Document Detail


Regulation of tissue- and stimulus-specific cell fate decisions by p53 in vivo.
MedLine Citation:
PMID:  20957626     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The tumour suppressor p53 pathway is often inactivated by multiple mechanisms in the genesis of human cancers. Aberrant cellular proliferation, DNA damage, hypoxia, and ribosomal stress cause activation of the p53 tumour suppressor with multiple possible consequences to the cell: cell death, cell cycle arrest, or senescence. These mechanisms ultimately ensure that the cell does not replicate, and are thus potent tumour suppressor mechanisms. An important question that has eluded the field is how p53 makes these cell fate decisions. This review summarizes the current status of knowledge regarding p53-mediated stress and tissue-dependent cell fate decisions in mouse models and human tumours.
Authors:
James G Jackson; Sean M Post; Guillermina Lozano
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Publication Detail:
Type:  Journal Article; Review     Date:  2010-10-18
Journal Detail:
Title:  The Journal of pathology     Volume:  223     ISSN:  1096-9896     ISO Abbreviation:  J. Pathol.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2010-12-02     Completed Date:  2011-02-03     Revised Date:  2014-10-10    
Medline Journal Info:
Nlm Unique ID:  0204634     Medline TA:  J Pathol     Country:  England    
Other Details:
Languages:  eng     Pagination:  127-36     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / genetics
Cell Aging / genetics
Cell Cycle / genetics
Genes, p53
Humans
Mice
Neoplasms / genetics*,  pathology
Neoplasms, Experimental / genetics,  pathology
Radiation Injuries / genetics,  pathology
Tumor Suppressor Protein p53 / physiology*
Grant Support
ID/Acronym/Agency:
P30 CA016672/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Tumor Suppressor Protein p53

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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