ReviewCurrent opinion in cell biology2015
What is the DNA repair defect underlying Fanconi anemia?
Review in Current opinion in cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
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
99 citing papers in PubMed, 138 citations in OpenAlex.
- Prenatal Diagnosis of a Fetus With Congenital Malformations Caused by Compound Heterozygous Mutations in FANCA: A Case Report and Literature Review.Molecular genetics & genomic medicine · 2026Review
- Examination of a Chimeric Bis-Electrophile for Selective DNA-Protein Cross-Linking and Mechlorethamine Reveals an Unknown Source of Nitrogen Mustard Cytotoxicity.Journal of the American Chemical Society · 2025Article
- Fanconi anemia patients with head and neck squamous cell carcinoma - a multi-center study.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2025Article
- Comprehensive review on Fanconi anemia: insights into DNA interstrand cross-links, repair pathways, and associated tumors.Orphanet journal of rare diseases · 2025Review
- Circadian rhythm and aryl hydrocarbon receptor crosstalk in bone marrow adipose tissue and implications in leukemia.Scientific reports · 2025Article
- AmNA-Modified Antisense Oligonucleotide Targeting MCM8 as a Cancer-Specific Chemosensitizer for Platinum Compounds.Cancer science · 2025Article
- Observational
- Repair of genomic interstrand crosslinks.DNA repair · 2024Review
- STIM1 translocation to the nucleus protects cells from DNA damage.Nucleic acids research · 2024Article
- FANCD2 and RAD51 recombinase directly inhibit DNA2 nuclease at stalled replication forks and FANCD2 acts as a novel RAD51 mediator in strand exchange to promote genome stability.Nucleic acids research · 2023Article
- Phosphorylation by ATR triggers FANCD2 chromatin loading and activates the Fanconi anemia pathway.Cell reports · 2023Article
- Mutations in AcrR and RNA Polymerase Confer High-Level Resistance to Psoralen-UVA Irradiation.Journal of bacteriology · 2023Article
- SNV/indel hypermutator phenotype in biallelic RAD51C variant: Fanconi anemia.Human genetics · 2023Article
- SPRTN-dependent DPC degradation precedes repair of damaged DNA: a proof of concept revealed by the STAR assay.Nucleic acids research · 2023Article
- SNV/indel hypermutator phenotype in biallelic RAD51C variant - Fanconi anemia.Research square · 2023Article
- A CRISPR-Cas9 screen identifies EXO1 as a formaldehyde resistance gene.Nature communications · 2023Article
- Fanconi anemia: current insights regarding epidemiology, cancer, and DNA repair.Human genetics · 2022Review
- Biological Functions of the DNA Glycosylase NEIL3 and Its Role in Disease Progression Including Cancer.Cancers · 2022Review
- The structure-specific endonuclease complex SLX4-XPF regulates Tus-Ter-induced homologous recombination.Nature structural & molecular biology · 2022Article
- MutatedCells · 2022Article
39 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Fanconi anemia (FA) is a rare human genetic disease characterized by bone marrow failure, cancer predisposition, and genomic instability. It has been known for many years that FA patient-derived cells are exquisitely sensitive to DNA interstrand cross-linking agents such as cisplatin and mitomycin C. On this basis, it was widely assumed that failure to repair endogenous interstrand cross-links (ICLs) causes FA, although the endogenous mutagen that generates these lesions remained elusive. Recent genetic evidence now suggests that endogenous aldehydes are the driving force behind FA. Importantly, aldehydes cause a variety of DNA lesions, including ICLs and DNA protein cross-links (DPCs), re-kindling the debate about which DNA lesions cause FA. In this review, we discuss new developments in our understanding of DPC and ICL repair, and how these findings bear on the question of which DNA lesion underlies FA.
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.