ReviewChemical research in toxicology2008
Genetic and epigenetic mechanisms in metal carcinogenesis and cocarcinogenesis: nickel, arsenic, and chromium.
Review in Chemical research in toxicology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 275 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
275 citing papers in PubMed, 3 syntheses or guidelines pooled it, 907 citations in OpenAlex.
- The preventive and carcinogenic effect of metals on cancer: a systematic review.BMC public health · 2024Pooled it
- Chromium as a Risk Factor for Breast Cancer: A Meta-Analysis.Asian Pacific journal of cancer prevention : APJCP · 2022Pooled it
- An integrative approach for the identification of prognostic and predictive biomarkers in rectal cancer.Oncotarget · 2015Pooled it
- Heavy metal contamination in cosmetic hair dyes, dermal health risk assessment, and in vivo toxicological implications among exposed women in Khartoum, Sudan.Toxicology reports · 2026Article
- Quantum dot sensors for heavy metal detection: from mechanistic design to field deployment: a review.RSC advances · 2026Review
- Identification of Key Indicators in the Adverse Outcome Pathway for Genetic Damage Induced by Chromate Exposure: A Machine Learning-Based Cross-Sectional Study.Environment & health (Washington, D.C.) · 2026Article
- Combined Occupational Exposure to Lead and Other Metals and Risk of Lung Cancer.La Medicina del lavoro · 2026Article
- Arsenic exposure and skin cancer: Mechanisms, clinical evidence and public health implications (Review).International journal of molecular medicine · 2026Review
- Environmental influences on macrophage epigenetics and trained immunity: a review.Molecular biology reports · 2026Review
- AB-Free Kava and Dihydromethysticin Inhibit Chronic Hexavalent Chromium Exposure-Induced Cell Malignant Transformation through Down-Regulating RNA Splicing Factor SNRPA1 Expression.Chemical research in toxicology · 2026Article
- Nickel exposure disrupts epigenetic repression of developmental genes in mouse embryonic stem cells.Toxicology and applied pharmacology · 2026Article
- Diverse stresses differentially regulate rRNA biogenesis and mRNA translation.Nucleic acids research · 2026Article
- Toward Smart Salivary Diagnostics: A Comprehensive Review of Heavy Metal Biomarkers and Digital Risk Modeling.Diagnostics (Basel, Switzerland) · 2026Review
- Metal carcinogens and cancer: integrating genetic and epigenetic perspectives.Frontiers in oncology · 2026Review
- Causal relationship between blood metal levels and breast cancer risk: a Mendelian randomization study in East Asian populations.Discover oncology · 2025Article
- Modification of Oxidative Stress Induced by Exposure to Arsenate in Rat Chondrocytes Treated With Chitosan-Glutathione Nanoparticles.Journal of applied toxicology : JAT · 2025Article
- Metals in the human liver: An underappreciated risk factor of hepatic insulin resistance and associated pathophysiology.Environmental pollution (Barking, Essex : 1987) · 2025Review
- Chronic arsenic exposure and hsa-miR-186 overexpression causes transcriptome-wide differential alternative splicing contributing to skin carcinogenesis in human HaCaT cell line.Archives of toxicology · 2025Article
- Health risk assessment of PAHs and heavy metal levels in periwinkles (Pachymelania fusca mutans) and crabs (Scylla serrata) consumed in crude oil-contaminated coastal regions of Southern Nigeria.Toxicology reports · 2025Article
- Nuclear SUMOylation and Proteotoxic Stress Responses to Metals with Different Ligand Preferences.Chemical research in toxicology · 2025Article
215 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Chronic exposure to nickel(II), chromium(VI), or inorganic arsenic (iAs) has long been known to increase cancer incidence among affected individuals. Recent epidemiological studies have found that carcinogenic risks associated with chromate and iAs exposures were substantially higher than previously thought, which led to major revisions of the federal standards regulating ambient and drinking water levels. Genotoxic effects of Cr(VI) and iAs are strongly influenced by their intracellular metabolism, which creates several reactive intermediates and byproducts. Toxic metals are capable of potent and surprisingly selective activation of stress-signaling pathways, which are known to contribute to the development of human cancers. Depending on the metal, ascorbate (vitamin C) has been found to act either as a strong enhancer or suppressor of toxic responses in human cells. In addition to genetic damage via both oxidative and nonoxidative (DNA adducts) mechanisms, metals can also cause significant changes in DNA methylation and histone modifications, leading to epigenetic silencing or reactivation of gene expression. In vitro genotoxicity experiments and recent animal carcinogenicity studies provided strong support for the idea that metals can act as cocarcinogens in combination with nonmetal carcinogens. Cocarcinogenic and comutagenic effects of metals are likely to stem from their ability to interfere with DNA repair processes. Overall, metal carcinogenesis appears to require the formation of specific metal complexes, chromosomal damage, and activation of signal transduction pathways promoting survival and expansion of genetically/epigenetically altered cells.
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What OpenQuestion holds
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.