ReviewEnvironmental and molecular mutagenesis2014
Chromatin modifications during repair of environmental exposure-induced DNA damage: a potential mechanism for stable epigenetic alterations.
Review in Environmental and molecular mutagenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 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
29 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Epigenetic alterations induced by genotoxic occupational and environmental human chemical carcinogens: A systematic literature review.Mutation research. Reviews in mutation researchPooled it
- Epigenetic alterations induced by genotoxic occupational and environmental human chemical carcinogens: An update of a systematic literature review.Mutation research. Reviews in mutation researchPooled it
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- Deciphering the potential role of post-translational modifications of histones in gastrointestinal cancers: a proteomics-based review with therapeutic challenges and opportunities.Frontiers in oncology · 2024Review
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- Making sense of the ageing methylome.Nature reviews. Genetics · 2022Review
- CK2 and the Hallmarks of Cancer.Biomedicines · 2022Review
- Novel acetylation-related gene signatures for predicting the prognosis of patients with colorectal cancer.Human cell · 2022Article
- Structural and functional specificity of H3K36 methylation.Epigenetics & chromatin · 2022Review
- Targeting Cell Death Mechanism Specifically in Triple Negative Breast Cancer Cell Lines.International journal of molecular sciences · 2022Article
- Influence of the sperm DNA fragmentation index on the outcome of rescue ICSI and the clinical value of rescue ICSI.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022Article
- Targeted Cancer Therapy Based on Acetylation and Deacetylation of Key Proteins Involved in Double-Strand Break Repair.Cancer management and research · 2022Review
- SIRT1 and gynecological malignancies (Review).Oncology reports · 2021Review
- Histone Modifications and their Role in Colorectal Cancer (Review).Pathology oncology research : POR · 2020Review
- Dietary antioxidants remodel DNA methylation patterns in chronic disease.British journal of pharmacology · 2020Review
- The Role of SIRT1 on DNA Damage Response and Epigenetic Alterations in Cancer.International journal of molecular sciences · 2019Review
- Galactic Cosmic Radiation Induces Persistent Epigenome Alterations Relevant to Human Lung Cancer.Scientific reports · 2018Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
Abstract
Exposures to environmental toxicants and toxins cause epigenetic changes that likely play a role in the development of diseases associated with exposure. The mechanism behind these exposure-induced epigenetic changes is currently unknown. One commonality between most environmental exposures is that they cause DNA damage either directly or through causing an increase in reactive oxygen species, which can damage DNA. Like transcription, DNA damage repair must occur in the context of chromatin requiring both histone modifications and ATP-dependent chromatin remodeling. These chromatin changes aid in DNA damage accessibility and signaling. Several proteins and complexes involved in epigenetic silencing during both development and cancer have been found to be localized to sites of DNA damage. The chromatin-based response to DNA damage is considered a transient event, with chromatin being restored to normal as DNA damage repair is completed. However, in individuals chronically exposed to environmental toxicants or with chronic inflammatory disease, repeated DNA damage-induced chromatin rearrangement may ultimately lead to permanent epigenetic alterations. Understanding the mechanism behind exposure-induced epigenetic changes will allow us to develop strategies to prevent or reverse these changes. This review focuses on epigenetic changes and DNA damage induced by environmental exposures, the chromatin changes that occur around sites of DNA damage, and how these transient chromatin changes may lead to heritable epigenetic alterations at sites of chronic exposure.
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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.