Making Young Tumors Old: A New Weapon Against Cancer?
Abstract
As the population of industrial nations ages, the incidence of cancer and cancer mortality is increasing. Intuitively, older organisms may be less able to cope with accumulated damage and thus be more prone to develop cancer. However, so far, the links between aging and cancer have been only partially explored. Strikingly, four recent studies now indicate that premature senescence accompanied by cell cycle arrest occurs in tumors initiated by an oncogenic mutation. Thus, senescence may act as a key tumor suppressor mechanism in young tumors in vivo.
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RB-E2F activity and chromatin-regulating complexes such as SUV39H1 are key regulators of senescence in cultured cells.
“strong evidence places RB–E2F activity and associated chromatin-regulating complexes, such as SUV39H1, as a key regulators of senescence in cells in culture121–124.”
From Cellular mechanisms of tumour suppression by the retinoblastoma gene (2008) · cites this paper as [121]
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CONSTITUTIVE AND SOMATIC GENETIC EVENTS IN RETINOMA AND RETINOBLASTOMA
Sampieri, K. (2008)
- Authors
- Sage, J.
- Affiliations
- Stanford Medicine (US)
- Corresponding author
- Sage, Julien
- ORCID
- Sage, Julien
- Venue
- Science of Aging Knowledge Environment
- Published
- 2005-08-17
- Volume
- 2005
- Issue
- 33
- Pages
- pe25-pe25
- ISSN
- 1539-6150 (ISSN-L)
- OpenAlex
- W1970110843
- Cited by
- 9
- References
- 25
- Citations by year
- 2016: 1 · 2015: 1 · 2013: 2
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science of Aging Knowledge Environment (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- cellular senescence, premature senescence, tumor suppression, cell cycle arrest, oncogenic mutations, cancer incidence, aging, cancer mortality
- MeSH terms
- Animals, Genetic Markers, Humans, Lymphoma, Male, Models, Biological, Neoplasms, Nevus, Oncogenes, Precancerous Conditions, Prostatic Neoplasms, Skin Neoplasms, Tumor Suppressor Protein p53, Cellular Senescence, Disease Progression, Mice
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