ArticleBlood advances2025
Hematological phenotypes in GATA2 deficiency syndrome arise from aging, maladaptation to proliferation, and somatic events.
Article in Blood advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- The Runx1-Gata2 axis: epigenetic architecture of lineage fate.Molecular biology reports · 2026Review
- X-linked SEPTIN6-related congenital neutropenia and B cell deficiency.Journal of human immunity · 2026Article
- GATA2 deficiency exacerbates chronic liver injuryWorld journal of stem cells · 2026Article
- ViableFrontiers in immunology · 2026Article
- Article
- Human iPSCs-based modeling unveils SETBP1 as a driver of chromatin rewiring in GATA2 deficiency.Nature communications · 2025Article
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26 authors.
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Abstract
abstractThe GATA2 transcription factor is a pivotal regulator of hematopoiesis. Disruptions in the GATA2 gene drive severe hematologic abnormalities and are associated with an increased risk of myelodysplastic syndromes and acute myeloid leukemia; however, the mechanisms underlying the pathophysiology of GATA2 deficiency still remain unclear. We developed 2 different mouse models that are based on serial and limiting donor-cell transplantation of (14-15 months) GATA2 haploinsufficient cells and mirror the symptoms of GATA2 deficiency. Similar to what has been observed in patients, our models showed that GATA2 haploinsufficiency leads to B lymphopenia, monocytopenia, lethal bone marrow failure (BMF), myelodysplasia, and lymphoblastic leukemia. Leukemia arises exclusively because of BMF, driven by somatic aberrations and accompanied by increased Myc target expression and genomic instability. These findings were confirmed in human GATA2+/- K562 cell lines showing defects in cytokinesis and are in line with the fact that monosomy 7 and trisomy 8 are frequent events in patients with myelodysplastic syndrome.
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