The DOI matches its Crossref record; 95 of the 96 references it cites were found in a registry or an index.
The age of cancer
Abstract
A striking link exists between advanced age and increased incidence of cancer. Here I review how several of the age-related molecular and physiological changes might act in concert to promote cancer, and in particular epithelial carcinogenesis. Experimental data indicate that the aged, cancer-prone phenotype might represent the combined pathogenetic effects of mutation load, epigenetic regulation, telomere dysfunction and altered stromal milieu. Further verification of the role of these effects should in turn lead to the design of effective therapeutics for the treatment and prevention of cancer in the aged.
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In the citing paper
“Both processes would function to impede the accumulation of a greater number of somatic mutations thought to be required for the development of epithelial cancers (50, 51).”
From Ink4a / Arf tumor suppressor does not modulate the degenerative conditions or tumor spectrum of the telomerase-deficient mouse (2007) · cites this paper as [51]
In the citing paper
“Age is a significant risk factor for the development of cancer.”
From Stromal senescence establishes an immunosuppressive microenvironment that drives tumorigenesis (2016) · cites this paper as [1]
Citations
Cites
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Telomeres shorten during ageing of human fibroblasts
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Research works printed but not linked: 1
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Genome maintenance mechanisms for preventing cancer
Hoeijmakers, J. H. J. (2001) · Nature · doi:10.1038/35077232 · Cited by 3,939
Proliferation, cell cycle and apoptosis in cancer
Evan, G. I., & Vousden, K. H. (2001) · Nature · doi:10.1038/35077213 · Cited by 3,417
Broken Limits to Life Expectancy
Oeppen, J., & Vaupel, J. W. (2002) · Science · doi:10.1126/science.1069675 · Cited by 2,819
Krtolica, A., Parrinello, S., Lockett, S., Desprez, P.-Y., & Campisi, J. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.211053698 · Cited by 1,730
The insulin-like growth factor system and cancer
LeRoith, D., & Roberts, C. T. (2003) · Cancer Letters · doi:10.1016/s0304-3835(03)00159-9 · Cited by 1,124
Metadata
- Authors
- DePinho, R. A.
- Affiliations
- Harvard University (US)
- Corresponding author
- DePinho, Ronald A.
- ORCID
- DePinho, Ronald A.
- Venue
- Nature
- Published
- 2000-11
- Volume
- 408
- Issue
- 6809
- Pages
- 248-254
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W1552282019
- Cited by
- 951
- References
- 96
- Citations by year
- 2026: 10 · 2025: 17 · 2024: 28 · 2023: 28 · 2022: 19 · 2021: 34 · 2020: 19 · 2019: 29 · 2018: 29 · 2017: 35 · 2016: 19 · 2015: 38 · 2014: 41 · 2013: 38 · 2012: 36
- FWCI
- 3.79
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › 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
- aging, cancer incidence, epithelial carcinogenesis, mutational burden, epigenetic regulation, telomere dysfunction, tumor microenvironment, cancer prevention
- MeSH terms
- Aging, Animals, Humans, Neoplasms, Incidence, Telomere, Genome, Mice
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