ArticleArchives of toxicology2013
The impact of FANCD2 deficiency on formaldehyde-induced toxicity in human lymphoblastoid cell lines.
Article in Archives of toxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Repair of genomic interstrand crosslinks.DNA repair · 2024Review
- Integrating PARP Inhibitors in mCRPC Therapy: Current Strategies and Emerging Trends.Cancer management and research · 2024Review
- Fanconi anemia: current insights regarding epidemiology, cancer, and DNA repair.Human genetics · 2022Review
- Evaluating the Sub-Acute Toxicity of Formaldehyde Fumes in an In Vitro Human Airway Epithelial Tissue Model.International journal of molecular sciences · 2022Article
- Endogenous formaldehyde scavenges cellular glutathione resulting in redox disruption and cytotoxicity.Nature communications · 2022Article
- Applying genome-wide CRISPR to identify known and novel genes and pathways that modulate formaldehyde toxicity.Chemosphere · 2021Article
- Combined exposure to formaldehyde and PMEnvironment international · 2020Article
- Mode of action-based risk assessment of genotoxic carcinogens.Archives of toxicology · 2020Review
- Genetic investigation of formaldehyde-induced DNA damage response in Schizosaccharomyces pombe.Current genetics · 2020Article
- Evaluation of inhaled low-dose formaldehyde-induced DNA adducts and DNA-protein cross-links by liquid chromatography-tandem mass spectrometry.Archives of toxicology · 2019Article
- An RNAi screen in human cell lines reveals conserved DNA damage repair pathways that mitigate formaldehyde sensitivity.DNA repair · 2018Article
- Estimation of formaldehyde occupational exposure limit based on genetic damage in some Iranian exposed workers using benchmark dose method.Environmental science and pollution research international · 2018Article
- Article
- Editor's Highlight: High-Throughput Functional Genomics Identifies Modulators of TCE Metabolite Genotoxicity and Candidate Susceptibility Genes.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
- Re-evaluation of the WHO (2010) formaldehyde indoor air quality guideline for cancer risk assessment.Archives of toxicology · 2017Review
- Complementation of hypersensitivity to DNA interstrand crosslinking agents demonstrates that XRCC2 is a Fanconi anaemia gene.Journal of medical genetics · 2016Article
- Identification of Genes That Modulate Susceptibility to Formaldehyde and Imatinib by Functional Genomic Screening in Human Haploid KBM7 Cells.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
- Functional Toxicogenomic Profiling Expands Insight into Modulators of Formaldehyde Toxicity in Yeast.Frontiers in genetics · 2016Article
- Induction of centrosome amplification by formaldehyde, but not hydroquinone, in human lymphoblastoid TK6 cells.Environmental and molecular mutagenesis · 2015Article
- Emerging approaches in predictive toxicology.Environmental and molecular mutagenesis · 2014Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Formaldehyde (FA), a major industrial chemical and ubiquitous environmental pollutant, has recently been classified by the International Agency for Research on Cancer as a human leukemogen. The major mode of action of FA is thought to be the formation of DNA-protein cross-links (DPCs). Repair of DPCs may be mediated by the Fanconi anemia pathway; however, data supporting the involvement of this pathway are limited, particularly in human hematopoietic cells. Therefore, we assessed the role of FANCD2, a critical component of the Fanconi anemia pathway, in FA-induced toxicity in human lymphoblast cell models of FANCD2 deficiency (PD20 cells) and FANCD2 sufficiency (PD20-D2 cells). After treatment of the cells with 0-150 μM FA for 24 h, DPCs were increased in a dose-dependent manner in both cell lines, with greater increases in FANCD2-deficient PD20 cells. FA also induced cytotoxicity, micronuclei, chromosome aberrations, and apoptosis in a dose-dependent manner in both cell lines, with greater increases in cytotoxicity and apoptosis in PD20 cells. Increased levels of γ-ATR and γ-H2AX in both cell lines suggested the recognition of FA-induced DNA damage; however, the induction of BRCA2 was compromised in FANCD2-deficient PD20 cells, potentially reducing the capacity to repair DPCs. Together, these findings suggest that FANCD2 protein and the Fanconi anemia pathway are essential to protect human lymphoblastoid cells against FA toxicity. Future studies are needed to delineate the role of this pathway in mitigating FA-induced toxicity, particularly in hematopoietic stem cells, the target cells in leukemia.
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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.