Mouse models of XRCC1 DNA repair polymorphisms and cancer
DNA damage plays a major role in mutagenesis, carcinogenesis and aging. A gene that is emerging as an essential element in the repair of both damaged bases and single-strand breaks (SSB) is XRCC1. XRCC1 has been shown to have a large number of single-nucleotide polymorphisms (SNPs), several of which...
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| Veröffentlicht in: | Oncogene 2006-03, Vol.25 (11), p.1612-1619 |
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| description | DNA damage plays a major role in mutagenesis, carcinogenesis and aging. A gene that is emerging as an essential element in the repair of both damaged bases and single-strand breaks (SSB) is XRCC1. XRCC1 has been shown to have a large number of single-nucleotide polymorphisms (SNPs), several of which are being increasingly studied in cancer epidemiology investigations, in part because of their relative high frequency in the population. Although association trends with specific cancer types have occasionally been shown in a variety of ethnic backgrounds, there are often conflicting reports that weaken any substantial conclusions. The functional significance of these SNPs is still largely unknown. XRCC1 is an excellent prototype to provide a forum for determining how epidemiological cancer association studies with DNA repair gene polymorphisms can be validated or refuted. The focus is on the utilization of
in silico
data and biochemical studies in cell lines and existing mouse models to help provide a framework for the development of new mutant mouse lines that mimic human polymorphisms. These mouse lines will provide the next generation of mammalian tools for carcinogen exposure studies relevant to human cancer and variations in XRCC1, and provide the basis for investigating groups of genes and polymorphisms in an animal model. |
| doi_str_mv | 10.1038/sj.onc.1209370 |
| format | Article |
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in silico
data and biochemical studies in cell lines and existing mouse models to help provide a framework for the development of new mutant mouse lines that mimic human polymorphisms. These mouse lines will provide the next generation of mammalian tools for carcinogen exposure studies relevant to human cancer and variations in XRCC1, and provide the basis for investigating groups of genes and polymorphisms in an animal model.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1209370</identifier><identifier>PMID: 16550161</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Aging ; Animal models ; Animals ; Apoptosis ; Biological and medical sciences ; Cancer ; Carcinogenesis ; Carcinogens ; Carcinogens - toxicity ; Cell Biology ; Cell physiology ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Deoxyribonucleic acid ; Disease Models, Animal ; DNA ; DNA Damage ; DNA Repair ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - physiology ; Epidemiologic Studies ; Epidemiology ; Fundamental and applied biological sciences. Psychology ; Gene polymorphism ; Human Genetics ; Humans ; Internal Medicine ; Mathematical models ; Medicine ; Medicine & Public Health ; Mice ; Molecular and cellular biology ; Mutagenesis ; Neoplasms - epidemiology ; Neoplasms - genetics ; Neoplasms - physiopathology ; Oncology ; Polymorphism, Single Nucleotide ; review ; Single-nucleotide polymorphism ; Trends ; X-ray Repair Cross Complementing Protein 1 ; XRCC1 protein</subject><ispartof>Oncogene, 2006-03, Vol.25 (11), p.1612-1619</ispartof><rights>Springer Nature Limited 2006</rights><rights>2006 INIST-CNRS</rights><rights>COPYRIGHT 2006 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Mar 13, 2006</rights><rights>Nature Publishing Group 2006.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c541t-90cd9ede84fbb4aa72f14fbdb7d225ab63a1ead3a72d5eb359f3ca662133be873</citedby><cites>FETCH-LOGICAL-c541t-90cd9ede84fbb4aa72f14fbdb7d225ab63a1ead3a72d5eb359f3ca662133be873</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/sj.onc.1209370$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/sj.onc.1209370$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,2725,27922,27923,41486,42555,51317</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17609508$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16550161$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ladiges, W C</creatorcontrib><title>Mouse models of XRCC1 DNA repair polymorphisms and cancer</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>DNA damage plays a major role in mutagenesis, carcinogenesis and aging. A gene that is emerging as an essential element in the repair of both damaged bases and single-strand breaks (SSB) is XRCC1. XRCC1 has been shown to have a large number of single-nucleotide polymorphisms (SNPs), several of which are being increasingly studied in cancer epidemiology investigations, in part because of their relative high frequency in the population. Although association trends with specific cancer types have occasionally been shown in a variety of ethnic backgrounds, there are often conflicting reports that weaken any substantial conclusions. The functional significance of these SNPs is still largely unknown. XRCC1 is an excellent prototype to provide a forum for determining how epidemiological cancer association studies with DNA repair gene polymorphisms can be validated or refuted. The focus is on the utilization of
in silico
data and biochemical studies in cell lines and existing mouse models to help provide a framework for the development of new mutant mouse lines that mimic human polymorphisms. These mouse lines will provide the next generation of mammalian tools for carcinogen exposure studies relevant to human cancer and variations in XRCC1, and provide the basis for investigating groups of genes and polymorphisms in an animal model.</description><subject>Aging</subject><subject>Animal models</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Cancer</subject><subject>Carcinogenesis</subject><subject>Carcinogens</subject><subject>Carcinogens - toxicity</subject><subject>Cell Biology</subject><subject>Cell physiology</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Deoxyribonucleic acid</subject><subject>Disease Models, Animal</subject><subject>DNA</subject><subject>DNA Damage</subject><subject>DNA Repair</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - physiology</subject><subject>Epidemiologic Studies</subject><subject>Epidemiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene polymorphism</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Mathematical models</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Molecular and cellular biology</subject><subject>Mutagenesis</subject><subject>Neoplasms - epidemiology</subject><subject>Neoplasms - genetics</subject><subject>Neoplasms - physiopathology</subject><subject>Oncology</subject><subject>Polymorphism, Single Nucleotide</subject><subject>review</subject><subject>Single-nucleotide polymorphism</subject><subject>Trends</subject><subject>X-ray Repair Cross Complementing Protein 1</subject><subject>XRCC1 protein</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkk2LFDEQhoMo7rh69aY0it56Nh-dpHMcxk9YFUTBW0gnlbWH7qQ3mT7svzfNNIwIi-SQUPXUW1W8Qeg5wVuCWXuVD9sY7JZQrJjED9CGNFLUnKvmIdpgxXGtKKMX6EnOB4yxVJg-RhdEcI6JIBukvsQ5QzVGB0Ouoq9-fd_vSfXu665KMJk-VVMc7saYpt99HnNlgqusCRbSU_TImyHDs_W-RD8_vP-x_1Rff_v4eb-7ri1vyLFW2DoFDtrGd11jjKSelKfrpKOUm04wQ8A4VhKOQ8e48swaIShhrINWskv09qQ7pXg7Qz7qsc8WhsEEKLPrBeQSs_-CREnWYC4K-Pof8BDnFMoSmoqGMM6lagv16l6KFqVW8KXn9gTdmAF0H3w8JmPLcTD2NgbwfYnvSKswb4n8q8CmmHMCr6fUjybdaYL14qjOB10c1aujpeDlOsbcjeDO-GphAd6sgMnWDD4Vd_p85qRYvsGyz9WJyyUVbiCd97m39YtTRTDHOcFZcs3_AdtbwCc</recordid><startdate>20060313</startdate><enddate>20060313</enddate><creator>Ladiges, W C</creator><general>Nature Publishing Group UK</general><general>Nature Publishing</general><general>Nature Publishing Group</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope></search><sort><creationdate>20060313</creationdate><title>Mouse models of XRCC1 DNA repair polymorphisms and cancer</title><author>Ladiges, W C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c541t-90cd9ede84fbb4aa72f14fbdb7d225ab63a1ead3a72d5eb359f3ca662133be873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Aging</topic><topic>Animal models</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Cancer</topic><topic>Carcinogenesis</topic><topic>Carcinogens</topic><topic>Carcinogens - toxicity</topic><topic>Cell Biology</topic><topic>Cell physiology</topic><topic>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</topic><topic>Deoxyribonucleic acid</topic><topic>Disease Models, Animal</topic><topic>DNA</topic><topic>DNA Damage</topic><topic>DNA Repair</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - physiology</topic><topic>Epidemiologic Studies</topic><topic>Epidemiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene polymorphism</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Mathematical models</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mice</topic><topic>Molecular and cellular biology</topic><topic>Mutagenesis</topic><topic>Neoplasms - epidemiology</topic><topic>Neoplasms - genetics</topic><topic>Neoplasms - physiopathology</topic><topic>Oncology</topic><topic>Polymorphism, Single Nucleotide</topic><topic>review</topic><topic>Single-nucleotide polymorphism</topic><topic>Trends</topic><topic>X-ray Repair Cross Complementing Protein 1</topic><topic>XRCC1 protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ladiges, W C</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ladiges, W C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mouse models of XRCC1 DNA repair polymorphisms and cancer</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2006-03-13</date><risdate>2006</risdate><volume>25</volume><issue>11</issue><spage>1612</spage><epage>1619</epage><pages>1612-1619</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>DNA damage plays a major role in mutagenesis, carcinogenesis and aging. A gene that is emerging as an essential element in the repair of both damaged bases and single-strand breaks (SSB) is XRCC1. XRCC1 has been shown to have a large number of single-nucleotide polymorphisms (SNPs), several of which are being increasingly studied in cancer epidemiology investigations, in part because of their relative high frequency in the population. Although association trends with specific cancer types have occasionally been shown in a variety of ethnic backgrounds, there are often conflicting reports that weaken any substantial conclusions. The functional significance of these SNPs is still largely unknown. XRCC1 is an excellent prototype to provide a forum for determining how epidemiological cancer association studies with DNA repair gene polymorphisms can be validated or refuted. The focus is on the utilization of
in silico
data and biochemical studies in cell lines and existing mouse models to help provide a framework for the development of new mutant mouse lines that mimic human polymorphisms. These mouse lines will provide the next generation of mammalian tools for carcinogen exposure studies relevant to human cancer and variations in XRCC1, and provide the basis for investigating groups of genes and polymorphisms in an animal model.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>16550161</pmid><doi>10.1038/sj.onc.1209370</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| language | eng |
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| source | MEDLINE; Nature; EZB-FREE-00999 freely available EZB journals; SpringerLink Journals - AutoHoldings |
| subjects | Aging Animal models Animals Apoptosis Biological and medical sciences Cancer Carcinogenesis Carcinogens Carcinogens - toxicity Cell Biology Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Deoxyribonucleic acid Disease Models, Animal DNA DNA Damage DNA Repair DNA-Binding Proteins - genetics DNA-Binding Proteins - physiology Epidemiologic Studies Epidemiology Fundamental and applied biological sciences. Psychology Gene polymorphism Human Genetics Humans Internal Medicine Mathematical models Medicine Medicine & Public Health Mice Molecular and cellular biology Mutagenesis Neoplasms - epidemiology Neoplasms - genetics Neoplasms - physiopathology Oncology Polymorphism, Single Nucleotide review Single-nucleotide polymorphism Trends X-ray Repair Cross Complementing Protein 1 XRCC1 protein |
| title | Mouse models of XRCC1 DNA repair polymorphisms and cancer |
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