ReviewOrphanet journal of rare diseases2025
Comprehensive review on Fanconi anemia: insights into DNA interstrand cross-links, repair pathways, and associated tumors.
Review in Orphanet journal of rare diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Aldehyde Detoxification in Cancer: Metabolic Guardians of the Genome.Biomolecules · 2026Review
- Xenobiotic Sulforaphane in Head and Neck Cancer: Beyond the Nrf2 Pathway.Journal of xenobiotics · 2026Review
- BAP1 and USP1 cooperate to regulate FANCD2 stability and cell proliferation in mesothelioma cells.Cell death & disease · 2026Article
- Fanconi Anemia in Mexican Patients: Molecular Spectrum and Clinical Manifestations in a Case Series.International journal of molecular sciences · 2026Article
- Fanconi Anemia: Interplay Between DNA Repair Defects, Mitochondrial Dysfunction, and Oxidative Stress.Cells · 2026Review
- Functional Germline DNA Repair Mutations as Predictors of Acute Radiodermatitis in Breast Cancer.Diagnostics (Basel, Switzerland) · 2026Article
- Clinical, cytogenetic, and molecular insights from 32 years of the Portuguese Fanconi anemia cohort.Genetics in medicine open · 2026Article
- Red Blood Cell Antioxidant State in Fanconi Anemia: The Highlighted Roles of Pi-Class Glutathione S-Transferase and Glutathione Peroxidase.Antioxidants (Basel, Switzerland) · 2025Article
- TSN Disrupts Fanconi Anemia Pathway Activation Through JAK/STAT1-Mediated Transcriptional Repression of FA Core Subunits in Bladder Cancer.Dose-response : a publication of International Hormesis SocietyArticle
- Concordant high-grade glioma in monozygotic twins with germline variants in ATM, FANCC, and FANCM: a case report on combined DNA repair deficiency.Neuro-oncology advancesArticle
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fanconi anemia (FA) is a rare genetic disorder caused by defects in the repair of DNA interstrand crosslinks (ICLs)-highly toxic lesions that impede essential processes like DNA replication and transcription, leading to severe genome instability. Clinically, FA presents with a broad spectrum of symptoms, including progressive bone marrow failure, congenital abnormalities, and an elevated predisposition to various malignancies, particularly acute myeloid leukemia and squamous cell carcinomas. This review provides a comprehensive overview of both the endogenous and exogenous sources of ICLs and the DNA repair pathways responsible for their resolution, with a primary focus on the FA pathway. We also discuss the tumorigenic consequences of FA pathway deficiencies, highlighting the molecular mechanisms that contribute to the heightened cancer risk observed in FA patients.
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