ArticleAnemia2012
Disrupted Signaling through the Fanconi Anemia Pathway Leads to Dysfunctional Hematopoietic Stem Cell Biology: Underlying Mechanisms and Potential Therapeutic Strategies.
Article in Anemia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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.
The trial behind it
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Fanconi Anemia: Interplay Between DNA Repair Defects, Mitochondrial Dysfunction, and Oxidative Stress.Cells · 2026Review
- Function and Regulation of Bone Marrow Adipose Tissue in Health and Disease: State of the Field and Clinical Considerations.Comprehensive Physiology · 2024Review
- The DNA helicase FANCJ (BRIP1) functions in double strand break repair processing, but not crossover formation during prophase I of meiosis in male mice.PLoS genetics · 2024Article
- The DNA helicase FANCJ (BRIP1) functions in Double Strand Break repair processing, but not crossover formation during Prophase I of meiosis in male mice.bioRxiv : the preprint server for biology · 2023Article
- The FANC/BRCA Pathway Releases Replication Blockades by Eliminating DNA Interstrand Cross-Links.Genes · 2020Review
- Peering through zebrafish to understand inherited bone marrow failure syndromes.Haematologica · 2019Review
- An abnormal bone marrow microenvironment contributes to hematopoietic dysfunction in Fanconi anemia.Haematologica · 2017Article
- Increased red cell distribution width in Fanconi anemia: a novel marker of stress erythropoiesis.Orphanet journal of rare diseases · 2016Article
- Telomere dysfunction drives aberrant hematopoietic differentiation and myelodysplastic syndrome.Cancer cell · 2015Article
- Article
- Epigenetic Alterations in Fanconi Anaemia: Role in Pathophysiology and Therapeutic Potential.PloS one · 2015Article
- The Fanconi anemia pathway is required for efficient repair of stress-induced DNA damage in haematopoietic stem cells.Cell cycle (Georgetown, Tex.) · 2015Article
- Pro-inflammatory cytokines: emerging players regulating HSC function in normal and diseased hematopoiesis.Experimental cell research · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fanconi anemia (FA) is the most common inherited bone marrow failure syndrome. FA patients suffer to varying degrees from a heterogeneous range of developmental defects and, in addition, have an increased likelihood of developing cancer. Almost all FA patients develop a severe, progressive bone marrow failure syndrome, which impacts upon the production of all hematopoietic lineages and, hence, is thought to be driven by a defect at the level of the hematopoietic stem cell (HSC). This hypothesis would also correlate with the very high incidence of MDS and AML that is observed in FA patients. In this paper, we discuss the evidence that supports the role of dysfunctional HSC biology in driving the etiology of the disease. Furthermore, we consider the different model systems currently available to study the biology of cells defective in the FA signaling pathway and how they are informative in terms of identifying the physiologic mediators of HSC depletion and dissecting their putative mechanism of action. Finally, we ask whether the insights gained using such disease models can be translated into potential novel therapeutic strategies for the treatment of the hematologic disorders in FA patients.
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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.