| Local regulation of homeostasis favors chromosomal instability. | |
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MedLine Citation:
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PMID: 12676089 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Tissues of long-lived multicellular organisms have to maintain a constant number of functioning cells for many years. This process is called homeostasis. Homeostasis breaks down when cells emerge with mutations in tumor suppressor genes or oncogenes. Such mutated cells can have increased net rates of proliferation, which is increased somatic fitness. We show that the best protection against such mutations is achieved when homeostasis is regulated locally via small compartments. Small compartments, on the other hand, allow the accumulation of cells with reduced somatic fitness. Cells with mutations conferring genetic instability normally have a reduced somatic fitness because they have an increased probability of producing deleterious mutations or triggering apoptosis. Thus, small compartments protect against mutations in tumor suppressor genes or oncogenes but promote the emergence of genetic instability. |
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Authors:
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Franziska Michor; Yoh Iwasa; Natalia L Komarova; Martin A Nowak |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Current biology : CB Volume: 13 ISSN: 0960-9822 ISO Abbreviation: Curr. Biol. Publication Date: 2003 Apr |
Date Detail:
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Created Date: 2003-04-04 Completed Date: 2003-12-02 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 9107782 Medline TA: Curr Biol Country: England |
Other Details:
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Languages: eng Pagination: 581-4 Citation Subset: IM |
Affiliation:
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Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, MA 02138, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Cell Transformation, Neoplastic
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genetics Chromosome Disorders / genetics* Genes, Tumor Suppressor / physiology* Homeostasis / genetics*, physiology* Humans Loss of Heterozygosity / genetics Models, Genetic Models, Theoretical Mutation / genetics*, physiology Oncogenes / genetics, physiology* |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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