ArticleMolecular and cellular biology1995
Carcinogenic nickel silences gene expression by chromatin condensation and DNA methylation: a new model for epigenetic carcinogens.
Article in Molecular and cellular biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 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
103 citing papers in PubMed, 3 syntheses or guidelines pooled it, 365 citations in OpenAlex.
- Association between Retinoic acid receptor-β hypermethylation and NSCLC risk: a meta-analysis and literature review.Oncotarget · 2017Pooled it
- Environmental Metals and Cardiovascular Disease in Adults: A Systematic Review Beyond Lead and Cadmium.Current environmental health reports · 2016Pooled it
- Clinicopathological significance and a potential drugtarget of RARβ in non-small-cell lung carcinoma: a meta-analysis and a systematic review.Drug design, development and therapy · 2016Pooled it
- Gene expression profiles in peripheral blood mononuclear cells of Chinese nickel refinery workers with high exposures to nickel and control subjects.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2013Trial
- Atmospheric Particulate Matter as a Carrier of Pb, Cd, and Ni: From Environmental Transfer and Bioaccessibility to Molecular Toxicity and Predictive Modeling.Journal of xenobiotics · 2026Review
- Skin Whitening Creams: Cosmetovigilance.Current pharmaceutical biotechnology · 2026Review
- Article
- Missing Causality and Heritability of Autoimmune Hepatitis.Digestive diseases and sciences · 2023Article
- Review
- The Roles of Histone Post-Translational Modifications in the Formation and Function of a Mitotic Chromosome.International journal of molecular sciences · 2022Review
- Plasma Nickel Levels Correlate with Low Muscular Strength and Renal Function Parameters in Patients with Prostate Cancer.Diseases (Basel, Switzerland) · 2022Article
- Relationships of multiple metals exposure, global DNA methylation, and urothelial carcinoma in central Taiwan.Archives of toxicology · 2022Article
- A comprehensive review on the sources, essentiality and toxicological profile of nickel.RSC advances · 2022Review
- Epithelial-mesenchymal transition: Insights into nickel-induced lung diseases.Seminars in cancer biology · 2021Review
- Integration of Epigenetic Mechanisms into Non-Genotoxic Carcinogenicity Hazard Assessment: Focus on DNA Methylation and Histone Modifications.International journal of molecular sciences · 2021Review
- Update of the risk assessment of nickel in food and drinking water.EFSA journal. European Food Safety Authority · 2020Article
- Metals and molecular carcinogenesis.Carcinogenesis · 2020Review
- Nickel-induced transcriptional changes persist post exposure through epigenetic reprogramming.Epigenetics & chromatin · 2019Article
- Article
- Epidemiology of Pancreatic Cancer: Global Trends, Etiology and Risk Factors.World journal of oncology · 2019Review
43 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
9 authors at 1 institution in 1 country.
Funding
Abstract
A transgenic gpt+ Chinese hamster cell line (G12) was found to be susceptible to carcinogenic nickel-induced inactivation of gpt expression without mutagenesis or deletion of the transgene. Many nickel-induced 6-thioguanine-resistant variants spontaneously reverted to actively express gpt, as indicated by both reversion assays and direct enzyme measurements. Since reversion was enhanced in many of the nickel-induced variant cell lines following 24-h treatment with the demethylating agent 5-azacytidine, the involvement of DNA methylation in silencing gpt expression was suspected. This was confirmed by demonstrations of increased DNA methylation, as well as by evidence indicating condensed chromatin and heterochromatinization of the gpt integration site in 6-thioguanine-resistant cells. Upon reversion to active gpt expression, DNA methylation and condensation are lost. We propose that DNA condensation and methylation result in heterochromatinization of the gpt sequence with subsequent inheritance of the now silenced gene. This mechanism is supported by direct evidence showing that acute nickel treatment of cultured cells, and of isolated nuclei in vitro, can indeed facilitate gpt sequence-specific chromatin condensation. Epigenetic mechanisms have been implicated in the actions of some nonmutagenic carcinogens, and DNA methylation changes are now known to be important in carcinogenesis. This paper further supports the emerging theory that nickel is a human carcinogen that can alter gene expression by enhanced DNA methylation and compaction, rather than by mutagenic mechanisms.
Indexed as
Identifiers
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.