A newly characterized human well-differentiated liposarcoma cell line contains amplifications of the 12q12-21 and 10p11-14 regions
Identifieur interne : 004D69 ( PascalFrancis/Curation ); précédent : 004D68; suivant : 004D70A newly characterized human well-differentiated liposarcoma cell line contains amplifications of the 12q12-21 and 10p11-14 regions
Auteurs : Florence Pedeutour [France] ; Georges Maire [Canada] ; Anne Pierron [France] ; David M. Thomas [Australie] ; Dale W. Garsed [Australie] ; Laurence Bianchini [France] ; Valérie Duranton-Tanneur [France] ; Annabelle Cortes-Maurel [France] ; Antoine Italiano [France] ; Jeremy A. Squire [Canada] ; Jean-Michel Coindre [France]Source :
- Virchows Archiv [ 0945-6317 ] ; 2012.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
Abstract
While surgery is the usual treatment for localized well-differentiated and dedifferentiated liposarcomas (WDLPS/DDLPS), the therapeutic options for patients with advanced disease are limited. The classical antimitotic treatments are most often inefficient. The establishment of genetically characterized cell lines is therefore crucial for providing in vitro models for novel targeted therapies. We have used spectral karyotyping, fluorescence in situ hybridization with whole chromosome painting and locus-specific probes, and array-comparative genomic hybridization to identify the chromosomal and molecular alterations of a novel cell line established from a recurring sclerosing WDLPS. The karyotype was hypertriploid and showed multiple structural anomalies. All cells retained the presence of a giant marker chromosome that had been previously identified in the primary cell cultures. This giant chromosome contained high-level amplification of chromosomal regions 12q13-21 and lacked the alpha-satellite centromeric sequences associated with WDLPS/DDLPS. The 12q amplicon was large, containing 370 amplified genes. The DNA copy number ranged from 3 to 57. The highest levels of amplification were observed at 12ql4.3 for GNS, WIF1, and HMGA2. We analyzed the mRNA expression status by real-time reverse transcription polymerase chain reaction for six genes from this amplicon: MDM2, HMGA2, CDK4, TSPAN31, WIF1, and YEATS4. mRNA overexpression was correlated with genomic amplification. A second amplicon originating from 10p11-14 was also present in the giant marker chromosome. The 10p amplicon contained 62 genes, including oncogenes such as MLLT10, previously described in chimeric fusion with MLL in leukemias, NEBL, and BMI1.
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amplification</term>
<term>Anatomic pathology</term>
<term>C-Onc gene</term>
<term>Cell line</term>
<term>Chromosome C10</term>
<term>Chromosome C12</term>
<term>Established cell line</term>
<term>Genetic mapping</term>
<term>Human</term>
<term>Liposarcoma</term>
<term>Protooncogene</term>
<term>Soft tissue sarcoma</term>
<term>mdm2 Gene</term>
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<keywords scheme="Pascal" xml:lang="fr"><term>Liposarcome</term>
<term>Homme</term>
<term>Lignée cellulaire</term>
<term>Sarcome des tissus mous</term>
<term>Lignée cellulaire établie</term>
<term>Amplification</term>
<term>Chromosome C12</term>
<term>Carte génétique</term>
<term>Chromosome C10</term>
<term>Gène onc cellulaire</term>
<term>Protooncogène</term>
<term>Gène mdm2</term>
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<front><div type="abstract" xml:lang="en">While surgery is the usual treatment for localized well-differentiated and dedifferentiated liposarcomas (WDLPS/DDLPS), the therapeutic options for patients with advanced disease are limited. The classical antimitotic treatments are most often inefficient. The establishment of genetically characterized cell lines is therefore crucial for providing in vitro models for novel targeted therapies. We have used spectral karyotyping, fluorescence in situ hybridization with whole chromosome painting and locus-specific probes, and array-comparative genomic hybridization to identify the chromosomal and molecular alterations of a novel cell line established from a recurring sclerosing WDLPS. The karyotype was hypertriploid and showed multiple structural anomalies. All cells retained the presence of a giant marker chromosome that had been previously identified in the primary cell cultures. This giant chromosome contained high-level amplification of chromosomal regions 12q13-21 and lacked the alpha-satellite centromeric sequences associated with WDLPS/DDLPS. The 12q amplicon was large, containing 370 amplified genes. The DNA copy number ranged from 3 to 57. The highest levels of amplification were observed at 12ql4.3 for GNS, WIF1, and HMGA2. We analyzed the mRNA expression status by real-time reverse transcription polymerase chain reaction for six genes from this amplicon: MDM2, HMGA2, CDK4, TSPAN31, WIF1, and YEATS4. mRNA overexpression was correlated with genomic amplification. A second amplicon originating from 10p11-14 was also present in the giant marker chromosome. The 10p amplicon contained 62 genes, including oncogenes such as MLLT10, previously described in chimeric fusion with MLL in leukemias, NEBL, and BMI1.</div>
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<fA45><s0>72 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>12-0326835</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Virchows Archiv</s0>
</fA64>
<fA66 i1="01"><s0>DEU</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>While surgery is the usual treatment for localized well-differentiated and dedifferentiated liposarcomas (WDLPS/DDLPS), the therapeutic options for patients with advanced disease are limited. The classical antimitotic treatments are most often inefficient. The establishment of genetically characterized cell lines is therefore crucial for providing in vitro models for novel targeted therapies. We have used spectral karyotyping, fluorescence in situ hybridization with whole chromosome painting and locus-specific probes, and array-comparative genomic hybridization to identify the chromosomal and molecular alterations of a novel cell line established from a recurring sclerosing WDLPS. The karyotype was hypertriploid and showed multiple structural anomalies. All cells retained the presence of a giant marker chromosome that had been previously identified in the primary cell cultures. This giant chromosome contained high-level amplification of chromosomal regions 12q13-21 and lacked the alpha-satellite centromeric sequences associated with WDLPS/DDLPS. The 12q amplicon was large, containing 370 amplified genes. The DNA copy number ranged from 3 to 57. The highest levels of amplification were observed at 12ql4.3 for GNS, WIF1, and HMGA2. We analyzed the mRNA expression status by real-time reverse transcription polymerase chain reaction for six genes from this amplicon: MDM2, HMGA2, CDK4, TSPAN31, WIF1, and YEATS4. mRNA overexpression was correlated with genomic amplification. A second amplicon originating from 10p11-14 was also present in the giant marker chromosome. The 10p amplicon contained 62 genes, including oncogenes such as MLLT10, previously described in chimeric fusion with MLL in leukemias, NEBL, and BMI1.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B24O</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B08A</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Liposarcome</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Liposarcoma</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Liposarcoma</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Homme</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Human</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Hombre</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Lignée cellulaire</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Cell line</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Línea celular</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Sarcome des tissus mous</s0>
<s2>NM</s2>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Soft tissue sarcoma</s0>
<s2>NM</s2>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Sarcoma de tejidos blandos</s0>
<s2>NM</s2>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Lignée cellulaire établie</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Established cell line</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Línea celular establecida</s0>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Amplification</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Amplification</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Amplificación</s0>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Chromosome C12</s0>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Chromosome C12</s0>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Cromosoma C12</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Carte génétique</s0>
<s5>09</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Genetic mapping</s0>
<s5>09</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Mapa genético</s0>
<s5>09</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Chromosome C10</s0>
<s5>11</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Chromosome C10</s0>
<s5>11</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Cromosoma C10</s0>
<s5>11</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Gène onc cellulaire</s0>
<s5>12</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>C-Onc gene</s0>
<s5>12</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Gen onc celular</s0>
<s5>12</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Protooncogène</s0>
<s5>17</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Protooncogene</s0>
<s5>17</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Protooncogen</s0>
<s5>17</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Gène mdm2</s0>
<s5>18</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>mdm2 Gene</s0>
<s5>18</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA"><s0>Gen mdm2</s0>
<s5>18</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE"><s0>Anatomopathologie</s0>
<s5>19</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG"><s0>Anatomic pathology</s0>
<s5>19</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA"><s0>Anatomía patológica</s0>
<s5>19</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Pathologie du tissu adipeux</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Adipose tissue disorders</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Tejido adiposo patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Tumeur maligne</s0>
<s2>NM</s2>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Malignant tumor</s0>
<s2>NM</s2>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Tumor maligno</s0>
<s2>NM</s2>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Cancer</s0>
<s2>NM</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Cancer</s0>
<s2>NM</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Cáncer</s0>
<s2>NM</s2>
</fC07>
<fN21><s1>247</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>
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