Non-homologous End-joining Genes are not Inactivated in Human Radiation-induced Sarcomas with Genomic Instability
DNA double-strand break (DSB) repair pathways are implicated in the maintenance of genomic stability. However the alterations of these pathways, as may occur in human tumor cells with strong genomic instability, remain poorly characterized. We analyzed the loss of heterozygosity (LOH) and the presen...
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| Veröffentlicht in: | Journal of radiation research 2005-06, Vol.46 (2), p.223-231 |
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| creator | Lefèvre, Sandrine H. Coquelle, Arnaud Gonin-Laurent, Nathalie Cör, Andrej Vogt, Nicolas Chauveinc, Laurent Anract, Philippe Dutrillaux, Bernard Chevillard, Sylvie Malfoy, Bernard |
| description | DNA double-strand break (DSB) repair pathways are implicated in the maintenance of genomic stability. However the alterations of these pathways, as may occur in human tumor cells with strong genomic instability, remain poorly characterized. We analyzed the loss of heterozygosity (LOH) and the presence of mutations for a series of genes implicated in DSB repair by non-homologous end-joining in five radiation-induced sarcomas devoid of both active Tp53 and Rb1. LOH was recurrently observed for 8 of the 9 studied genes (KU70, KU80, XRCC4, LIG4, Artemis, MRE11, RAD50, NBS1) but not for DNA-PKcs. No mutation was found in the remaining allele of the genes with LOH and the mRNA expression did not correlate with the allelic status. Our findings suggest that non-homologous end-joining repair pathway alteration is unlikely to be involved in the high genomic instability observed in these tumors. |
| doi_str_mv | 10.1269/jrr.46.223 |
| format | Article |
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However the alterations of these pathways, as may occur in human tumor cells with strong genomic instability, remain poorly characterized. We analyzed the loss of heterozygosity (LOH) and the presence of mutations for a series of genes implicated in DSB repair by non-homologous end-joining in five radiation-induced sarcomas devoid of both active Tp53 and Rb1. LOH was recurrently observed for 8 of the 9 studied genes (KU70, KU80, XRCC4, LIG4, Artemis, MRE11, RAD50, NBS1) but not for DNA-PKcs. No mutation was found in the remaining allele of the genes with LOH and the mRNA expression did not correlate with the allelic status. Our findings suggest that non-homologous end-joining repair pathway alteration is unlikely to be involved in the high genomic instability observed in these tumors.</description><identifier>ISSN: 0449-3060</identifier><identifier>EISSN: 1349-9157</identifier><identifier>DOI: 10.1269/jrr.46.223</identifier><identifier>PMID: 15988141</identifier><language>eng</language><publisher>England: The Japan Radiation Research Society and Japanese Society for Therapeutic Radiology and Oncology</publisher><subject>DNA Damage - genetics ; DNA Mutational Analysis - methods ; Gene Expression Regulation, Neoplastic - genetics ; Gene Expression Regulation, Neoplastic - radiation effects ; Gene mutations ; Gene Silencing - radiation effects ; Genetic aspects ; Genetic Variation - genetics ; Genomic Instability - genetics ; Genomic Instability - radiation effects ; Humans ; Ionizing radiation ; Neoplasms, Radiation-Induced - genetics ; Physiological aspects ; Risk factors ; Sarcoma ; Sarcoma - genetics ; Tumor Cells, Cultured</subject><ispartof>Journal of radiation research, 2005-06, Vol.46 (2), p.223-231</ispartof><rights>Copyright © 2005 Japan Radiation Research Society 2005</rights><rights>COPYRIGHT 2005 Oxford University Press</rights><rights>Copyright Japan Science and Technology Agency 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c567t-231aef9e555f88cd0b9588ffc84f99ed8ec55458f8ca9e1ad7d2584d462c6c353</citedby><cites>FETCH-LOGICAL-c567t-231aef9e555f88cd0b9588ffc84f99ed8ec55458f8ca9e1ad7d2584d462c6c353</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,860,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15988141$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lefèvre, Sandrine H.</creatorcontrib><creatorcontrib>Coquelle, Arnaud</creatorcontrib><creatorcontrib>Gonin-Laurent, Nathalie</creatorcontrib><creatorcontrib>Cör, Andrej</creatorcontrib><creatorcontrib>Vogt, Nicolas</creatorcontrib><creatorcontrib>Chauveinc, Laurent</creatorcontrib><creatorcontrib>Anract, Philippe</creatorcontrib><creatorcontrib>Dutrillaux, Bernard</creatorcontrib><creatorcontrib>Chevillard, Sylvie</creatorcontrib><creatorcontrib>Malfoy, Bernard</creatorcontrib><title>Non-homologous End-joining Genes are not Inactivated in Human Radiation-induced Sarcomas with Genomic Instability</title><title>Journal of radiation research</title><addtitle>J Radiat Res</addtitle><description>DNA double-strand break (DSB) repair pathways are implicated in the maintenance of genomic stability. However the alterations of these pathways, as may occur in human tumor cells with strong genomic instability, remain poorly characterized. We analyzed the loss of heterozygosity (LOH) and the presence of mutations for a series of genes implicated in DSB repair by non-homologous end-joining in five radiation-induced sarcomas devoid of both active Tp53 and Rb1. LOH was recurrently observed for 8 of the 9 studied genes (KU70, KU80, XRCC4, LIG4, Artemis, MRE11, RAD50, NBS1) but not for DNA-PKcs. No mutation was found in the remaining allele of the genes with LOH and the mRNA expression did not correlate with the allelic status. Our findings suggest that non-homologous end-joining repair pathway alteration is unlikely to be involved in the high genomic instability observed in these tumors.</description><subject>DNA Damage - genetics</subject><subject>DNA Mutational Analysis - methods</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Gene Expression Regulation, Neoplastic - radiation effects</subject><subject>Gene mutations</subject><subject>Gene Silencing - radiation effects</subject><subject>Genetic aspects</subject><subject>Genetic Variation - genetics</subject><subject>Genomic Instability - genetics</subject><subject>Genomic Instability - radiation effects</subject><subject>Humans</subject><subject>Ionizing radiation</subject><subject>Neoplasms, Radiation-Induced - genetics</subject><subject>Physiological aspects</subject><subject>Risk factors</subject><subject>Sarcoma</subject><subject>Sarcoma - genetics</subject><subject>Tumor Cells, Cultured</subject><issn>0449-3060</issn><issn>1349-9157</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kV9rHCEUxaW0NJu0L_0AZaA0D4XZ6ow6-hhCmgRCAv3zLK5eNy4zulEnJd--bnchtJTig3L9ncO99yD0juAl6bj8vElpSfmy6_oXaEF6KltJ2PASLTCt7x5zfISOc95g3A2Y4dfoiDApBKFkgR5uY2jv4xTHuI5zbi6CbTfRBx_WzSUEyI1O0IRYmuugTfGPuoBtfGiu5kmH5qu2XhdfPXyws6lf33QycdK5-enL_c4iTt5UcS565Udfnt6gV06PGd4e7hP048vF9_Or9ubu8vr87KY1jA-l7XqiwUlgjDkhjMUryYRwzgjqpAQrwDBGmXDCaAlE28F2TFBLeWe46Vl_gk73vtsUH2bIRU0-GxhHHaBOqsjAOeO_wQ9_gZs4p1B7U4TWDfaDYPKZWusRlA8ulqTNzlKdsZ4TRqkYKrX8B1WPhbqGGMD5Wv9D8GkvMCnmnMCpbfKTTk-KYLVLV9V0FeWqplvh94dO59UE9hk9xFmBj3sgztv_Gf0CzE6rkA</recordid><startdate>20050601</startdate><enddate>20050601</enddate><creator>Lefèvre, Sandrine H.</creator><creator>Coquelle, Arnaud</creator><creator>Gonin-Laurent, Nathalie</creator><creator>Cör, Andrej</creator><creator>Vogt, Nicolas</creator><creator>Chauveinc, Laurent</creator><creator>Anract, Philippe</creator><creator>Dutrillaux, Bernard</creator><creator>Chevillard, Sylvie</creator><creator>Malfoy, Bernard</creator><general>The Japan Radiation Research Society and Japanese Society for Therapeutic Radiology and Oncology</general><general>Oxford University Press</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><scope>K9.</scope><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>20050601</creationdate><title>Non-homologous End-joining Genes are not Inactivated in Human Radiation-induced Sarcomas with Genomic Instability</title><author>Lefèvre, Sandrine H. ; Coquelle, Arnaud ; Gonin-Laurent, Nathalie ; Cör, Andrej ; Vogt, Nicolas ; Chauveinc, Laurent ; Anract, Philippe ; Dutrillaux, Bernard ; Chevillard, Sylvie ; Malfoy, Bernard</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c567t-231aef9e555f88cd0b9588ffc84f99ed8ec55458f8ca9e1ad7d2584d462c6c353</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>DNA Damage - genetics</topic><topic>DNA Mutational Analysis - methods</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Gene Expression Regulation, Neoplastic - radiation effects</topic><topic>Gene mutations</topic><topic>Gene Silencing - radiation effects</topic><topic>Genetic aspects</topic><topic>Genetic Variation - genetics</topic><topic>Genomic Instability - genetics</topic><topic>Genomic Instability - radiation effects</topic><topic>Humans</topic><topic>Ionizing radiation</topic><topic>Neoplasms, Radiation-Induced - genetics</topic><topic>Physiological aspects</topic><topic>Risk factors</topic><topic>Sarcoma</topic><topic>Sarcoma - genetics</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lefèvre, Sandrine H.</creatorcontrib><creatorcontrib>Coquelle, Arnaud</creatorcontrib><creatorcontrib>Gonin-Laurent, Nathalie</creatorcontrib><creatorcontrib>Cör, Andrej</creatorcontrib><creatorcontrib>Vogt, Nicolas</creatorcontrib><creatorcontrib>Chauveinc, Laurent</creatorcontrib><creatorcontrib>Anract, Philippe</creatorcontrib><creatorcontrib>Dutrillaux, Bernard</creatorcontrib><creatorcontrib>Chevillard, Sylvie</creatorcontrib><creatorcontrib>Malfoy, Bernard</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Journal of radiation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lefèvre, Sandrine H.</au><au>Coquelle, Arnaud</au><au>Gonin-Laurent, Nathalie</au><au>Cör, Andrej</au><au>Vogt, Nicolas</au><au>Chauveinc, Laurent</au><au>Anract, Philippe</au><au>Dutrillaux, Bernard</au><au>Chevillard, Sylvie</au><au>Malfoy, Bernard</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Non-homologous End-joining Genes are not Inactivated in Human Radiation-induced Sarcomas with Genomic Instability</atitle><jtitle>Journal of radiation research</jtitle><addtitle>J Radiat Res</addtitle><date>2005-06-01</date><risdate>2005</risdate><volume>46</volume><issue>2</issue><spage>223</spage><epage>231</epage><pages>223-231</pages><issn>0449-3060</issn><eissn>1349-9157</eissn><abstract>DNA double-strand break (DSB) repair pathways are implicated in the maintenance of genomic stability. However the alterations of these pathways, as may occur in human tumor cells with strong genomic instability, remain poorly characterized. We analyzed the loss of heterozygosity (LOH) and the presence of mutations for a series of genes implicated in DSB repair by non-homologous end-joining in five radiation-induced sarcomas devoid of both active Tp53 and Rb1. LOH was recurrently observed for 8 of the 9 studied genes (KU70, KU80, XRCC4, LIG4, Artemis, MRE11, RAD50, NBS1) but not for DNA-PKcs. No mutation was found in the remaining allele of the genes with LOH and the mRNA expression did not correlate with the allelic status. 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| subjects | DNA Damage - genetics DNA Mutational Analysis - methods Gene Expression Regulation, Neoplastic - genetics Gene Expression Regulation, Neoplastic - radiation effects Gene mutations Gene Silencing - radiation effects Genetic aspects Genetic Variation - genetics Genomic Instability - genetics Genomic Instability - radiation effects Humans Ionizing radiation Neoplasms, Radiation-Induced - genetics Physiological aspects Risk factors Sarcoma Sarcoma - genetics Tumor Cells, Cultured |
| title | Non-homologous End-joining Genes are not Inactivated in Human Radiation-induced Sarcomas with Genomic Instability |
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