The DOI matches its Crossref record; 145 of the 145 references it cites were found in a registry or an index.
Telomeres: Cancer to Human Aging
Abstract
The cell phenotypes of senescence and crisis operate to circumscribe the proliferative potential of mammalian cells, suggesting that both are capable of operating in vivo to suppress the formation of tumors. The key regulators of these phenotypes are the telomeres, which are located at the ends of chromosomes and operate to protect the chromosomes from end-to-end fusions. Telomere erosion below a certain length can trigger crisis. The relationship between senescence and telomere function is more complex, however: Cell-physiological stresses as well as dysfunction of the complex molecular structures at the ends of telomeric DNA can trigger senescence. Cells can escape senescence by inactivating the Rb and p53 tumor suppressor proteins and can surmount crisis by activating a telomere maintenance mechanism. The resulting cell immortalization is an essential component of the tumorigenic phenotype of human cancer cells. Here we discuss how telomeres are monitored and maintained and how loss of a functional telomere influences biological functions as diverse as aging and carcinogenesis.
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Cites
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Cited by
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A crucial role for adipose tissue p53 in the regulation of insulin resistance
Minamino, T., Orimo, M., Shimizu, I., Kunieda, T., Yokoyama, M., Ito, T., Nojima, A., Nabetani, A., Oike, Y., Matsubara, H., et al. (2009) · Nature Medicine · doi:10.1038/nm.2014 · Cited by 891
Comprehensive Pan-Genomic Characterization of Adrenocortical Carcinoma
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Systematic analysis of telomere length and somatic alterations in 31 cancer types
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Metadata
- Authors
- Stewart, S. A., & Weinberg, R. A.
- Venue
- Annual Review of Cell and Developmental Biology
- Publisher
- Annual Reviews
- Published
- 2006-11-01
- Volume
- 22
- Issue
- 1
- Pages
- 531-557
- ISSN
- 1081-0706 (ISSN-L)
- 1530-8995
- OpenAlex
- W2080370285
- Cited by
- 334
- References
- 145
- FWCI
- 3.30
- Type
- journal article
- Language
- en
- Open access
- closed
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