Senescence as a mode of tumor suppression.
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Two independent lines of experimental evidence are presented in support of the hypothesis that senescence is a normal mechanism of tumor suppression, a homeostatic device designed through evolution to limit cell proliferation irreversibly and thereby to protect the organism against cancer. One set of experiments uses normal human foreskin fibroblasts, transfected at early passage with SV40 DNA and subsequently infected with the K-ras virus. If the cells are immortal prior to infection, they become tumorigenic and make large tumors in nude mice, whereas if they are not immortal, though expressing SV40 T-antigen, they make tiny tumors that senesce in the test mouse after as many doublings as similar cells make in culture. This result demonstrates that immortalization is essential for progressive tumor growth in vivo. The second set of experiments demonstrate that normal human mammary epithelial cells can be immortalized by transfection with viral DNA from human papilloma virus 16 or 18, although these viruses have not been associated with breast cancer. The effective immortalization and other premalignant changes induced by human papilloma virus transfection are accompanied by chromosome changes that may contribute to the partially transformed phenotypes. None of the cloned or pooled transfectants have been tumorigenic in the nude mouse assay. Here, too, immortalization is experimentally separable from tumor-forming ability.
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The permanence of senescence arrest supports that senescence evolved partly to suppress cancer.
“The permanence of the senescence growth arrest enforces the idea that the senescence response evolved at least in part to suppress the development of cancer (9).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [9]
The idea that senescence is tumor suppressive was speculative 50 years ago but became more firmly grounded.
“Hence, the idea that the senescence response is tumor suppressive, although still speculative 50 years ago, was more firmly grounded (9).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [9]
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Biliary Epithelial Senescence in Liver Disease: There Will Be SASP
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- Authors
- Sager, R.
- Affiliations
- Dana-Farber Cancer Institute (US)
- Corresponding author
- Sager, R
- Venue
- Environmental Health Perspectives
- Publisher
- American Chemical Society (ACS)
- Published
- 1991-06
- Volume
- 93
- Pages
- 59-62
- ISSN
- 0091-6765 (ISSN-L)
- 1552-9924
- PMC
- PMC1568048
- OpenAlex
- W2070012290
- Cited by
- 213
- References
- 14
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 6 · 2023: 6 · 2022: 13 · 2021: 8 · 2020: 11 · 2019: 8 · 2018: 4 · 2017: 3 · 2016: 3 · 2015: 4 · 2014: 10 · 2013: 5 · 2012: 6
- FWCI
- 0.50
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- public-domain
- Locations
- Environmental Health Perspectives (publishedVersion, public-domain)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r35ca039814-07)
- National Cancer Institute (CA 39814)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- cellular senescence, tumor suppression, cell immortalization, SV40 T antigen, K-ras oncogene, HPV16, HPV 18, mammary epithelial cells, foreskin fibroblasts, tumorigenicity, chromosomal abnormalities, cancer prevention
- MeSH terms
- Animals, Antigens, Polyomavirus Transforming, Breast, Cell Differentiation, Cell Division, Cell Line, Transformed, Cells, Cultured, DNA-Binding Proteins, Epithelium, Fibroblasts, Genes, Dominant, Humans, Kirsten murine sarcoma virus, Mice, Nude, Neoplasm Transplantation, Neoplasms, Experimental, Oncogene Proteins, Viral, Oncogenes, Genes, ras, Simian virus 40, Transfection, Genes, Tumor Suppressor, Cellular Senescence, Papillomaviridae, Papillomavirus E7 Proteins, Mice
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