ArticlePloS one2014
DNA-damage foci to detect and characterize DNA repair alterations in children treated for pediatric malignancies.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Association Between PARP1 Single Nucleotide Polymorphism and Brain Tumors.Molecular neurobiology · 2016Pooled it
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- Evaluation of predictive biomarkers for late radiation toxicity in breast cancer patients.Scientific reports · 2025Article
- The human RAD52 complex undergoes phase separation and facilitates bundling and end-to-end tethering of RAD51 presynaptic filaments.bioRxiv : the preprint server for biology · 2024Article
- Navigating the Complexities of Radiation Injuries: Therapeutic Principles and Reconstructive Strategies.Journal of personalized medicine · 2024Review
- Radiation Dermatitis: Radiation-Induced Effects on the Structural and Immunological Barrier Function of the Epidermis.International journal of molecular sciences · 2024Review
- Human skin aging is associated with increased expression of the histone variant H2A.J in the epidermis.NPJ aging and mechanisms of disease · 2021Article
- Article
- Prediction of the Acute or Late Radiation Toxicity Effects in Radiotherapy Patients Using Ex Vivo Induced Biodosimetric Markers: A Review.Journal of personalized medicine · 2020Review
- Individual response of humans to ionising radiation: governing factors and importance for radiological protection.Radiation and environmental biophysics · 2020Review
- Spontaneous and Radiation-Induced Chromosome Aberrations in Primary Fibroblasts of Patients With Pediatric First and Second Neoplasms.Frontiers in oncology · 2020Article
- AutoFoci, an automated high-throughput foci detection approach for analyzing low-dose DNA double-strand break repair.Scientific reports · 2018Article
- Clinical and Functional Assays of Radiosensitivity and Radiation-Induced Second Cancer.Cancers · 2017Review
- A novel automatic quantification method for high-content screening analysis of DNA double strand-break response.Scientific reports · 2017Article
- Complex DNA Damage: A Route to Radiation-Induced Genomic Instability and Carcinogenesis.Cancers · 2017Review
- Compromized DNA repair as a basis for identification of cancer radiotherapy patients with extreme radiosensitivity.Cancer letters · 2016Article
- DNA Damage Response Assessments in Human Tumor Samples Provide Functional Biomarkers of Radiosensitivity.Seminars in radiation oncology · 2015Review
- Molecular Pathways: Overcoming Radiation Resistance by Targeting DNA Damage Response Pathways.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015Review
- High-throughput detection of DNA double-strand breaks using image cytometry.BioTechniques · 2015Article
- Constitutional mismatch repair deficiency-associated brain tumors: report from the European C4CMMRD consortium.Neuro-oncology advancesArticle
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeIn children diagnosed with cancer, we evaluated the DNA damage foci approach to identify patients with double-strand break (DSB) repair deficiencies, who may overreact to DNA-damaging radio- and chemotherapy. In one patient with Fanconi anemia (FA) suffering relapsing squamous cell carcinomas of the oral cavity we also characterized the repair defect in biopsies of skin, mucosa and tumor. METHODS AND MATERIALS: In children with histologically confirmed tumors or leukemias and healthy control-children DSB repair was investigated by counting γH2AX-, 53BP1- and pATM-foci in blood lymphocytes at defined time points after ex-vivo irradiation. This DSB repair capacity was correlated with treatment-related normal-tissue responses. For the FA patient the defective repair was also characterized in tissue biopsies by analyzing DNA damage response proteins by light and electron microscopy.
resultsBetween tumor-children and healthy control-children we observed significant differences in mean DSB repair capacity, suggesting that childhood cancer is based on genetic alterations affecting DNA repair. Only 1 out of 4 patients with grade-4 normal-tissue toxicities revealed an impaired DSB repair capacity. The defective DNA repair in FA patient was verified in irradiated blood lymphocytes as well as in non-irradiated mucosa and skin biopsies leading to an excessive accumulation of heterochromatin-associated DSBs in rapidly cycling cells.
conclusionsAnalyzing human tissues we show that DSB repair alterations predispose to cancer formation at younger ages and affect the susceptibility to normal-tissue toxicities. DNA damage foci analysis of blood and tissue samples allows one to detect and characterize DSB repair deficiencies and enables identification of patients at risk for high-grade toxicities. However, not all treatment-associated normal-tissue toxicities can be explained by DSB repair deficiencies.
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