Baird, Duncan ![]() |
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Abstract
Telomere function is critical for genomic stability; in the context of a functional TP53 response, telomere erosion leads to a G1/S cell-cycle arrest and the induction of replicative senescence, a process that is considered to underpin the ageing process in long-lived species. Abrogation of the TP53 pathway allows for continued cell division, telomere erosion, and the complete loss of telomere function; the ensuing genomic instability facilitates clonal evolution and malignant progression. Telomeres display extensive length heterogeneity in the population that is established at birth, and this affects the individual risk of a broad range of diseases, including cardiovascular disease and cancer. In this perspective, I discuss telomere length heterogeneity at the levels of the population, individual, and cell, and consider how the dynamics of these essential chromosomal structures contribute to human disease.
Item Type: | Article |
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Date Type: | Published Online |
Status: | In Press |
Schools: | Schools > Medicine |
Publisher: | Cold Spring Harbor Laboratory Press |
ISSN: | 1943-0264 |
Date of First Compliant Deposit: | 22 October 2024 |
Date of Acceptance: | 16 October 2024 |
Last Modified: | 08 Jan 2025 12:15 |
URI: | https://orca.cardiff.ac.uk/id/eprint/173240 |
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