Document Detail

Molecular signaling and genetic pathways of senescence: Its role in tumorigenesis and aging.
MedLine Citation:
PMID:  17133363     Owner:  NLM     Status:  MEDLINE    
In response to progressive telomere shortening in successive cell divisions, normal somatic cells enter senescence, during which they cease to proliferate irreversibly and undergo dramatic changes in gene expression. Senescence can also be activated by various types of stressful stimuli, including aberrant oncogenic signaling, oxidative stress, and DNA damage. Because of the limited proliferative capacity imposed by senescence, as well as the ability of senescent cells to influence neighboring non-senescent cells, senescence has been proposed to play an important role in tumorigenesis and to contribute to aging. Considerable effort has been put into elucidating the molecular mechanisms of senescence, including the signals that trigger senescence, the molecular pathways by which cells enter senescence, and evidence that supports its role in tumorigenesis and aging.
Hong Zhang
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Journal of cellular physiology     Volume:  210     ISSN:  0021-9541     ISO Abbreviation:  J. Cell. Physiol.     Publication Date:  2007 Mar 
Date Detail:
Created Date:  2007-01-02     Completed Date:  2007-03-08     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0050222     Medline TA:  J Cell Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  567-74     Citation Subset:  IM    
Copyright Information:
Copyright 2006 Wiley-Liss, Inc.
Department of Cell Biology, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA.
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MeSH Terms
Aging / genetics*,  physiology*
Cell Proliferation
Cell Transformation, Neoplastic / genetics,  pathology*
Cyclin-Dependent Kinase Inhibitor p16 / genetics,  physiology
Cyclin-Dependent Kinase Inhibitor p21 / genetics,  physiology
Retinoblastoma Protein / genetics,  physiology
Signal Transduction / genetics*,  physiology*
Tumor Suppressor Protein p53 / genetics,  physiology
Reg. No./Substance:
0/Cyclin-Dependent Kinase Inhibitor p16; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/Retinoblastoma Protein; 0/Tumor Suppressor Protein p53

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