Systemic DNA damage responses in aging and diseases
Open accessAbstract
The genome is constantly attacked by a variety of genotoxic insults. The causal role for DNA damage in aging and cancer is exemplified by genetic defects in DNA repair that underlie a broad spectrum of acute and chronic human disorders that are characterized by developmental abnormalities, premature aging, and cancer predisposition. The disease symptoms are typically tissue-specific with uncertain genotype-phenotype correlation. The cellular DNA damage response (DDR) has been extensively investigated ever since yeast geneticists discovered DNA damage checkpoint mechanisms, several decades ago. In recent years, it has become apparent that not only cell-autonomous but also systemic DNA damage responses determine the outcome of genome instability in organisms. Understanding the mechanisms of non-cell-autonomous DNA damage responses will provide important new insights into the role of genome instability in human aging and a host of diseases including cancer and might better explain the complex phenotypes caused by genome instability.
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Half of all human tumors are estimated to carry a mutation in the TP53 gene.
“It is estimated that half of all human tumors carry a mutation in the TP53 gene [62].”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [62]
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“It is estimated that half of all human tumors carry a mutation in the TP53 gene [62].”
BackgroundDNA Damage Response and Autophagy: A Meaningful Partnership
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- Authors
- Ribezzo, F., Shiloh, Y., & Schumacher, B.
- Affiliations
- University of Cologne (DE)
- Tel Aviv University (IL)
- Corresponding author
- Schumacher, Björn
- Venue
- Seminars in Cancer Biology
- Publisher
- Elsevier BV
- Published
- 2016-06
- Volume
- 37-38
- Pages
- 26-35
- ISSN
- 1044-579X (ISSN-L)
- PMC
- PMC4886830
- OpenAlex
- W2227508297
- Cited by
- 116
- References
- 147
- Citations by year
- 2026: 4 · 2025: 10 · 2024: 5 · 2023: 11 · 2022: 13 · 2021: 11 · 2020: 15 · 2019: 8 · 2018: 14 · 2017: 14 · 2016: 11
- FWCI
- 1.42
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Seminars in Cancer Biology (publishedVersion)
- PubMed (publishedVersion)
- Kölner Universitäts PublikationsServer (Universität zu Köln) (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- European Research Council (260383)
- Marie Curie (316354, 316390, 316964)
- German-Israeli Foundation for Scientific Research and Development (GIF 1104-68.11/2010)
- Deutsche Krebshilfe (109453)
- Bundesministerium für Forschung und Bildung (FKZ0315893A-B)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Keywords
- DNA damage response, aging, genomic instability, DNA repair deficiency, premature aging, cancer susceptibility, genotoxicity, DNA damage checkpoint, cancer
- MeSH terms
- Aging, Animals, DNA Damage, DNA Repair, Humans, Immunity, Innate, Mutation, Neoplasms, Cellular Senescence, Genomic Instability, DNA Breaks, Double-Stranded, Genetic Association Studies
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