ArticleNucleic acids research2002
Mutational fingerprints of aging.
Article in Nucleic acids research, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 89 citations in OpenAlex.
- Review
- The functional mutational landscape of theiScience · 2023Article
- From DNA damage to mutations: All roads lead to aging.Ageing research reviews · 2021Review
- Stem Cell DNA Damage and Genome Mutation in the Context of Aging and Cancer Initiation.Cold Spring Harbor perspectives in biology · 2020Review
- Chemically induced mutations in a MutaMouse reporter gene inform mechanisms underlying human cancer mutational signatures.Communications biology · 2020Article
- Single-cell analysis reveals different age-related somatic mutation profiles between stem and differentiated cells in human liver.Science advances · 2020Article
- Protein synthesis and quality control in aging.Aging · 2018Review
- Somatic Mutagenesis in Mammals and Its Implications for Human Disease and Aging.Annual review of genetics · 2018Review
- Genomic variations in the counterpart normal controls of lung squamous cell carcinomas.Frontiers of medicine · 2018Article
- Aging and neurodegeneration are associated with increased mutations in single human neurons.Science (New York, N.Y.) · 2018Article
- Article
- Genome instability: a conserved mechanism of ageing?Essays in biochemistry · 2017Review
- A high-fidelity method for genomic sequencing of single somatic cells reveals a very high mutational burden.Experimental biology and medicine (Maywood, N.J.) · 2017Review
- Accumulation of DNA damage in the aged hematopoietic stem cell compartment.Seminars in hematology · 2017Review
- Article
- Somatic Variants in the Human Lens Epithelium: A Preliminary Assessment.Investigative ophthalmology & visual science · 2016Article
- Using measures of single-cell physiology and physiological state to understand organismic aging.Aging cell · 2016Review
- Breast Cancer beyond the Age of Mutation.Gerontology · 2016Article
- Age-related somatic mutations in the cancer genome.Oncotarget · 2015Article
- Alterations in the mutagenicity and mutation spectrum induced by benzo[a]pyrene instilled in the lungs of gpt delta mice of various ages.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Using a lacZ plasmid transgenic mouse model, spectra of spontaneous point mutations were determined in brain, heart, liver, spleen and small intestine in young and old mice. While similar at a young age, the mutation spectra among these organs were significantly different in old age. In brain and heart G:C-->A:T transitions at CpG sites were the predominant mutation, suggesting that oxidative damage is not a major mutagenic event in these tissues. Other base changes, especially those affecting A:T base pairs, positively correlated with increasing proliferative activity of the different tissues. A relatively high percentage of base changes at A:T base pairs and compound mutants were found in both spleen and spontaneous lymphoma, suggesting a possible role of the hypermutation process in splenocytes in carcinogenesis. The similar mutant spectra observed at a young age may reflect a common mutation mechanism for all tissues that could be driven by the rapid cell division that takes place during development. However, the spectra of the young tissues did not resemble that of the most proliferative aged tissue, implying that replicative history per se is not the underlying causal factor of age-related organ-specific differences in mutation spectra. Rather, differences in organ function, possibly in association with replicative history, may explain the divergence in mutation spectra during aging.
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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.