ArticleBlood2013
Perturbation of fetal hematopoiesis in a mouse model of Down syndrome's transient myeloproliferative disorder.
Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed.
- Single cell transcriptional evolution of myeloid leukemia of Down syndrome.Nature communications · 2026Article
- Genome-wide association study of somatic GATA1s mutations in newborns with Down syndrome.Blood advances · 2025Article
- Organoids in Haematologic Research: Advances and Future Directions.Cell proliferation · 2025Review
- Down syndrome-associated leukaemias: current evidence and challenges.Therapeutic advances in hematology · 2024Review
- Synergistic roles of DYRK1A and GATA1 in trisomy 21 megakaryopoiesis.JCI insight · 2023Article
- The NCOR-HDAC3 co-repressive complex modulates the leukemogenic potential of the transcription factor ERG.Nature communications · 2023Article
- Cellular and metabolic characteristics of pre-leukemic hematopoietic progenitors with GATA2 haploinsufficiency.Haematologica · 2023Article
- Gata1s mutant mice display persistent defects in the erythroid lineage.Blood advances · 2023Article
- RUNX1 isoform disequilibrium promotes the development of trisomy 21-associated myeloid leukemia.Blood · 2023Article
- Leukemogenesis in infants and young children with trisomy 21.Hematology. American Society of Hematology. Education Program · 2022Article
- Amplified EPOR/JAK2 Genes Define a Unique Subtype of Acute Erythroid Leukemia.Blood cancer discovery · 2022Article
- Article
- Review
- The Fetal-to-Adult Hematopoietic Stem Cell Transition and its Role in Childhood Hematopoietic Malignancies.Stem cell reviews and reports · 2021Review
- Molecular Landscapes and Models of Acute Erythroleukemia.HemaSphere · 2021Review
- Molecular Mechanisms of the Genetic Predisposition to Acute Megakaryoblastic Leukemia in Infants With Down Syndrome.Frontiers in oncology · 2021Review
- Gain of chromosome 21 in hematological malignancies: lessons from studying leukemia in children with Down syndrome.Leukemia · 2020Review
- A non-mosaic transchromosomic mouse model of down syndrome carrying the long arm of human chromosome 21.eLife · 2020Article
- Influence of allelic differences in Down syndrome.Progress in brain research · 2020Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Children with Down syndrome develop a unique congenital clonal megakaryocytic proliferation disorder (transient myeloproliferative disorder [TMD]). It is caused by an expansion of fetal megakaryocyte-erythroid progenitors (MEPs) triggered by trisomy of chromosome 21 and is further enhanced by the somatic acquisition of a mutation in GATA1. These mutations result in the expression of a short-isoform GATA1s lacking the N-terminal domain. To examine the hypothesis that the Hsa21 ETS transcription factor ERG cooperates with GATA1s in this process, we generated double-transgenic mice expressing hERG and Gata1s. We show that increased expression of ERG by itself is sufficient to induce expansion of MEPs in fetal livers. Gata1s expression synergizes with ERG in enhancing the expansion of fetal MEPs and megakaryocytic precursors, resulting in hepatic fibrosis, transient postnatal thrombocytosis, anemia, a gene expression profile that is similar to that of human TMD and progression to progenitor myeloid leukemia by 3 months of age. This ERG/Gata1s transgenic mouse model also uncovers an essential role for the N terminus of Gata1 in erythropoiesis and the antagonistic role of ERG in fetal erythroid differentiation and survival. The human relevance of this finding is underscored by the recent discovery of similar mutations in GATA1 in patients with Diamond-Blackfan anemia.
Indexed as
Identifiers
What OpenQuestion holds
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.