ArticleBlood2012
Overcoming reprogramming resistance of Fanconi anemia cells.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
What it found
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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.
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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.
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Who cites it
81 citing papers in PubMed.
- Embryoid bodies as a model system for exploring early human embryonic development.Journal of assisted reproduction and genetics · 2025Review
- Examining patient-specific responses to PARP inhibitors in a novel, human induced pluripotent stem cell-based model of breast cancer.NPJ precision oncology · 2025Article
- BRCA1 and 53BP1 regulate reprogramming efficiency by mediating DNA repair pathway choice at replication-associated double-strand breaks.Cell reports · 2024Article
- Applications of Innovation Technologies for Personalized Cancer Medicine: Stem Cells and Gene-Editing Tools.ACS pharmacology & translational science · 2023Review
- Replication stress in mammalian embryo development, differentiation, and reprogramming.Trends in cell biology · 2023Review
- RUNX1 mutations mitigate quiescence to promote transformation of hematopoietic progenitors in Fanconi anemia.Leukemia · 2023Article
- Patient-Derived iPSCs Faithfully Represent the Genetic Diversity and Cellular Architecture of Human Acute Myeloid Leukemia.Blood cancer discovery · 2023Article
- Transcription-replication conflicts in primordial germ cells necessitate the Fanconi anemia pathway to safeguard genome stability.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Developing Bottom-Up Induced Pluripotent Stem Cell Derived Solid Tumor Models Using Precision Genome Editing Technologies.The CRISPR journal · 2022Review
- The Use of Stem Cell-Derived Organoids in Disease Modeling: An Update.International journal of molecular sciences · 2021Review
- Induced pluripotent stem cell models of myeloid malignancies and clonal evolution.Stem cell research · 2021Review
- Inherited DNA Repair Defects Disrupt the Structure and Function of Human Skin.Cell stem cell · 2021Article
- Modeling cancer progression using human pluripotent stem cell-derived cells and organoids.Stem cell research · 2020Review
- An induced pluripotent stem cell model of Fanconi anemia reveals mechanisms of p53-driven progenitor cell differentiation.Blood advances · 2020Article
- Canonical and Noncanonical Roles of Fanconi Anemia Proteins: Implications in Cancer Predisposition.Cancers · 2020Review
- Article
- Rescue of premature aging defects in Cockayne syndrome stem cells by CRISPR/Cas9-mediated gene correction.Protein & cell · 2020Article
- DNA cross-link repair safeguards genomic stability during premeiotic germ cell development.Nature genetics · 2019Article
- Induced pluripotent stem cells in disease modelling and drug discovery.Nature reviews. Genetics · 2019Review
- Modeling blood diseases with human induced pluripotent stem cells.Disease models & mechanisms · 2019Review
21 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Fanconi anemia (FA) is a recessive syndrome characterized by progressive fatal BM failure and chromosomal instability. FA cells have inactivating mutations in a signaling pathway that is critical for maintaining genomic integrity and protecting cells from the DNA damage caused by cross-linking agents. Transgenic expression of the implicated genes corrects the phenotype of hematopoietic cells, but previous attempts at gene therapy have failed largely because of inadequate numbers of hematopoietic stem cells available for gene correction. Induced pluripotent stem cells (iPSCs) constitute an alternate source of autologous cells that are amenable to ex vivo expansion, genetic correction, and molecular characterization. In the present study, we demonstrate that reprogramming leads to activation of the FA pathway, increased DNA double-strand breaks, and senescence. We also demonstrate that defects in the FA DNA-repair pathway decrease the reprogramming efficiency of murine and human primary cells. FA pathway complementation reduces senescence and restores the reprogramming efficiency of somatic FA cells to normal levels. Disease-specific iPSCs derived in this fashion maintain a normal karyotype and are capable of hematopoietic differentiation. These data define the role of the FA pathway in reprogramming and provide a strategy for future translational applications of patient-specific FA iPSCs.
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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.