| Aging and cancer: the double-edged sword of replicative senescence. | |
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MedLine Citation:
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PMID: 9100719 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Normal cells do not divide indefinitely. This trait, termed the finite replicative life span of cells, limits the capacity for cell division by a process termed cellular or replicative senescence. Replicative senescence is thought to be a tumor suppression mechanism and also a contributor to organismic aging. This article reviews what is known about the genetics and molecular biology of cell senescence. It discusses the evidence that replicative senescence suppresses tumorigenesis, at least in young organisms, and that it also contributes to the aging of mitotic tissues. Finally, it puts forth the somewhat unorthodox view that, in older organisms, senescent cells may actually contribute to carcinogenesis. |
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Authors:
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J Campisi |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.; Review |
Journal Detail:
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Title: Journal of the American Geriatrics Society Volume: 45 ISSN: 0002-8614 ISO Abbreviation: J Am Geriatr Soc Publication Date: 1997 Apr |
Date Detail:
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Created Date: 1997-04-30 Completed Date: 1997-04-30 Revised Date: 2008-03-10 |
Medline Journal Info:
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Nlm Unique ID: 7503062 Medline TA: J Am Geriatr Soc Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 482-8 Citation Subset: IM |
Affiliation:
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Berkeley National Laboratory, University of California 94720, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Aging
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physiology* Cell Aging / physiology* Cell Division / physiology* Genes, Tumor Suppressor / physiology Humans Mitosis Neoplasms / physiopathology* |
| Grant Support | |
ID/Acronym/Agency:
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AG09909/AG/NIA NIH HHS; AG11658/AG/NIA NIH HHS |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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