The Causes and Consequences of Polyploidy in Normal Development and Cancer
Although nearly all mammalian species are diploid, whole-genome duplications occur in select mammalian tissues as part of normal development. Such programmed polyploidization involves changes in the regulatory pathways that normally maintain the diploid state of the mammalian genome. Unscheduled who...
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Veröffentlicht in: | Annual review of cell and developmental biology 2011-01, Vol.27 (1), p.585-610 |
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description | Although nearly all mammalian species are diploid, whole-genome duplications occur in select mammalian tissues as part of normal development. Such programmed polyploidization involves changes in the regulatory pathways that normally maintain the diploid state of the mammalian genome. Unscheduled whole-genome duplications, which lead primarily to tetraploid cells, also take place in a substantial fraction of human tumors and have been proposed to constitute an important step in the development of cancer aneuploidy. The origins of these polyploidization events and their consequences for tumor progression are explored in this review. |
doi_str_mv | 10.1146/annurev-cellbio-092910-154234 |
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Such programmed polyploidization involves changes in the regulatory pathways that normally maintain the diploid state of the mammalian genome. Unscheduled whole-genome duplications, which lead primarily to tetraploid cells, also take place in a substantial fraction of human tumors and have been proposed to constitute an important step in the development of cancer aneuploidy. The origins of these polyploidization events and their consequences for tumor progression are explored in this review.</description><identifier>ISSN: 1081-0706</identifier><identifier>EISSN: 1530-8995</identifier><identifier>DOI: 10.1146/annurev-cellbio-092910-154234</identifier><identifier>PMID: 21801013</identifier><language>eng</language><publisher>United States: Annual Reviews</publisher><subject>Aging - genetics ; Aneuploidy ; Animals ; Cell Cycle - physiology ; Cell Transformation, Neoplastic - genetics ; Diploidy ; DNA Damage ; Genome ; Humans ; Karyotyping ; Morphogenesis - genetics ; Neoplasms - genetics ; Polyploidy ; Stress, Physiological - genetics ; telomere ; tetraploidy ; Tumor Suppressor Protein p53 - genetics ; Tumor Suppressor Protein p53 - metabolism</subject><ispartof>Annual review of cell and developmental biology, 2011-01, Vol.27 (1), p.585-610</ispartof><rights>Copyright © 2011 by Annual Reviews. 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The origins of these polyploidization events and their consequences for tumor progression are explored in this review.</description><subject>Aging - genetics</subject><subject>Aneuploidy</subject><subject>Animals</subject><subject>Cell Cycle - physiology</subject><subject>Cell Transformation, Neoplastic - genetics</subject><subject>Diploidy</subject><subject>DNA Damage</subject><subject>Genome</subject><subject>Humans</subject><subject>Karyotyping</subject><subject>Morphogenesis - genetics</subject><subject>Neoplasms - genetics</subject><subject>Polyploidy</subject><subject>Stress, Physiological - genetics</subject><subject>telomere</subject><subject>tetraploidy</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><issn>1081-0706</issn><issn>1530-8995</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkMtOwzAQRS0EoqXwCygbloZx7Dy8YAHhrQpYlHXkxBMR5MTBJkX9e1ylsGflkXXPHc0h5IzBOWMivVB9Pzpc0xqNqVpLQcaSAWWJiLnYI3OWcKC5lMl-mCFnFDJIZ-TI-w8AkJwnh2QWsxwYMD4nT6t3jAo1evSR6nVU2N7j54h9HT5sE71asxmMbfUmavvo2bpOmegG12js0GH_NUEqxN0xOWiU8Xiyexfk7e52VTzQ5cv9Y3G1pEoI-UV1KiRLGwUZcsGyTECOSZXquuYiixusdc4USq3iHDjEMlzHhYKA1ZWWjeQLcjn11s5677ApB9d2ym1KBuXWUblzVO4clZOjcnIU-NOJH8aqQ_1H_0oJgespsO1RJjS1-O3_ueUHcK1-gg</recordid><startdate>20110101</startdate><enddate>20110101</enddate><creator>Davoli, Teresa</creator><creator>de Lange, Titia</creator><general>Annual Reviews</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>20110101</creationdate><title>The Causes and Consequences of Polyploidy in Normal Development and Cancer</title><author>Davoli, Teresa ; de Lange, Titia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-a449t-d64916fa07e34177408e5b6dcc3472fecd81ae9da280302991034a0d64cbd9f93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Aging - genetics</topic><topic>Aneuploidy</topic><topic>Animals</topic><topic>Cell Cycle - physiology</topic><topic>Cell Transformation, Neoplastic - genetics</topic><topic>Diploidy</topic><topic>DNA Damage</topic><topic>Genome</topic><topic>Humans</topic><topic>Karyotyping</topic><topic>Morphogenesis - genetics</topic><topic>Neoplasms - genetics</topic><topic>Polyploidy</topic><topic>Stress, Physiological - genetics</topic><topic>telomere</topic><topic>tetraploidy</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Davoli, Teresa</creatorcontrib><creatorcontrib>de Lange, Titia</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Annual review of cell and developmental biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Davoli, Teresa</au><au>de Lange, Titia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Causes and Consequences of Polyploidy in Normal Development and Cancer</atitle><jtitle>Annual review of cell and developmental biology</jtitle><addtitle>Annu Rev Cell Dev Biol</addtitle><date>2011-01-01</date><risdate>2011</risdate><volume>27</volume><issue>1</issue><spage>585</spage><epage>610</epage><pages>585-610</pages><issn>1081-0706</issn><eissn>1530-8995</eissn><abstract>Although nearly all mammalian species are diploid, whole-genome duplications occur in select mammalian tissues as part of normal development. 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source | Annual Reviews; MEDLINE |
subjects | Aging - genetics Aneuploidy Animals Cell Cycle - physiology Cell Transformation, Neoplastic - genetics Diploidy DNA Damage Genome Humans Karyotyping Morphogenesis - genetics Neoplasms - genetics Polyploidy Stress, Physiological - genetics telomere tetraploidy Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism |
title | The Causes and Consequences of Polyploidy in Normal Development and Cancer |
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