ReviewFree radical biology & medicine2012
Redox regulation of the epigenetic landscape in cancer: a role for metabolic reprogramming in remodeling the epigenome.
Review in Free radical biology & medicine, 2012. 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
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.
- Evaluation of DNA Methylation Profiles of LINE-1, Alu and Ribosomal DNA Repeats in Human Cell Lines Exposed to Radiofrequency Radiation.International journal of molecular sciences · 2023Article
- Nutriepigenomics in Environmental-Associated Oxidative Stress.Antioxidants (Basel, Switzerland) · 2023Review
- Integrated Multi-Omics Analysis Reveals the Effect of Maternal Gestational Diabetes on Fetal Mouse Hippocampi.Frontiers in cell and developmental biology · 2022Article
- Connections between metabolism and epigenetic modifications in cancer.Medical review (2021) · 2021Review
- Mitochondria signaling to the epigenome: A novel role for an old organelle.Free radical biology & medicine · 2021Review
- The roles of inducible chromatin and transcriptional memory in cellular defense system responses to redox-active pollutants.Free radical biology & medicine · 2021Review
- Redox-related biomarkers in human cardiovascular disease - classical footprints and beyond.Redox biology · 2021Review
- Single Nucleotide Resolution Analysis Reveals Pervasive, Long-Lasting DNA Methylation Changes by Developmental Exposure to a Mitochondrial Toxicant.Cell reports · 2020Article
- Mitochondrial acetyl-CoA reversibly regulates locus-specific histone acetylation and gene expression.Life science alliance · 2019Article
- Modulators of Redox Metabolism in Head and Neck Cancer.Antioxidants & redox signaling · 2018Review
- Mitochondrial nicotinamide adenine dinucleotide reduced (NADH) oxidation links the tricarboxylic acid (TCA) cycle with methionine metabolism and nuclear DNA methylation.PLoS biology · 2018Article
- Abnormal Epigenetic Regulation of Immune System during Aging.Frontiers in immunology · 2018Review
- Excess iron: considerations related to development and early growth.The American journal of clinical nutrition · 2017Review
- ROS homeostasis and metabolism: a critical liaison for cancer therapy.Experimental & molecular medicine · 2016Review
- Renal Carcinogenesis, Tumor Heterogeneity, and Reactive Oxygen Species: Tactics Evolved.Antioxidants & redox signaling · 2016Review
- Oxidative stress signaling to chromatin in health and disease.Epigenomics · 2016Review
- Biological chemistry and functionality of protein sulfenic acids and related thiol modifications.Free radical research · 2016Review
- Redox regulation of genome stability by effects on gene expression, epigenetic pathways and DNA damage/repair.Redox biology · 2015Review
- Metabolic restructuring and cell fate conversion.Cellular and molecular life sciences : CMLS · 2015Review
- Oxidative stress and the unfulfilled promises of antioxidant agents.Ecancermedicalscience · 2015Review
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.
Funding
Abstract
Cancer arises from normal cells that acquire a series of molecular changes; however, the founding events that create the clonogens from which a tumor will arise and progress have been the subject of speculation. Through the efforts of several generations of cancer biologists it has been established that the malignant phenotype is an amalgamation of genetic and metabolic alterations. Numerous theories have suggested that either, or both, of these elements might serve as the impetus for cancer formation. Recently, the epigenetic origins of cancer have been suggested as an additional mechanism giving rise to the malignant phenotype. When the discovery that the enzymes responsible for initiating and perpetuating epigenetic events is linked to metabolism by their cofactors, a new paradigm for the origins of cancer can be created. Here, we summarize the foundation of such a paradigm on the origins of cancer, in which metabolic alterations create an epigenetic progenitor that clonally expands to become cancer. We suggest that metabolic alterations disrupt the production and availability of cofactors such as S-adenosylmethionine, α-ketoglutarate, NAD(+), and acetyl-CoA to modify the epigenotype of cells. We further speculate that redox biology can change epigenetic events through oxidation of enzymes and alterations in metabolic cofactors that affect epigenetic events such as DNA methylation. Combined, these metabolic and redox changes serve as the foundation for altering the epigenotype of normal cells and creating the epigenetic progenitor of cancer.
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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.