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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“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]
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“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]
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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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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