ArticleBlood advances2020
An induced pluripotent stem cell model of Fanconi anemia reveals mechanisms of p53-driven progenitor cell differentiation.
Article in Blood advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Modeling myeloid cell development in health and disease using induced pluripotent stem cells.Frontiers in immunology · 2026Review
- Beyond Hematologic Malignancies: Colorectal Cancer as a Solid Tumor Manifestation of Inherited Bone Marrow Failure Syndromes.International journal of molecular sciences · 2025Review
- Article
- Efficient gene editing in induced pluripotent stem cells enabled by an inducible adenine base editor with tunable expression.Scientific reports · 2023Article
- p53 in the Molecular Circuitry of Bone Marrow Failure Syndromes.International journal of molecular sciences · 2023Review
- RUNX1 mutations mitigate quiescence to promote transformation of hematopoietic progenitors in Fanconi anemia.Leukemia · 2023Article
- Fanca deficiency is associated with alterations in osteoclastogenesis that are rescued by TNFα.Cell & bioscience · 2023Article
- ARID1B, a molecular suppressor of erythropoiesis, is essential for the prevention of Monge's disease.Experimental & molecular medicine · 2022Article
- Review
- Pediatric Tumors as Disorders of Development: The Case for In Vitro Modeling Based on Human Stem Cells.Cancer control : journal of the Moffitt Cancer CenterReview
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Authors and funding
18 authors at 4 institutions in 1 country.
Funding
Abstract
Fanconi anemia (FA) is a disorder of DNA repair that manifests as bone marrow (BM) failure. The lack of accurate murine models of FA has refocused efforts toward differentiation of patient-derived induced pluripotent stem cells (IPSCs) to hematopoietic progenitor cells (HPCs). However, an intact FA DNA repair pathway is required for efficient IPSC derivation, hindering these efforts. To overcome this barrier, we used inducible complementation of FANCA-deficient IPSCs, which permitted robust maintenance of IPSCs. Modulation of FANCA during directed differentiation to HPCs enabled the production of FANCA-deficient human HPCs that recapitulated FA genotoxicity and hematopoietic phenotypes relative to isogenic FANCA-expressing HPCs. FANCA-deficient human HPCs underwent accelerated terminal differentiation driven by activation of p53/p21. We identified growth arrest specific 6 (GAS6) as a novel target of activated p53 in FANCA-deficient HPCs and modulate GAS6 signaling to rescue hematopoiesis in FANCA-deficient cells. This study validates our strategy to derive a sustainable, highly faithful human model of FA, uncovers a mechanism of HPC exhaustion in FA, and advances toward future cell therapy in FA.
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