Delineation of a 1Mb breakpoint region at 1p13 in Wilms tumors by fine‐tiling oligonucleotide array CGH
Identifieur interne : 002524 ( Istex/Corpus ); précédent : 002523; suivant : 002525Delineation of a 1Mb breakpoint region at 1p13 in Wilms tumors by fine‐tiling oligonucleotide array CGH
Auteurs : Rachael Natrajan ; Richard D. Williams ; Anita Grigoriadis ; Alan Mackay ; Kerry Fenwick ; Alan Ashworth ; Jeffrey S. Dome ; Paul E. Grundy ; Kathy Pritchard-Jones ; Chris JonesSource :
- [ 1045-2257 ]
Abstract
Wilms tumor karyotypes frequently exhibit recurrent, large‐scale chromosomal imbalances, among the most common of which are concurrent loss of 1p and gain of 1q. We have previously identified a novel breakpoint at 1p13 by 1 Mb‐spaced array CGH, and have now undertaken a fine‐tiling oligonucleotide array approach to map the region accurately in four tumors exhibiting rearrangements at this locus. The use of a 10 bp‐spaced platform revealed that all four tumors in fact harbored different breakpoints, which targeted intragenic sequences in PHTF1, DCLRE1B, and NRAS, and an intergenic region immediately downstream of TRIM33. All four genes and breakpoints were within the 1.78 Mb intervals identified by the genome‐wide BAC arrays. The precise breakpoint interval was in each case mapped to a 200–1,200 bp region and was confirmed for one case to lie within intron 3 of DCLRE1B by quantitative PCR. Analysis of local genome architecture revealed no convincing conservation of repetitive sequences or specific translocation/recombination‐associated elements within the breakpoint regions. This study highlights the power of fine‐tiling oligonucleotide arrays to delineate breakpoint regions identified by genome‐wide screens. © 2007 Wiley‐Liss, Inc.
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DOI: 10.1002/gcc.20446
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Williams</name><affiliation><mods:affiliation>Paediatric Oncology, Institute of Cancer Research/Royal Marsden NHS Trust, Sutton, UK</mods:affiliation></affiliation></author><author><name sortKey="Grigoriadis, Anita" sort="Grigoriadis, Anita" uniqKey="Grigoriadis A" first="Anita" last="Grigoriadis">Anita Grigoriadis</name><affiliation><mods:affiliation>Ludwig Institute for Cancer Research, University College London, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Mackay, Alan" sort="Mackay, Alan" uniqKey="Mackay A" first="Alan" last="Mackay">Alan Mackay</name><affiliation><mods:affiliation>Breakthrough Breast Cancer Research Centre, Institute of Cancer Research, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Fenwick, Kerry" sort="Fenwick, Kerry" uniqKey="Fenwick K" first="Kerry" last="Fenwick">Kerry Fenwick</name><affiliation><mods:affiliation>Breakthrough Breast Cancer Research Centre, Institute of Cancer Research, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Ashworth, Alan" sort="Ashworth, Alan" uniqKey="Ashworth A" first="Alan" last="Ashworth">Alan Ashworth</name><affiliation><mods:affiliation>Breakthrough Breast Cancer Research Centre, Institute of Cancer Research, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Dome, Jeffrey S" sort="Dome, Jeffrey S" uniqKey="Dome J" first="Jeffrey S." last="Dome">Jeffrey S. 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Williams</name><affiliation><mods:affiliation>Paediatric Oncology, Institute of Cancer Research/Royal Marsden NHS Trust, Sutton, UK</mods:affiliation></affiliation></author><author><name sortKey="Grigoriadis, Anita" sort="Grigoriadis, Anita" uniqKey="Grigoriadis A" first="Anita" last="Grigoriadis">Anita Grigoriadis</name><affiliation><mods:affiliation>Ludwig Institute for Cancer Research, University College London, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Mackay, Alan" sort="Mackay, Alan" uniqKey="Mackay A" first="Alan" last="Mackay">Alan Mackay</name><affiliation><mods:affiliation>Breakthrough Breast Cancer Research Centre, Institute of Cancer Research, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Fenwick, Kerry" sort="Fenwick, Kerry" uniqKey="Fenwick K" first="Kerry" last="Fenwick">Kerry Fenwick</name><affiliation><mods:affiliation>Breakthrough Breast Cancer Research Centre, Institute of Cancer Research, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Ashworth, Alan" sort="Ashworth, Alan" uniqKey="Ashworth A" first="Alan" last="Ashworth">Alan Ashworth</name><affiliation><mods:affiliation>Breakthrough Breast Cancer Research Centre, Institute of Cancer Research, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Dome, Jeffrey S" sort="Dome, Jeffrey S" uniqKey="Dome J" first="Jeffrey S." last="Dome">Jeffrey S. Dome</name><affiliation><mods:affiliation>Division of Oncology, Children's National Medical Center, Washington DC</mods:affiliation></affiliation></author><author><name sortKey="Grundy, Paul E" sort="Grundy, Paul E" uniqKey="Grundy P" first="Paul E." last="Grundy">Paul E. Grundy</name><affiliation><mods:affiliation>Departments of Paediatrics and Oncology, University of Alberta, Edmonton, Canada</mods:affiliation></affiliation></author><author><name sortKey="Pritchard Ones, Kathy" sort="Pritchard Ones, Kathy" uniqKey="Pritchard Ones K" first="Kathy" last="Pritchard-Jones">Kathy Pritchard-Jones</name><affiliation><mods:affiliation>Paediatric Oncology, Institute of Cancer Research/Royal Marsden NHS Trust, Sutton, UK</mods:affiliation></affiliation></author><author><name sortKey="Jones, Chris" sort="Jones, Chris" uniqKey="Jones C" first="Chris" last="Jones">Chris Jones</name><affiliation><mods:affiliation>Paediatric Oncology, Institute of Cancer Research/Royal Marsden NHS Trust, Sutton, UK</mods:affiliation></affiliation><affiliation><mods:affiliation>Paediatric Oncology, Institute of Cancer Research, 15 Costwold Road, Sutton, Surrey, SM2 5NG, UK</mods:affiliation></affiliation></author></analytic><series><idno type="ISSN">1045-2257</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1045-2257</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Wilms tumor karyotypes frequently exhibit recurrent, large‐scale chromosomal imbalances, among the most common of which are concurrent loss of 1p and gain of 1q. We have previously identified a novel breakpoint at 1p13 by 1 Mb‐spaced array CGH, and have now undertaken a fine‐tiling oligonucleotide array approach to map the region accurately in four tumors exhibiting rearrangements at this locus. The use of a 10 bp‐spaced platform revealed that all four tumors in fact harbored different breakpoints, which targeted intragenic sequences in PHTF1, DCLRE1B, and NRAS, and an intergenic region immediately downstream of TRIM33. All four genes and breakpoints were within the 1.78 Mb intervals identified by the genome‐wide BAC arrays. The precise breakpoint interval was in each case mapped to a 200–1,200 bp region and was confirmed for one case to lie within intron 3 of DCLRE1B by quantitative PCR. Analysis of local genome architecture revealed no convincing conservation of repetitive sequences or specific translocation/recombination‐associated elements within the breakpoint regions. 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We have previously identified a novel breakpoint at 1p13 by 1 Mb‐spaced array CGH, and have now undertaken a fine‐tiling oligonucleotide array approach to map the region accurately in four tumors exhibiting rearrangements at this locus. The use of a 10 bp‐spaced platform revealed that all four tumors in fact harbored different breakpoints, which targeted intragenic sequences in PHTF1, DCLRE1B, and NRAS, and an intergenic region immediately downstream of TRIM33. All four genes and breakpoints were within the 1.78 Mb intervals identified by the genome‐wide BAC arrays. The precise breakpoint interval was in each case mapped to a 200–1,200 bp region and was confirmed for one case to lie within intron 3 of DCLRE1B by quantitative PCR. Analysis of local genome architecture revealed no convincing conservation of repetitive sequences or specific translocation/recombination‐associated elements within the breakpoint regions. 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version="3.6"><titleInfo lang="en"><title>Delineation of a 1Mb breakpoint region at 1p13 in Wilms tumors by fine‐tiling oligonucleotide array CGH</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Fine‐Tiling 1p13 aCGH in Wilms Tumor</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Delineation of a 1Mb breakpoint region at 1p13 in Wilms tumors by fine‐tiling oligonucleotide array CGH</title></titleInfo><name type="personal"><namePart type="given">Rachael</namePart><namePart type="family">Natrajan</namePart><affiliation>Paediatric Oncology, Institute of Cancer Research/Royal Marsden NHS Trust, Sutton, UK</affiliation><description>R.N. and R.D.W. contributed equally this work.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Richard D.</namePart><namePart type="family">Williams</namePart><affiliation>Paediatric Oncology, Institute of Cancer Research/Royal Marsden NHS Trust, Sutton, UK</affiliation><description>R.N. and R.D.W. contributed equally this work.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Anita</namePart><namePart type="family">Grigoriadis</namePart><affiliation>Ludwig Institute for Cancer Research, University College London, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alan</namePart><namePart type="family">Mackay</namePart><affiliation>Breakthrough Breast Cancer Research Centre, Institute of Cancer Research, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kerry</namePart><namePart type="family">Fenwick</namePart><affiliation>Breakthrough Breast Cancer Research Centre, Institute of Cancer Research, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alan</namePart><namePart type="family">Ashworth</namePart><affiliation>Breakthrough Breast Cancer Research Centre, Institute of Cancer Research, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jeffrey S.</namePart><namePart type="family">Dome</namePart><affiliation>Division of Oncology, Children's National Medical Center, Washington DC</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paul E.</namePart><namePart type="family">Grundy</namePart><affiliation>Departments of Paediatrics and Oncology, University of Alberta, Edmonton, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kathy</namePart><namePart type="family">Pritchard‐Jones</namePart><affiliation>Paediatric Oncology, Institute of Cancer Research/Royal Marsden NHS Trust, Sutton, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Chris</namePart><namePart type="family">Jones</namePart><affiliation>Paediatric Oncology, Institute of Cancer Research/Royal Marsden NHS Trust, Sutton, UK</affiliation><affiliation>Paediatric Oncology, Institute of Cancer Research, 15 Costwold Road, Sutton, Surrey, SM2 5NG, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2007-06</dateIssued><dateCaptured encoding="w3cdtf">2007-01-03</dateCaptured><dateValid encoding="w3cdtf">2007-02-27</dateValid><copyrightDate encoding="w3cdtf">2007</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">5</extent><extent unit="tables">2</extent><extent unit="references">24</extent><extent unit="words">5299</extent></physicalDescription><abstract lang="en">Wilms tumor karyotypes frequently exhibit recurrent, large‐scale chromosomal imbalances, among the most common of which are concurrent loss of 1p and gain of 1q. We have previously identified a novel breakpoint at 1p13 by 1 Mb‐spaced array CGH, and have now undertaken a fine‐tiling oligonucleotide array approach to map the region accurately in four tumors exhibiting rearrangements at this locus. The use of a 10 bp‐spaced platform revealed that all four tumors in fact harbored different breakpoints, which targeted intragenic sequences in PHTF1, DCLRE1B, and NRAS, and an intergenic region immediately downstream of TRIM33. All four genes and breakpoints were within the 1.78 Mb intervals identified by the genome‐wide BAC arrays. The precise breakpoint interval was in each case mapped to a 200–1,200 bp region and was confirmed for one case to lie within intron 3 of DCLRE1B by quantitative PCR. Analysis of local genome architecture revealed no convincing conservation of repetitive sequences or specific translocation/recombination‐associated elements within the breakpoint regions. This study highlights the power of fine‐tiling oligonucleotide arrays to delineate breakpoint regions identified by genome‐wide screens. © 2007 Wiley‐Liss, Inc.</abstract><note type="funding">Cancer Research UK</note><note type="funding">Breakthrough Breast Cancer</note><note type="funding">Lisa Thaxter Trust</note><relatedItem type="host"><titleInfo><title>Genes, Chromosomes and Cancer</title></titleInfo><titleInfo type="abbreviated"><title>Genes Chromosom. Cancer</title></titleInfo><genre type="journal">journal</genre><subject><genre>article-category</genre><topic>Research Article</topic></subject><identifier type="ISSN">1045-2257</identifier><identifier type="eISSN">1098-2264</identifier><identifier type="DOI">10.1002/(ISSN)1098-2264</identifier><identifier type="PublisherID">GCC</identifier><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>46</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>607</start><end>615</end><total>9</total></extent></part></relatedItem><identifier type="istex">F5CEC1ED5BB14FBB1AA8F7830851736E0F5A8172</identifier><identifier type="DOI">10.1002/gcc.20446</identifier><identifier type="ArticleID">GCC20446</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2007 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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