Comprehensive genomic analysis of desmoplastic medulloblastomas: identification of novel amplified genes and separate evaluation of the different histological components
Identifieur interne : 000763 ( Main/Corpus ); précédent : 000762; suivant : 000764Comprehensive genomic analysis of desmoplastic medulloblastomas: identification of novel amplified genes and separate evaluation of the different histological components
Auteurs : A. Ehrbrecht ; U. Müller ; M. Wolter ; A. Hoischen ; A. Koch ; B. Radlwimmer ; B. Actor ; A. Mincheva ; T. Pietsch ; P. Lichter ; G. Reifenberger ; Rg WeberSource :
- The Journal of Pathology [ 0022-3417 ] ; 2006-03.
English descriptors
- KwdEn :
Abstract
Desmoplastic medulloblastoma (DMB) is a malignant cerebellar tumour composed of two distinct tissue components, pale islands and desmoplastic areas. Previous studies revealed mutations in genes encoding members of the sonic hedgehog pathway, including PTCH, SMOH and SUFUH in DMBs. However, little is known about other genomic aberrations. We performed comparative genomic hybridization (CGH) analysis of 22 sporadic DMBs and identified chromosomal imbalances in 20 tumours (91%; mean, 4.9 imbalances/tumour). Recurrent chromosomal gains were found on chromosomes 3, 9 (six tumours each), 20, 22 (five tumours each), 2, 6, 7, 17 (four tumours each) and 1 (three tumours). Recurrent losses involved chromosomes X (eight tumours), Y (six of eleven tumours from male patients), 9, 12 (four tumours each), as well as 10, 13 and 17 (three tumours each). Four tumours demonstrated high‐level amplifications involving sequences from 1p22, 5p15, 9p, 12p13, 13q33‐q34 and 17q22‐q24, respectively. Further analysis of the 9p and 17q22‐q24 amplicons by array‐based CGH (matrix‐CGH) and candidate gene analyses revealed amplification of JMJD2C at 9p24 in one DMB and amplification of RPS6KB1, APPBP2, PPM1D and BCAS3 from 17q23 in three DMBs. Among the 17q23 genes, RPS6KB1 showed markedly elevated transcript levels as compared to normal cerebellum in five of six DMBs and four of five classic medulloblastomas investigated. Finally, CGH analysis of microdissected pale islands and desmoplastic areas showed common chromosomal imbalances in five of six informative tumours. In summary, we have identified several novel genetic alterations in DMBs and provide genetic evidence for a monoclonal origin of their different tissue components. Copyright © 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Url:
DOI: 10.1002/path.1925
Links to Exploration step
ISTEX:0862DF71DEC52E56F75C017A8EB7CBB528800972Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Comprehensive genomic analysis of desmoplastic medulloblastomas: identification of novel amplified genes and separate evaluation of the different histological components</title><author><name sortKey="Ehrbrecht, A" sort="Ehrbrecht, A" uniqKey="Ehrbrecht A" first="A" last="Ehrbrecht">A. Ehrbrecht</name><affiliation><mods:affiliation>Institute of Human Genetics, Rheinische Friedrich‐Wilhelms‐University, Wilhelmstrasse 31, D‐53111 Bonn, Germany</mods:affiliation></affiliation></author><author><name sortKey="Muller, U" sort="Muller, U" uniqKey="Muller U" first="U" last="Müller">U. Müller</name><affiliation><mods:affiliation>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Wolter, M" sort="Wolter, M" uniqKey="Wolter M" first="M" last="Wolter">M. Wolter</name><affiliation><mods:affiliation>Department of Neuropathology, Heinrich‐Heine‐University, Moorenstrasse 5, D‐40225 Düsseldorf, Germany</mods:affiliation></affiliation></author><author><name sortKey="Hoischen, A" sort="Hoischen, A" uniqKey="Hoischen A" first="A" last="Hoischen">A. Hoischen</name><affiliation><mods:affiliation>Institute of Human Genetics, Rheinische Friedrich‐Wilhelms‐University, Wilhelmstrasse 31, D‐53111 Bonn, Germany</mods:affiliation></affiliation></author><author><name sortKey="Koch, A" sort="Koch, A" uniqKey="Koch A" first="A" last="Koch">A. Koch</name><affiliation><mods:affiliation>Department of Neuropathology, Rheinische Friedrich‐Wilhelms‐University, Sigmund‐Freud‐Strasse 25, D‐53105 Bonn, Germany</mods:affiliation></affiliation></author><author><name sortKey="Radlwimmer, B" sort="Radlwimmer, B" uniqKey="Radlwimmer B" first="B" last="Radlwimmer">B. Radlwimmer</name><affiliation><mods:affiliation>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Actor, B" sort="Actor, B" uniqKey="Actor B" first="B" last="Actor">B. Actor</name><affiliation><mods:affiliation>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Mincheva, A" sort="Mincheva, A" uniqKey="Mincheva A" first="A" last="Mincheva">A. Mincheva</name><affiliation><mods:affiliation>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Pietsch, T" sort="Pietsch, T" uniqKey="Pietsch T" first="T" last="Pietsch">T. Pietsch</name><affiliation><mods:affiliation>Department of Neuropathology, Rheinische Friedrich‐Wilhelms‐University, Sigmund‐Freud‐Strasse 25, D‐53105 Bonn, Germany</mods:affiliation></affiliation></author><author><name sortKey="Lichter, P" sort="Lichter, P" uniqKey="Lichter P" first="P" last="Lichter">P. Lichter</name><affiliation><mods:affiliation>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Reifenberger, G" sort="Reifenberger, G" uniqKey="Reifenberger G" first="G" last="Reifenberger">G. Reifenberger</name><affiliation><mods:affiliation>Department of Neuropathology, Heinrich‐Heine‐University, Moorenstrasse 5, D‐40225 Düsseldorf, Germany</mods:affiliation></affiliation></author><author><name sortKey="Weber, Rg" sort="Weber, Rg" uniqKey="Weber R" first="Rg" last="Weber">Rg Weber</name><affiliation><mods:affiliation>Institute of Human Genetics, Rheinische Friedrich‐Wilhelms‐University, Wilhelmstrasse 31, D‐53111 Bonn, Germany</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:0862DF71DEC52E56F75C017A8EB7CBB528800972</idno><date when="2006" year="2006">2006</date><idno type="doi">10.1002/path.1925</idno><idno type="url">https://api.istex.fr/document/0862DF71DEC52E56F75C017A8EB7CBB528800972/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000763</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Comprehensive genomic analysis of desmoplastic medulloblastomas: identification of novel amplified genes and separate evaluation of the different histological components</title><author><name sortKey="Ehrbrecht, A" sort="Ehrbrecht, A" uniqKey="Ehrbrecht A" first="A" last="Ehrbrecht">A. Ehrbrecht</name><affiliation><mods:affiliation>Institute of Human Genetics, Rheinische Friedrich‐Wilhelms‐University, Wilhelmstrasse 31, D‐53111 Bonn, Germany</mods:affiliation></affiliation></author><author><name sortKey="Muller, U" sort="Muller, U" uniqKey="Muller U" first="U" last="Müller">U. Müller</name><affiliation><mods:affiliation>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Wolter, M" sort="Wolter, M" uniqKey="Wolter M" first="M" last="Wolter">M. Wolter</name><affiliation><mods:affiliation>Department of Neuropathology, Heinrich‐Heine‐University, Moorenstrasse 5, D‐40225 Düsseldorf, Germany</mods:affiliation></affiliation></author><author><name sortKey="Hoischen, A" sort="Hoischen, A" uniqKey="Hoischen A" first="A" last="Hoischen">A. Hoischen</name><affiliation><mods:affiliation>Institute of Human Genetics, Rheinische Friedrich‐Wilhelms‐University, Wilhelmstrasse 31, D‐53111 Bonn, Germany</mods:affiliation></affiliation></author><author><name sortKey="Koch, A" sort="Koch, A" uniqKey="Koch A" first="A" last="Koch">A. Koch</name><affiliation><mods:affiliation>Department of Neuropathology, Rheinische Friedrich‐Wilhelms‐University, Sigmund‐Freud‐Strasse 25, D‐53105 Bonn, Germany</mods:affiliation></affiliation></author><author><name sortKey="Radlwimmer, B" sort="Radlwimmer, B" uniqKey="Radlwimmer B" first="B" last="Radlwimmer">B. Radlwimmer</name><affiliation><mods:affiliation>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Actor, B" sort="Actor, B" uniqKey="Actor B" first="B" last="Actor">B. Actor</name><affiliation><mods:affiliation>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Mincheva, A" sort="Mincheva, A" uniqKey="Mincheva A" first="A" last="Mincheva">A. Mincheva</name><affiliation><mods:affiliation>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Pietsch, T" sort="Pietsch, T" uniqKey="Pietsch T" first="T" last="Pietsch">T. Pietsch</name><affiliation><mods:affiliation>Department of Neuropathology, Rheinische Friedrich‐Wilhelms‐University, Sigmund‐Freud‐Strasse 25, D‐53105 Bonn, Germany</mods:affiliation></affiliation></author><author><name sortKey="Lichter, P" sort="Lichter, P" uniqKey="Lichter P" first="P" last="Lichter">P. Lichter</name><affiliation><mods:affiliation>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Reifenberger, G" sort="Reifenberger, G" uniqKey="Reifenberger G" first="G" last="Reifenberger">G. Reifenberger</name><affiliation><mods:affiliation>Department of Neuropathology, Heinrich‐Heine‐University, Moorenstrasse 5, D‐40225 Düsseldorf, Germany</mods:affiliation></affiliation></author><author><name sortKey="Weber, Rg" sort="Weber, Rg" uniqKey="Weber R" first="Rg" last="Weber">Rg Weber</name><affiliation><mods:affiliation>Institute of Human Genetics, Rheinische Friedrich‐Wilhelms‐University, Wilhelmstrasse 31, D‐53111 Bonn, Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">The Journal of Pathology</title><title level="j" type="sub">A Journal of the Pathological Society of Great Britain and Ireland</title><title level="j" type="abbrev">J. Pathol.</title><idno type="ISSN">0022-3417</idno><idno type="eISSN">1096-9896</idno><imprint><publisher>John Wiley & Sons, Ltd.</publisher><pubPlace>Chichester, UK</pubPlace><date type="published" when="2006-03">2006-03</date><biblScope unit="volume">208</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="554">554</biblScope><biblScope unit="page" to="563">563</biblScope></imprint><idno type="ISSN">0022-3417</idno></series><idno type="istex">0862DF71DEC52E56F75C017A8EB7CBB528800972</idno><idno type="DOI">10.1002/path.1925</idno><idno type="ArticleID">PATH1925</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-3417</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>RPS6KB1</term><term>comparative genomic hybridization</term><term>gene amplification</term><term>medulloblastoma</term><term>molecular genetics</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Desmoplastic medulloblastoma (DMB) is a malignant cerebellar tumour composed of two distinct tissue components, pale islands and desmoplastic areas. Previous studies revealed mutations in genes encoding members of the sonic hedgehog pathway, including PTCH, SMOH and SUFUH in DMBs. However, little is known about other genomic aberrations. We performed comparative genomic hybridization (CGH) analysis of 22 sporadic DMBs and identified chromosomal imbalances in 20 tumours (91%; mean, 4.9 imbalances/tumour). Recurrent chromosomal gains were found on chromosomes 3, 9 (six tumours each), 20, 22 (five tumours each), 2, 6, 7, 17 (four tumours each) and 1 (three tumours). Recurrent losses involved chromosomes X (eight tumours), Y (six of eleven tumours from male patients), 9, 12 (four tumours each), as well as 10, 13 and 17 (three tumours each). Four tumours demonstrated high‐level amplifications involving sequences from 1p22, 5p15, 9p, 12p13, 13q33‐q34 and 17q22‐q24, respectively. Further analysis of the 9p and 17q22‐q24 amplicons by array‐based CGH (matrix‐CGH) and candidate gene analyses revealed amplification of JMJD2C at 9p24 in one DMB and amplification of RPS6KB1, APPBP2, PPM1D and BCAS3 from 17q23 in three DMBs. Among the 17q23 genes, RPS6KB1 showed markedly elevated transcript levels as compared to normal cerebellum in five of six DMBs and four of five classic medulloblastomas investigated. Finally, CGH analysis of microdissected pale islands and desmoplastic areas showed common chromosomal imbalances in five of six informative tumours. In summary, we have identified several novel genetic alterations in DMBs and provide genetic evidence for a monoclonal origin of their different tissue components. Copyright © 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>A Ehrbrecht</name><affiliations><json:string>Institute of Human Genetics, Rheinische Friedrich‐Wilhelms‐University, Wilhelmstrasse 31, D‐53111 Bonn, Germany</json:string></affiliations></json:item><json:item><name>U Müller</name><affiliations><json:string>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</json:string></affiliations></json:item><json:item><name>M Wolter</name><affiliations><json:string>Department of Neuropathology, Heinrich‐Heine‐University, Moorenstrasse 5, D‐40225 Düsseldorf, Germany</json:string></affiliations></json:item><json:item><name>A Hoischen</name><affiliations><json:string>Institute of Human Genetics, Rheinische Friedrich‐Wilhelms‐University, Wilhelmstrasse 31, D‐53111 Bonn, Germany</json:string></affiliations></json:item><json:item><name>A Koch</name><affiliations><json:string>Department of Neuropathology, Rheinische Friedrich‐Wilhelms‐University, Sigmund‐Freud‐Strasse 25, D‐53105 Bonn, Germany</json:string></affiliations></json:item><json:item><name>B Radlwimmer</name><affiliations><json:string>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</json:string></affiliations></json:item><json:item><name>B Actor</name><affiliations><json:string>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</json:string></affiliations></json:item><json:item><name>A Mincheva</name><affiliations><json:string>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</json:string></affiliations></json:item><json:item><name>T Pietsch</name><affiliations><json:string>Department of Neuropathology, Rheinische Friedrich‐Wilhelms‐University, Sigmund‐Freud‐Strasse 25, D‐53105 Bonn, Germany</json:string></affiliations></json:item><json:item><name>P Lichter</name><affiliations><json:string>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</json:string></affiliations></json:item><json:item><name>G Reifenberger</name><affiliations><json:string>Department of Neuropathology, Heinrich‐Heine‐University, Moorenstrasse 5, D‐40225 Düsseldorf, Germany</json:string></affiliations></json:item><json:item><name>RG Weber</name><affiliations><json:string>Institute of Human Genetics, Rheinische Friedrich‐Wilhelms‐University, Wilhelmstrasse 31, D‐53111 Bonn, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>comparative genomic hybridization</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>gene amplification</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>medulloblastoma</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>molecular genetics</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>RPS6KB1</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Desmoplastic medulloblastoma (DMB) is a malignant cerebellar tumour composed of two distinct tissue components, pale islands and desmoplastic areas. Previous studies revealed mutations in genes encoding members of the sonic hedgehog pathway, including PTCH, SMOH and SUFUH in DMBs. However, little is known about other genomic aberrations. We performed comparative genomic hybridization (CGH) analysis of 22 sporadic DMBs and identified chromosomal imbalances in 20 tumours (91%; mean, 4.9 imbalances/tumour). Recurrent chromosomal gains were found on chromosomes 3, 9 (six tumours each), 20, 22 (five tumours each), 2, 6, 7, 17 (four tumours each) and 1 (three tumours). Recurrent losses involved chromosomes X (eight tumours), Y (six of eleven tumours from male patients), 9, 12 (four tumours each), as well as 10, 13 and 17 (three tumours each). Four tumours demonstrated high‐level amplifications involving sequences from 1p22, 5p15, 9p, 12p13, 13q33‐q34 and 17q22‐q24, respectively. Further analysis of the 9p and 17q22‐q24 amplicons by array‐based CGH (matrix‐CGH) and candidate gene analyses revealed amplification of JMJD2C at 9p24 in one DMB and amplification of RPS6KB1, APPBP2, PPM1D and BCAS3 from 17q23 in three DMBs. Among the 17q23 genes, RPS6KB1 showed markedly elevated transcript levels as compared to normal cerebellum in five of six DMBs and four of five classic medulloblastomas investigated. Finally, CGH analysis of microdissected pale islands and desmoplastic areas showed common chromosomal imbalances in five of six informative tumours. In summary, we have identified several novel genetic alterations in DMBs and provide genetic evidence for a monoclonal origin of their different tissue components. Copyright © 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</abstract><qualityIndicators><score>8</score><pdfVersion>1.3</pdfVersion><pdfPageSize>595 x 842 pts (A4)</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>1831</abstractCharCount><pdfWordCount>6067</pdfWordCount><pdfCharCount>39447</pdfCharCount><pdfPageCount>10</pdfPageCount><abstractWordCount>269</abstractWordCount></qualityIndicators><title>Comprehensive genomic analysis of desmoplastic medulloblastomas: identification of novel amplified genes and separate evaluation of the different histological components</title><genre><json:string>article</json:string></genre><host><volume>208</volume><pages><total>10</total><last>563</last><first>554</first></pages><issn><json:string>0022-3417</json:string></issn><issue>4</issue><subject><json:item><value>Original Paper</value></json:item></subject><genre></genre><language><json:string>unknown</json:string></language><eissn><json:string>1096-9896</json:string></eissn><title>The Journal of Pathology</title><doi><json:string>10.1002/(ISSN)1096-9896</json:string></doi></host><publicationDate>2006</publicationDate><copyrightDate>2006</copyrightDate><doi><json:string>10.1002/path.1925</json:string></doi><id>0862DF71DEC52E56F75C017A8EB7CBB528800972</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/0862DF71DEC52E56F75C017A8EB7CBB528800972/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/0862DF71DEC52E56F75C017A8EB7CBB528800972/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/0862DF71DEC52E56F75C017A8EB7CBB528800972/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Comprehensive genomic analysis of desmoplastic medulloblastomas: identification of novel amplified genes and separate evaluation of the different histological components</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>John Wiley & Sons, Ltd.</publisher><pubPlace>Chichester, UK</pubPlace><availability><p>WILEY</p></availability><date>2006</date></publicationStmt><notesStmt><note>Deutsche Forschungsgemeinschaft - No. SFB503/B7; No. SFB400;</note><note>Deutsche Krebshilfe/Dr Mildred Scheel Stiftung - No. 10‐1639‐Re3; No. 70‐3088‐Sa1; No. 70‐3163‐Wi3;</note><note>German Ministry for Education and Research</note><note>Competence Network Pediatric Oncology</note><note>BONFOR programme, Rheinische Friedrich‐Wilhelms‐Universitat, Bonn - No. O‐149.0058; No. O‐154.0031;</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Comprehensive genomic analysis of desmoplastic medulloblastomas: identification of novel amplified genes and separate evaluation of the different histological components</title><author><persName><forename type="first">A</forename><surname>Ehrbrecht</surname></persName><affiliation>Institute of Human Genetics, Rheinische Friedrich‐Wilhelms‐University, Wilhelmstrasse 31, D‐53111 Bonn, Germany</affiliation></author><author><persName><forename type="first">U</forename><surname>Müller</surname></persName><affiliation>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</affiliation></author><author><persName><forename type="first">M</forename><surname>Wolter</surname></persName><affiliation>Department of Neuropathology, Heinrich‐Heine‐University, Moorenstrasse 5, D‐40225 Düsseldorf, Germany</affiliation></author><author><persName><forename type="first">A</forename><surname>Hoischen</surname></persName><affiliation>Institute of Human Genetics, Rheinische Friedrich‐Wilhelms‐University, Wilhelmstrasse 31, D‐53111 Bonn, Germany</affiliation></author><author><persName><forename type="first">A</forename><surname>Koch</surname></persName><affiliation>Department of Neuropathology, Rheinische Friedrich‐Wilhelms‐University, Sigmund‐Freud‐Strasse 25, D‐53105 Bonn, Germany</affiliation></author><author><persName><forename type="first">B</forename><surname>Radlwimmer</surname></persName><affiliation>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</affiliation></author><author><persName><forename type="first">B</forename><surname>Actor</surname></persName><affiliation>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</affiliation></author><author><persName><forename type="first">A</forename><surname>Mincheva</surname></persName><affiliation>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</affiliation></author><author><persName><forename type="first">T</forename><surname>Pietsch</surname></persName><affiliation>Department of Neuropathology, Rheinische Friedrich‐Wilhelms‐University, Sigmund‐Freud‐Strasse 25, D‐53105 Bonn, Germany</affiliation></author><author><persName><forename type="first">P</forename><surname>Lichter</surname></persName><affiliation>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</affiliation></author><author><persName><forename type="first">G</forename><surname>Reifenberger</surname></persName><affiliation>Department of Neuropathology, Heinrich‐Heine‐University, Moorenstrasse 5, D‐40225 Düsseldorf, Germany</affiliation></author><author><persName><forename type="first">RG</forename><surname>Weber</surname></persName><note type="correspondence"><p>Correspondence: Institute of Human Genetics, Rheinische Friedrich‐Wilhelms‐University, Wilhelmstrasse 31, D‐53111 Bonn, Germany.</p></note><affiliation>Institute of Human Genetics, Rheinische Friedrich‐Wilhelms‐University, Wilhelmstrasse 31, D‐53111 Bonn, Germany</affiliation></author></analytic><monogr><title level="j">The Journal of Pathology</title><title level="j" type="sub">A Journal of the Pathological Society of Great Britain and Ireland</title><title level="j" type="abbrev">J. Pathol.</title><idno type="pISSN">0022-3417</idno><idno type="eISSN">1096-9896</idno><idno type="DOI">10.1002/(ISSN)1096-9896</idno><imprint><publisher>John Wiley & Sons, Ltd.</publisher><pubPlace>Chichester, UK</pubPlace><date type="published" when="2006-03"></date><biblScope unit="volume">208</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="554">554</biblScope><biblScope unit="page" to="563">563</biblScope></imprint></monogr><idno type="istex">0862DF71DEC52E56F75C017A8EB7CBB528800972</idno><idno type="DOI">10.1002/path.1925</idno><idno type="ArticleID">PATH1925</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2006</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Desmoplastic medulloblastoma (DMB) is a malignant cerebellar tumour composed of two distinct tissue components, pale islands and desmoplastic areas. Previous studies revealed mutations in genes encoding members of the sonic hedgehog pathway, including PTCH, SMOH and SUFUH in DMBs. However, little is known about other genomic aberrations. We performed comparative genomic hybridization (CGH) analysis of 22 sporadic DMBs and identified chromosomal imbalances in 20 tumours (91%; mean, 4.9 imbalances/tumour). Recurrent chromosomal gains were found on chromosomes 3, 9 (six tumours each), 20, 22 (five tumours each), 2, 6, 7, 17 (four tumours each) and 1 (three tumours). Recurrent losses involved chromosomes X (eight tumours), Y (six of eleven tumours from male patients), 9, 12 (four tumours each), as well as 10, 13 and 17 (three tumours each). Four tumours demonstrated high‐level amplifications involving sequences from 1p22, 5p15, 9p, 12p13, 13q33‐q34 and 17q22‐q24, respectively. Further analysis of the 9p and 17q22‐q24 amplicons by array‐based CGH (matrix‐CGH) and candidate gene analyses revealed amplification of JMJD2C at 9p24 in one DMB and amplification of RPS6KB1, APPBP2, PPM1D and BCAS3 from 17q23 in three DMBs. Among the 17q23 genes, RPS6KB1 showed markedly elevated transcript levels as compared to normal cerebellum in five of six DMBs and four of five classic medulloblastomas investigated. Finally, CGH analysis of microdissected pale islands and desmoplastic areas showed common chromosomal imbalances in five of six informative tumours. In summary, we have identified several novel genetic alterations in DMBs and provide genetic evidence for a monoclonal origin of their different tissue components. Copyright © 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>comparative genomic hybridization</term></item><item><term>gene amplification</term></item><item><term>medulloblastoma</term></item><item><term>molecular genetics</term></item><item><term>RPS6KB1</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Original Paper</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2005-08-24">Received</change><change when="2005-10-21">Registration</change><change when="2006-03">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/0862DF71DEC52E56F75C017A8EB7CBB528800972/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>John Wiley & Sons, Ltd.</publisherName><publisherLoc>Chichester, UK</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1096-9896</doi><issn type="print">0022-3417</issn><issn type="electronic">1096-9896</issn><idGroup><id type="product" value="PATH"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="JOURNAL OF PATHOLOGY, THE">The Journal of Pathology</title><title type="subtitle">A Journal of the Pathological Society of Great Britain and Ireland</title><title type="short">J. Pathol.</title></titleGroup></publicationMeta><publicationMeta level="part" position="40"><doi origin="wiley" registered="yes">10.1002/path.v208:4</doi><numberingGroup><numbering type="journalVolume" number="208">208</numbering><numbering type="journalIssue">4</numbering></numberingGroup><coverDate startDate="2006-03">March 2006</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="110" status="forIssue"><doi origin="wiley" registered="yes">10.1002/path.1925</doi><idGroup><id type="unit" value="PATH1925"></id></idGroup><countGroup><count type="pageTotal" number="10"></count></countGroup><titleGroup><title type="articleCategory">Original Paper</title><title type="tocHeading1">Original Papers</title></titleGroup><copyright ownership="thirdParty">Copyright © 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</copyright><eventGroup><event type="manuscriptReceived" date="2005-08-24"></event><event type="manuscriptRevised" date="2005-10-12"></event><event type="manuscriptAccepted" date="2005-10-21"></event><event type="publishedOnlineEarlyUnpaginated" date="2006-01-06"></event><event type="firstOnline" date="2006-01-06"></event><event type="publishedOnlineFinalForm" date="2006-02-10"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.1 mode:FullText source:FullText result:FullText" date="2010-02-22"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-06"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-11-04"></event></eventGroup><numberingGroup><numbering type="pageFirst">554</numbering><numbering type="pageLast">563</numbering></numberingGroup><correspondenceTo>Institute of Human Genetics, Rheinische Friedrich‐Wilhelms‐University, Wilhelmstrasse 31, D‐53111 Bonn, Germany.</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:PATH.PATH1925.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="66"></count></countGroup><titleGroup><title type="main" xml:lang="en">Comprehensive genomic analysis of desmoplastic medulloblastomas: identification of novel amplified genes and separate evaluation of the different histological components</title><title type="short" xml:lang="en">Genomic alterations in desmoplastic medulloblastoma</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>A</givenNames><familyName>Ehrbrecht</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>U</givenNames><familyName>Müller</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af3"><personName><givenNames>M</givenNames><familyName>Wolter</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>A</givenNames><familyName>Hoischen</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af4"><personName><givenNames>A</givenNames><familyName>Koch</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af2"><personName><givenNames>B</givenNames><familyName>Radlwimmer</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af2"><personName><givenNames>B</givenNames><familyName>Actor</familyName></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af2"><personName><givenNames>A</givenNames><familyName>Mincheva</familyName></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af4"><personName><givenNames>T</givenNames><familyName>Pietsch</familyName></personName></creator><creator xml:id="au10" creatorRole="author" affiliationRef="#af2"><personName><givenNames>P</givenNames><familyName>Lichter</familyName></personName></creator><creator xml:id="au11" creatorRole="author" affiliationRef="#af3"><personName><givenNames>G</givenNames><familyName>Reifenberger</familyName></personName></creator><creator xml:id="au12" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>RG</givenNames><familyName>Weber</familyName></personName><contactDetails><email normalForm="ruthild.weber@ukb.uni-bonn.de">ruthild.weber@ukb.uni‐bonn.de</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="DE" type="organization"><unparsedAffiliation>Institute of Human Genetics, Rheinische Friedrich‐Wilhelms‐University, Wilhelmstrasse 31, D‐53111 Bonn, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="DE" type="organization"><unparsedAffiliation>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neuropathology, Heinrich‐Heine‐University, Moorenstrasse 5, D‐40225 Düsseldorf, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neuropathology, Rheinische Friedrich‐Wilhelms‐University, Sigmund‐Freud‐Strasse 25, D‐53105 Bonn, Germany</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">comparative genomic hybridization</keyword><keyword xml:id="kwd2">gene amplification</keyword><keyword xml:id="kwd3">medulloblastoma</keyword><keyword xml:id="kwd4">molecular genetics</keyword><keyword xml:id="kwd5"><i>RPS6KB1</i></keyword></keywordGroup><fundingInfo><fundingAgency>Deutsche Forschungsgemeinschaft</fundingAgency><fundingNumber>SFB503/B7</fundingNumber><fundingNumber>SFB400</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Deutsche Krebshilfe/Dr Mildred Scheel Stiftung</fundingAgency><fundingNumber>10‐1639‐Re3</fundingNumber><fundingNumber>70‐3088‐Sa1</fundingNumber><fundingNumber>70‐3163‐Wi3</fundingNumber></fundingInfo><fundingInfo><fundingAgency>German Ministry for Education and Research</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Competence Network Pediatric Oncology</fundingAgency></fundingInfo><fundingInfo><fundingAgency>BONFOR programme, Rheinische Friedrich‐Wilhelms‐Universitat, Bonn</fundingAgency><fundingNumber>O‐149.0058</fundingNumber><fundingNumber>O‐154.0031</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Desmoplastic medulloblastoma (DMB) is a malignant cerebellar tumour composed of two distinct tissue components, pale islands and desmoplastic areas. Previous studies revealed mutations in genes encoding members of the sonic hedgehog pathway, including <i>PTCH, SMOH</i> and <i>SUFUH</i> in DMBs. However, little is known about other genomic aberrations. We performed comparative genomic hybridization (CGH) analysis of 22 sporadic DMBs and identified chromosomal imbalances in 20 tumours (91%; mean, 4.9 imbalances/tumour). Recurrent chromosomal gains were found on chromosomes 3, 9 (six tumours each), 20, 22 (five tumours each), 2, 6, 7, 17 (four tumours each) and 1 (three tumours). Recurrent losses involved chromosomes X (eight tumours), Y (six of eleven tumours from male patients), 9, 12 (four tumours each), as well as 10, 13 and 17 (three tumours each). Four tumours demonstrated high‐level amplifications involving sequences from 1p22, 5p15, 9p, 12p13, 13q33‐q34 and 17q22‐q24, respectively. Further analysis of the 9p and 17q22‐q24 amplicons by array‐based CGH (matrix‐CGH) and candidate gene analyses revealed amplification of <i>JMJD2C</i> at 9p24 in one DMB and amplification of <i>RPS6KB1, APPBP2, PPM1D</i> and <i>BCAS3</i> from 17q23 in three DMBs. Among the 17q23 genes, <i>RPS6KB1</i> showed markedly elevated transcript levels as compared to normal cerebellum in five of six DMBs and four of five classic medulloblastomas investigated. Finally, CGH analysis of microdissected pale islands and desmoplastic areas showed common chromosomal imbalances in five of six informative tumours. In summary, we have identified several novel genetic alterations in DMBs and provide genetic evidence for a monoclonal origin of their different tissue components. Copyright © 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Comprehensive genomic analysis of desmoplastic medulloblastomas: identification of novel amplified genes and separate evaluation of the different histological components</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Genomic alterations in desmoplastic medulloblastoma</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Comprehensive genomic analysis of desmoplastic medulloblastomas: identification of novel amplified genes and separate evaluation of the different histological components</title></titleInfo><name type="personal"><namePart type="given">A</namePart><namePart type="family">Ehrbrecht</namePart><affiliation>Institute of Human Genetics, Rheinische Friedrich‐Wilhelms‐University, Wilhelmstrasse 31, D‐53111 Bonn, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">U</namePart><namePart type="family">Müller</namePart><affiliation>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Wolter</namePart><affiliation>Department of Neuropathology, Heinrich‐Heine‐University, Moorenstrasse 5, D‐40225 Düsseldorf, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Hoischen</namePart><affiliation>Institute of Human Genetics, Rheinische Friedrich‐Wilhelms‐University, Wilhelmstrasse 31, D‐53111 Bonn, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Koch</namePart><affiliation>Department of Neuropathology, Rheinische Friedrich‐Wilhelms‐University, Sigmund‐Freud‐Strasse 25, D‐53105 Bonn, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Radlwimmer</namePart><affiliation>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Actor</namePart><affiliation>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Mincheva</namePart><affiliation>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Pietsch</namePart><affiliation>Department of Neuropathology, Rheinische Friedrich‐Wilhelms‐University, Sigmund‐Freud‐Strasse 25, D‐53105 Bonn, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Lichter</namePart><affiliation>Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D‐69120 Heidelberg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G</namePart><namePart type="family">Reifenberger</namePart><affiliation>Department of Neuropathology, Heinrich‐Heine‐University, Moorenstrasse 5, D‐40225 Düsseldorf, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RG</namePart><namePart type="family">Weber</namePart><affiliation>Institute of Human Genetics, Rheinische Friedrich‐Wilhelms‐University, Wilhelmstrasse 31, D‐53111 Bonn, Germany</affiliation><description>Correspondence: Institute of Human Genetics, Rheinische Friedrich‐Wilhelms‐University, Wilhelmstrasse 31, D‐53111 Bonn, Germany.</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>John Wiley & Sons, Ltd.</publisher><place><placeTerm type="text">Chichester, UK</placeTerm></place><dateIssued encoding="w3cdtf">2006-03</dateIssued><dateCaptured encoding="w3cdtf">2005-08-24</dateCaptured><dateValid encoding="w3cdtf">2005-10-21</dateValid><copyrightDate encoding="w3cdtf">2006</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">4</extent><extent unit="tables">2</extent><extent unit="references">66</extent></physicalDescription><abstract lang="en">Desmoplastic medulloblastoma (DMB) is a malignant cerebellar tumour composed of two distinct tissue components, pale islands and desmoplastic areas. Previous studies revealed mutations in genes encoding members of the sonic hedgehog pathway, including PTCH, SMOH and SUFUH in DMBs. However, little is known about other genomic aberrations. We performed comparative genomic hybridization (CGH) analysis of 22 sporadic DMBs and identified chromosomal imbalances in 20 tumours (91%; mean, 4.9 imbalances/tumour). Recurrent chromosomal gains were found on chromosomes 3, 9 (six tumours each), 20, 22 (five tumours each), 2, 6, 7, 17 (four tumours each) and 1 (three tumours). Recurrent losses involved chromosomes X (eight tumours), Y (six of eleven tumours from male patients), 9, 12 (four tumours each), as well as 10, 13 and 17 (three tumours each). Four tumours demonstrated high‐level amplifications involving sequences from 1p22, 5p15, 9p, 12p13, 13q33‐q34 and 17q22‐q24, respectively. Further analysis of the 9p and 17q22‐q24 amplicons by array‐based CGH (matrix‐CGH) and candidate gene analyses revealed amplification of JMJD2C at 9p24 in one DMB and amplification of RPS6KB1, APPBP2, PPM1D and BCAS3 from 17q23 in three DMBs. Among the 17q23 genes, RPS6KB1 showed markedly elevated transcript levels as compared to normal cerebellum in five of six DMBs and four of five classic medulloblastomas investigated. Finally, CGH analysis of microdissected pale islands and desmoplastic areas showed common chromosomal imbalances in five of six informative tumours. In summary, we have identified several novel genetic alterations in DMBs and provide genetic evidence for a monoclonal origin of their different tissue components. Copyright © 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</abstract><note type="funding">Deutsche Forschungsgemeinschaft - No. SFB503/B7; No. SFB400; </note><note type="funding">Deutsche Krebshilfe/Dr Mildred Scheel Stiftung - No. 10‐1639‐Re3; No. 70‐3088‐Sa1; No. 70‐3163‐Wi3; </note><note type="funding">German Ministry for Education and Research</note><note type="funding">Competence Network Pediatric Oncology</note><note type="funding">BONFOR programme, Rheinische Friedrich‐Wilhelms‐Universitat, Bonn - No. O‐149.0058; No. O‐154.0031; </note><subject lang="en"><genre>Keywords</genre><topic>comparative genomic hybridization</topic><topic>gene amplification</topic><topic>medulloblastoma</topic><topic>molecular genetics</topic><topic>RPS6KB1</topic></subject><relatedItem type="host"><titleInfo><title>The Journal of Pathology</title><subTitle>A Journal of the Pathological Society of Great Britain and Ireland</subTitle></titleInfo><titleInfo type="abbreviated"><title>J. Pathol.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Original Paper</topic></subject><identifier type="ISSN">0022-3417</identifier><identifier type="eISSN">1096-9896</identifier><identifier type="DOI">10.1002/(ISSN)1096-9896</identifier><identifier type="PublisherID">PATH</identifier><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>208</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>554</start><end>563</end><total>10</total></extent></part></relatedItem><identifier type="istex">0862DF71DEC52E56F75C017A8EB7CBB528800972</identifier><identifier type="DOI">10.1002/path.1925</identifier><identifier type="ArticleID">PATH1925</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>John Wiley & Sons, Ltd.</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Musique/explor/SchutzV1/Data/Main/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000763 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 000763 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Musique
|area= SchutzV1
|flux= Main
|étape= Corpus
|type= RBID
|clé= ISTEX:0862DF71DEC52E56F75C017A8EB7CBB528800972
|texte= Comprehensive genomic analysis of desmoplastic medulloblastomas: identification of novel amplified genes and separate evaluation of the different histological components
}}
| This area was generated with Dilib version V0.6.38. |  |