Abstract
Historically, the senescent state has been associated with, and was named after, the cell-cycle arrest that occurs after cells have undergone an intrinsically defined number of divisions in vitro. More recently, however, it has been shown that extrinsic factors, including those encountered in normal tissue-culture environments, can prematurely induce an indistinguishable senescent phenotype. In this review, we discuss the pathways of cell senescence, the mechanisms involved and the role that these pathways have in regulating the initiation and progression of cancer.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Antineoplastic Agents / pharmacology
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Antineoplastic Agents / therapeutic use
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Cell Transformation, Neoplastic / genetics
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Cellular Senescence / physiology*
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DNA Damage
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DNA Replication
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Enzyme Inhibitors / pharmacology
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Enzyme Inhibitors / therapeutic use
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Fibroblasts / cytology
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Humans
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Mice
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Mice, Knockout
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Models, Genetic
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Neoplasm Proteins / physiology
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Neoplasms / drug therapy
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Neoplasms / enzymology
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Neoplasms / genetics
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Neoplasms / pathology*
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Phenotype
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RNA / genetics
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Telomerase / deficiency
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Telomerase / genetics
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Telomerase / physiology
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Telomere / ultrastructure
Substances
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Antineoplastic Agents
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Enzyme Inhibitors
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Neoplasm Proteins
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telomerase RNA
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RNA
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Telomerase