Mice without telomerase: what can they teach us about human cancer?
Abstract
Unicellular organisms, human cells and mice have provided insights into the processes of senescence, crisis, genomic instability and cancer in humans. Here, Artandi and DePinho discuss how studies in mice have uncovered a complex interplay between the ARF-p53 pathway, genomic instability due to telomere dysfunction, and the suppression or promotion of cancer.
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In cells lacking genome checkpoint functions, telomere dysfunction accelerates genomic instability and promotes cancer initiation.
“Thus, in the absence of genome checkpoint functions, telomere dysfunction accelerates genomic instability, facilitating cancer initiation.(4)”
From Understanding and exploiting <i>hTERT</i> promoter regulation for diagnosis and treatment of human cancers (2008) · cites this paper as [4]
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- Authors
- Artandi, S. E., & DePinho, R. A.
- Affiliations
- Dana-Farber Cancer Institute (US)
- Harvard University (US)
- Venue
- Nature Medicine
- Published
- 2000-08
- Volume
- 6
- Issue
- 8
- Pages
- 852-855
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W1594827217
- Cited by
- 126
- References
- 41
- Citations by year
- 2026: 1 · 2022: 2 · 2021: 3 · 2020: 3 · 2019: 1 · 2017: 1 · 2016: 2 · 2015: 1 · 2014: 4 · 2013: 5 · 2012: 5
- FWCI
- 9.82
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- 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
- telomerase, telomere dysfunction, genomic instability, cellular senescence, ARF-p53 pathway, tumor suppression, tumor promotion, mouse tumor model, human cancer
- MeSH terms
- Animals, Cell Division, Humans, Neoplasms, Species Specificity, Genes, p53, Telomere, Cellular Senescence, Mice, Knockout, Telomerase, Mice
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