatin Immunoprecipitation Sequencing (ChIP-seq) indicated reduced GATA1s occupancy at the MYC promoter. Knockdown of MYC, or the obligate E2F-cooperation partner DP1, rescued the GATA1s-induced hyperproliferative phenotype. In agreement, terminal eosinophil maturation was blocked in Gata1(Δe2) knockin mice, exclusively expressing Gata1s, leading to accumulation of eosinophil precursors in blood and bone marrow. These data suggest a direct relationship between the N-terminal truncating mutations of GATA1 and clonal eosinophilia in DS patients.
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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.