ArticleCancer research2018
Hexavalent Chromium-Induced Chromosome Instability Drives Permanent and Heritable Numerical and Structural Changes and a DNA Repair-Deficient Phenotype.
Article in Cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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.
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
29 citing papers in PubMed, 66 citations in OpenAlex.
- Remediating effects of coral fossils on hematobiochemical, histo accumulation and organ histomorphological changes in Chromium intoxicated broilers.Poultry science · 2026Article
- Particulate Hexavalent Chromium Inhibits RAD51 Paralogs Necessary for RAD51 Filament Formation and Stabilization During Homologous Recombination Repair.Occupational Health · 2026Article
- It's a gator tale: Alligator lung cells resist hexavalent chromium-induced DNA repair inhibition and chromosome instability.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2026Article
- Pollutant-regulated mitophagy: new perspectives in environmental toxicology.Apoptosis : an international journal on programmed cell death · 2026Review
- Arylamine N-Acetyltransferase 1 Knockout in Immortalized Human Bronchial Cells Results in a Reduction of Cellular Growth.Gene reports · 2025Article
- Article
- PLK1-mediated PDHA1 phosphorylation drives mitochondrial dysfunction, mitophagy, and cancer progression in Cr(VI)-associated lung cancer.The Journal of biological chemistry · 2025Article
- Particulate hexavalent chromium inhibits global transcription of genes in DNA repair pathways, particularly targeting homologous recombination repair, base excision repair, mismatch repair and microhomology-mediated end-joining.Journal of hazardous materials · 2025Article
- Particulate hexavalent chromium exposure induces DNA double-strand breaks and inhibits homologous recombination repair in rat and human lung tissues.Chemosphere · 2025Article
- Prolonged Particulate Hexavalent Chromium Exposure Induces DNA Double-Strand Breaks and Inhibits Homologous Recombination Repair in Primary Rodent Lung Cells.Biological trace element research · 2024Article
- Carcinogenic Mechanisms of Hexavalent Chromium: From DNA Breaks to Chromosome Instability and Neoplastic Transformation.Current environmental health reports · 2024Review
- Chromate Affects Gene Expression and DNA Methylation in Long-Term In Vitro Experiments in A549 Cells.International journal of molecular sciences · 2024Article
- Acute particulate hexavalent chromium exposure induces DNA double-strand breaks and activates homologous recombination repair in rat lung tissue.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- A whale of a tale: whale cells evade the driving mechanism for hexavalent chromium-induced chromosome instability.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Hexavalent Chromium Targets Securin to Drive Numerical Chromosome Instability in Human Lung Cells.International journal of molecular sciences · 2023Article
- Prolonged particulate hexavalent chromium exposure induces RAD51 foci inhibition and cytoplasmic accumulation in immortalized and primary human lung bronchial epithelial cells.Toxicology and applied pharmacology · 2023Article
- miR-186 induces tetraploidy in arsenic exposed human keratinocytes.Ecotoxicology and environmental safety · 2023Article
- Exposure to Heavy Metals and Serum Adiponectin Levels among Workers: A 2-Year Follow-Up Study.Metabolites · 2023Article
- HBM4EU Chromates Study-Genotoxicity and Oxidative Stress Biomarkers in Workers Exposed to Hexavalent Chromium.Toxics · 2022Article
- Impact of Nano- and Micro-Sized Chromium(III) Particles on Cytotoxicity and Gene Expression Profiles Related to Genomic Stability in Human Keratinocytes and Alveolar Epithelial Cells.Nanomaterials (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
A key hypothesis for how hexavalent chromium [Cr(VI)] causes cancer is that it drives chromosome instability (CIN), which leads to neoplastic transformation. Studies show chronic Cr(VI) can affect DNA repair and induce centrosome amplification, which can lead to structural and numerical CIN. However, no studies have considered whether these outcomes are transient or permanent. In this study, we exposed human lung cells to particulate Cr(VI) for three sequential 24-hour periods, each separated by about a month. After each treatment, cells were seeded at colony-forming density, cloned, expanded, and retreated, creating three generations of clonal cell lines. Each generation of clones was tested for chromium sensitivity, chromosome complement, DNA repair capacity, centrosome amplification, and the ability to grow in soft agar. After the first treatment, Cr(VI)-treated clones exhibited a normal chromosome complement, but some clones showed a repair-deficient phenotype and amplified centrosomes. After the second exposure, more than half of the treated clones acquired an abnormal karyotype including numerical and structural alterations, with many exhibiting deficient DNA double-strand break repair and amplified centrosomes. The third treatment produced new abnormal clones, with previously abnormal clones acquiring additional abnormalities and most clones exhibiting repair deficiency. CIN, repair deficiency, and amplified centrosomes were all permanent and heritable phenotypes of repeated Cr(VI) exposure. These outcomes support the hypothesis that CIN is a key mechanism of Cr(VI)-induced carcinogenesis.
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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.