ArticleCarcinogenesis2009
Large-scale evaluation of candidate genes identifies associations between DNA repair and genomic maintenance and development of benzene hematotoxicity.
Article in Carcinogenesis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 54 citations in OpenAlex.
- Acute lymphoblastic leukemia: an update on treatment and Brazilian perspective.Frontiers in oncology · 2026Review
- Towards a toxic-free environment: perspectives for chemical risk assessment approaches.La Medicina del lavoro · 2022Article
- The effects of genetic polymorphisms on benzene-exposed workers: A systematic review.Health science reports · 2021Review
- Personalised Medicine: implication and perspectives in the field of occupational health.La Medicina del lavoro · 2020Article
- Response to Comments on Zheng et al. "Association between Promoter Methylation of Gene ERCC3 and Benzene Hematotoxicity" Int. J. Environ. Res. Public Health 2017, 14, 1393.International journal of environmental research and public health · 2017Article
- Different non-synonymous polymorphisms modulate the interaction of the WRN protein to its protein partners and its enzymatic activities.Oncotarget · 2016Article
- A mechanism for 1,4-Benzoquinone-induced genotoxicity.Oncotarget · 2016Article
- Overexpression of the scaffold WD40 protein WRAP53β enhances the repair of and cell survival from DNA double-strand breaks.Cell death & disease · 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
- A missense single nucleotide polymorphism, V114I of the Werner syndrome gene, is associated with risk of osteoporosis and femoral fracture in the Japanese population.Journal of bone and mineral metabolism · 2015Article
- Diversity Outbred Mice Identify Population-Based Exposure Thresholds and Genetic Factors that Influence Benzene-Induced Genotoxicity.Environmental health perspectives · 2015Article
- Article
- Applying a Weight-of-Evidence Approach to Evaluate Relevance of Molecular Landscapes in the Exposure-Disease Paradigm.BioMed research international · 2015Review
- On the road with WRAP53β: guardian of Cajal bodies and genome integrity.Frontiers in genetics · 2015Review
- The scaffold protein WRAP53β orchestrates the ubiquitin response critical for DNA double-strand break repair.Genes & development · 2014Article
- Emerging approaches in predictive toxicology.Environmental and molecular mutagenesis · 2014Article
- Application of toxicogenomic profiling to evaluate effects of benzene and formaldehyde: from yeast to human.Annals of the New York Academy of Sciences · 2014Review
- Hydroquinone: environmental pollution, toxicity, and microbial answers.BioMed research international · 2013Review
- Current understanding of the mechanism of benzene-induced leukemia in humans: implications for risk assessment.Carcinogenesis · 2012Review
- Comparison of proliferation and genomic instability responses to WRN silencing in hematopoietic HL60 and TK6 cells.PloS one · 2011Article
Corrections and comments
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Authors and funding
19 authors at 5 institutions in 3 countries.
Funding
Abstract
Benzene is an established human hematotoxicant and leukemogen but its mechanism of action is unclear. To investigate the role of single-nucleotide polymorphisms (SNPs) on benzene-induced hematotoxicity, we analyzed 1395 SNPs in 411 genes using an Illumina GoldenGate assay in 250 benzene-exposed workers and 140 unexposed controls. Highly significant findings clustered in five genes (BLM, TP53, RAD51, WDR79 and WRN) that play a critical role in DNA repair and genomic maintenance, and these regions were then further investigated with tagSNPs. One or more SNPs in each gene were associated with highly significant 10-20% reductions (P values ranged from 0.0011 to 0.0002) in the white blood cell (WBC) count among benzene-exposed workers but not controls, with evidence for gene-environment interactions for SNPs in BLM, WRN and RAD51. Further, among workers exposed to benzene, the genotype-associated risk of having a WBC count <4000 cells/microl increased when using individuals with progressively higher WBC counts as the comparison group, with some odds ratios >8-fold. In vitro functional studies revealed that deletion of SGS1 in yeast, equivalent to lacking BLM and WRN function in humans, caused reduced cellular growth in the presence of the toxic benzene metabolite hydroquinone, and knockdown of WRN using specific short hairpin RNA increased susceptibility of human TK6 cells to hydroquinone toxicity. Our findings suggest that SNPs involved in DNA repair and genomic maintenance, with particular clustering in the homologous DNA recombination pathway, play an important role in benzene-induced hematotoxicity.
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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.