ReviewEnvironmental and molecular mutagenesis2020
Fanconi anemia and the underlying causes of genomic instability.
Review in Environmental and molecular mutagenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Cancer Trends in Inborn Errors of Immunity: A Systematic Review and Meta-Analysis.Journal of clinical immunology · 2024Pooled it
- Translational Research on Azacitidine Post-Remission Therapy of Acute Myeloid Leukemia in Elderly Patients (QOL-ONE Trans-2).International journal of molecular sciences · 2024Trial
- Iron, inflammation, and intestinal tumors: the crucial triad in colorectal cancer progression and therapy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Fanconi Anemia: Interplay Between DNA Repair Defects, Mitochondrial Dysfunction, and Oxidative Stress.Cells · 2026Review
- Evaluation of predictive biomarkers for late radiation toxicity in breast cancer patients.Scientific reports · 2025Article
- Epithelial competition determines gene therapy potential to suppress Fanconi Anemia oral cancer risk.PLoS computational biology · 2025Article
- Epithelial competition determines gene therapy potential to suppress Fanconi Anemia oral cancer risk.bioRxiv : the preprint server for biology · 2025Article
- Critical role of alpha spectrin in DNA repair: the importance of μ-calpain and Fanconi anemia proteins.Experimental biology and medicine (Maywood, N.J.) · 2025Review
- Unraveling the Role of Ubiquitin-Conjugating Enzyme UBE2T in Tumorigenesis: A Comprehensive Review.Cells · 2024Review
- Review
- Further Evidence forMolecular syndromology · 2023Article
- SNV/indel hypermutator phenotype in biallelic RAD51C variant: Fanconi anemia.Human genetics · 2023Article
- SNV/indel hypermutator phenotype in biallelic RAD51C variant - Fanconi anemia.Research square · 2023Article
- Whole-exome sequencing identifies FANC heterozygous germline mutation as an adverse factor for immunosuppressive therapy in Chinese aplastic anemia patients aged 40 or younger: a single-center retrospective study.Annals of hematology · 2023Article
- Computed cancer interactome explains the effects of somatic mutations in cancers.Protein science : a publication of the Protein Society · 2022Article
- Review
- SCAI promotes error-free repair of DNA interstrand crosslinks via the Fanconi anemia pathway.EMBO reports · 2022Article
- Alcohol Consumption,Life (Basel, Switzerland) · 2022Review
- Genome-wide whole-blood transcriptome profiling across inherited bone marrow failure subtypes.Blood advances · 2021Article
- Cell and Gene Therapy for Anemia: Hematopoietic Stem Cells and Gene Editing.International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Fanconi anemia (FA) is a rare genetic disorder, characterized by birth defects, progressive bone marrow failure, and a predisposition to cancer. This devastating disease is caused by germline mutations in any one of the 22 known FA genes, where the gene products are primarily responsible for the resolution of DNA interstrand cross-links (ICLs), a type of DNA damage generally formed by cytotoxic chemotherapeutic agents. However, the identity of endogenous mutagens that generate DNA ICLs remains largely elusive. In addition, whether DNA ICLs are indeed the primary cause behind FA phenotypes is still a matter of debate. Recent genetic studies suggest that naturally occurring reactive aldehydes are a primary source of DNA damage in hematopoietic stem cells, implicating that they could play a role in genome instability and FA. Emerging lines of evidence indicate that the FA pathway constitutes a general surveillance mechanism for the genome by protecting against a variety of DNA replication stresses. Therefore, understanding the DNA repair signaling that is regulated by the FA pathway, and the types of DNA lesions underlying the FA pathophysiology is crucial for the treatment of FA and FA-associated cancers. Here, we review recent advances in our understanding of the relationship between reactive aldehydes, bone marrow dysfunction, and FA biology in the context of signaling pathways triggered during FA-mediated DNA repair and maintenance of the genomic integrity. Environ. Mol. Mutagen. 2020. © 2020 Wiley Periodicals, Inc.
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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 Socratic graph.