Download Chromosomal Instability and Aging: Basic Science and by Fuki Hisama, Sherman M. Weissman, George M. Martin PDF

By Fuki Hisama, Sherman M. Weissman, George M. Martin

This article examines the connection among DNA harm and service, mobile senescence, genomic instability and ageing. It contains in-depth discussions of assorted sorts of DNA harm, the DNA fix community, and mobile responses to genetic harm to evaluate their influence at the modulation of ageing procedures and age-related ailment, together with melanoma improvement.

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Chromosomal Instability and Aging: Basic Science and Clinical Implications

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Extra info for Chromosomal Instability and Aging: Basic Science and Clinical Implications

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These findings suggest that telomerase may act preferentially on the shortest telomeres. The mechanisms by which dysfunctional telomeres signal cells to undergo cellular senescence or cell death are poorly understood. B. DNA Damage Certain types and/or levels of damage to genomic DNA can cause normal mammalian cells to undergo a senescence arrest. This damage may derive from endogenous or exogenous sources and includes DNA base and sugar modifications as well as single- or double-strand breaks in the DNA (19,20,24).

Some of the phenotypic changes that are characteristic of senescent cells are common to most, if not all, cell types. These changes include an enlarged cell size, an increase in lysosome biogenesis, and a decrease in the rates of protein synthesis and degradation (27,91,92,124). In addition, most senescent cells express a neutral beta-galactosidase, termed the senescence-associated beta-galactosidase (118). The function of this enzyme is unknown, but, because it can be detected by a simple histochemical reaction, it is a useful marker for the senescent phenotype.

Thus, damage, telomeric dysfunction, or errors in mitogenic signaling may cause senescent cells to accumulate, but their influence may become significant and deleterious only later in life when they reach sufficient numbers. Simultaneously, it is well established that mutations, including potentially oncogenic mutations, accumulate with age (174–177). Thus, the probability that senescent cells and cells with oncogenic mutations occur in close proximity very likely also increases with age. When this occurs, senescent cells may create a microenvironment that promotes the proliferation and neoplastic progression of the mutant cells.

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