ReviewMutation research2009
Mouse models of Fanconi anemia.
Review in Mutation research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 1 of them a synthesis that pooled it.
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
107 citing papers in PubMed, 1 synthesis or guideline pooled it, 166 citations in OpenAlex.
- The Coming of Age of Preclinical Models of MDS.Frontiers in oncology · 2022Pooled it
- Homozygosity for the WRN Helicase-Inactivating Variant, R834C, does not confer a Werner syndrome clinical phenotype.Scientific reports · 2017Trial
- CRISPR-Cas9-mediated homology-directed repair rescues the induced bone marrow failure inMolecular therapy. Nucleic acids · 2026Article
- Insights and modulation of RNA polymerase-dependent R-loop and dsRNA in Fanconi anemia hematopoietic stem cells.JCI insight · 2026Article
- Metabolite-induced DNA damage drives stochastic stem cell loss and clonal hematopoiesis.Cell stem cell · 2026Article
- The tight bond between Fanconi anemia and aging.Frontiers in aging · 2026Review
- Rbm8a deficiency causes hematopoietic defects by modulating Wnt/PCP signaling.Developmental biology · 2025Article
- The Converging Roles of Nucleases and Helicases in Genome Maintenance and the Aging Process.Life (Basel, Switzerland) · 2025Review
- MDM4 overexpression alleviates developmental and hematopoietic defects in Fancg deficient mice.Leukemia · 2025Article
- Distinct developmental outcomes in DNA repair-deficient FANCC c.67delG mutant and FANCCCell death and differentiation · 2025Article
- A porcine model of Fanconi anemia.PloS one · 2025Article
- In utero hematopoietic stem cell transplantation for Fanconi anemia.Blood advances · 2024Article
- Reduced levels of MRE11 cause disease phenotypes distinct from ataxia telangiectasia-like disorder.Human molecular genetics · 2024Article
- Hematopoiesis after anti-CD117 monoclonal antibody treatment in the settings of wild-type and Fanconi anemia mice.Haematologica · 2024Article
- Article
- New insights into the all-testis differentiation in zebrafish with compromised endogenous androgen and estrogen synthesis.PLoS genetics · 2024Article
- Primary hepatoid adenocarcinoma of the lung in patient with silicosis: a case report and literature review.Frontiers in oncology · 2024Article
- A murine model to evaluate immunotherapy effectiveness for human Fanconi anemia-mutated acute myeloid leukemia.PloS one · 2024Article
- Base Excision Repair: Mechanisms and Impact in Biology, Disease, and Medicine.International journal of molecular sciences · 2023Review
- FANCA deficiency promotes leukaemic progression by allowing the emergence of cells carrying oncogenic driver mutations.Oncogene · 2023Article
47 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Fanconi anemia is a rare inherited disease characterized by congenital anomalies, growth retardation, aplastic anemia and an increased risk of acute myeloid leukemia and squamous cell carcinomas. The disease is caused by mutation in genes encoding proteins required for the Fanconi anemia pathway, a response mechanism to replicative stress, including that caused by genotoxins that cause DNA interstrand crosslinks. Defects in the Fanconi anemia pathway lead to genomic instability and apoptosis of proliferating cells. To date, 13 complementation groups of Fanconi anemia were identified. Five of these genes have been deleted or mutated in the mouse, as well as a sixth key regulatory gene, to create mouse models of Fanconi anemia. This review summarizes the phenotype of each of the Fanconi anemia mouse models and highlights how genetic and interventional studies using the strains have yielded novel insight into therapeutic strategies for Fanconi anemia and into how the Fanconi anemia pathway protects against genomic instability.
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.