Document Detail


Mechanisms by which energy restriction inhibits carcinogenesis.
MedLine Citation:
PMID:  10709676     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cancer that occurs at numerous organ sites, including the colon and breast, is inhibited by energy restriction, and the inhibition is proportional to the degree of restriction imposed. In an effort to identify the mechanism(s) by which energy restriction exerts this effect, a short term model system of experimentally induced mammary carcinogenesis was used. Given that carcinogenesis is known to involve a dysregulation to tissue size homeostasis in which cell proliferation and cell death are in dysequilibrium, we hypothesized that energy restriction exerts its effect by altering one or more aspects of cell cycle regulation. It was observed that energy restriction inhibited cell proliferation and increased cell death due to apoptosis. Thus attention was next focused on aspects of cell cycle regulation that might be affected by energy restriction. It was observed that the amount of p27 protein, one member of the Cip/Kip family of genes that are involved in cell cycle arrest, was increased dose dependently by energy restriction. Based on this and related observations, the hypothesis is advanced that energy restriction inhibits carcinogenesis, at least in part, by delaying cell cycle progression via shifting cell populations into a G(0)/G(1)state. Ongoing work indicates that corticosteroids, which are produced in increased amounts in response to energy restriction, may be involved in mediating this effect.
Authors:
H J Thompson; W Jiang; Z Zhu
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  Advances in experimental medicine and biology     Volume:  470     ISSN:  0065-2598     ISO Abbreviation:  Adv. Exp. Med. Biol.     Publication Date:  1999  
Date Detail:
Created Date:  2000-04-04     Completed Date:  2000-04-04     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0121103     Medline TA:  Adv Exp Med Biol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  77-84     Citation Subset:  IM    
Affiliation:
Center for Nutrition in the Prevention of Disease, AMC Cancer Research Center, Lakewood, Colorado 80214, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Breast Neoplasms / metabolism*,  prevention & control*
Energy Intake*
Energy Metabolism
Humans
Mammary Neoplasms, Experimental / metabolism*,  prevention & control*
Grant Support
ID/Acronym/Agency:
CA 52626/CA/NCI NIH HHS

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


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