Identification of novel candidate target genes in amplicons of Glioblastoma multiforme tumors detected by expression and CGH microarray profiling

<p<Abstract</p< <p<Background</p< <p<Conventional cytogenetic and comparative genomic hybridization (CGH) studies in brain malignancies have shown that glioblastoma multiforme (GBM) is characterized by complex structural and numerical alterations. However, the limited resolution of these techniques has precluded the precise identification of detailed specific gene copy number alterations.</p< <p<Results</p< <p<We performed a genome-wide survey of gene copy number changes in 20 primary GBMs by CGH on cDNA microarrays. A novel amplicon at 4p15, and previously uncharacterized amplicons at 13q32-34 and 1q32 were detected and are analyzed here. These amplicons contained amplified genes not previously reported. Other amplified regions containg well-known oncogenes in GBMs were also detected at 7p12 (<it<EGFR</it<), 7q21 (<it<CDK6</it<), 4q12 (<it<PDGFRA</it<), and 12q13-15 (<it<MDM2 </it<and <it<CDK4</it<). In order to identify the putative target genes of the amplifications, and to determine the changes in gene expression levels associated with copy number change events, we carried out parallel gene expression profiling analyses using the same cDNA microarrays. We detected overexpression of the novel amplified genes <it<SLA/LP </it<and <it<STIM2 </it<(4p15), and <it<TNFSF13B </it<and <it<COL4A2 </it<(13q32-34). Some of the candidate target genes of amplification (<it<EGFR, CDK6, MDM2</it<, <it<CDK4</it<, and <it<TNFSF13B</it<) were tested in an independent set of 111 primary GBMs by using FISH and immunohistological assays. The novel candidate 13q-amplification target <it<TNFSF13B </it<was amplified in 8% of the tumors, and showed protein expression in 20% of the GBMs.</p< <p<Conclusion</p< <p<This high-resolution analysis allowed us to propose novel candidate target genes such as <it<STIM2 </it<at 4p15, and <it<TNFSF13B </it<or <it<COL4A2 </it<at 13q32-34 that could potentially contribute to the pathogenesis of these tumors and which would require futher investigations. We showed that overexpression of the amplified genes could be attributable to gene dosage and speculate that deregulation of those genes could be important in the development and progression of GBM. Our findings highlight the important influence in GBM of signaling pathways such as the PI3K/AKT, consistent with the invasive features of this tumor.</p< Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Hernández-Moneo Jose-Luis [verfasserIn] de Lope Angel [verfasserIn] Gómez Elena [verfasserIn] Camacho Francisca I [verfasserIn] Fiaño Concepción [verfasserIn] Ribalta Teresa [verfasserIn] Mollejo Manuela [verfasserIn] Ruano Yolanda [verfasserIn] Martínez Pedro [verfasserIn] Meléndez Bárbara [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2006

Übergeordnetes Werk:	In: Molecular Cancer - BMC, 2003, 5(2006), 1, p 39
Übergeordnetes Werk:	volume:5 ; year:2006 ; number:1, p 39

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/1476-4598-5-39

Katalog-ID:	DOAJ043278345

Internformat


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520			\|a <p<Abstract</p< <p<Background</p< <p<Conventional cytogenetic and comparative genomic hybridization (CGH) studies in brain malignancies have shown that glioblastoma multiforme (GBM) is characterized by complex structural and numerical alterations. However, the limited resolution of these techniques has precluded the precise identification of detailed specific gene copy number alterations.</p< <p<Results</p< <p<We performed a genome-wide survey of gene copy number changes in 20 primary GBMs by CGH on cDNA microarrays. A novel amplicon at 4p15, and previously uncharacterized amplicons at 13q32-34 and 1q32 were detected and are analyzed here. These amplicons contained amplified genes not previously reported. Other amplified regions containg well-known oncogenes in GBMs were also detected at 7p12 (<it<EGFR</it<), 7q21 (<it<CDK6</it<), 4q12 (<it<PDGFRA</it<), and 12q13-15 (<it<MDM2 </it<and <it<CDK4</it<). In order to identify the putative target genes of the amplifications, and to determine the changes in gene expression levels associated with copy number change events, we carried out parallel gene expression profiling analyses using the same cDNA microarrays. We detected overexpression of the novel amplified genes <it<SLA/LP </it<and <it<STIM2 </it<(4p15), and <it<TNFSF13B </it<and <it<COL4A2 </it<(13q32-34). Some of the candidate target genes of amplification (<it<EGFR, CDK6, MDM2</it<, <it<CDK4</it<, and <it<TNFSF13B</it<) were tested in an independent set of 111 primary GBMs by using FISH and immunohistological assays. The novel candidate 13q-amplification target <it<TNFSF13B </it<was amplified in 8% of the tumors, and showed protein expression in 20% of the GBMs.</p< <p<Conclusion</p< <p<This high-resolution analysis allowed us to propose novel candidate target genes such as <it<STIM2 </it<at 4p15, and <it<TNFSF13B </it<or <it<COL4A2 </it<at 13q32-34 that could potentially contribute to the pathogenesis of these tumors and which would require futher investigations. We showed that overexpression of the amplified genes could be attributable to gene dosage and speculate that deregulation of those genes could be important in the development and progression of GBM. Our findings highlight the important influence in GBM of signaling pathways such as the PI3K/AKT, consistent with the invasive features of this tumor.</p<
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allfields	10.1186/1476-4598-5-39 doi (DE-627)DOAJ043278345 (DE-599)DOAJ7896976e49dd44c3849c20d5f2ee3a9d DE-627 ger DE-627 rakwb eng RC254-282 Hernández-Moneo Jose-Luis verfasserin aut Identification of novel candidate target genes in amplicons of Glioblastoma multiforme tumors detected by expression and CGH microarray profiling 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<Conventional cytogenetic and comparative genomic hybridization (CGH) studies in brain malignancies have shown that glioblastoma multiforme (GBM) is characterized by complex structural and numerical alterations. However, the limited resolution of these techniques has precluded the precise identification of detailed specific gene copy number alterations.</p< <p<Results</p< <p<We performed a genome-wide survey of gene copy number changes in 20 primary GBMs by CGH on cDNA microarrays. A novel amplicon at 4p15, and previously uncharacterized amplicons at 13q32-34 and 1q32 were detected and are analyzed here. These amplicons contained amplified genes not previously reported. Other amplified regions containg well-known oncogenes in GBMs were also detected at 7p12 (<it<EGFR</it<), 7q21 (<it<CDK6</it<), 4q12 (<it<PDGFRA</it<), and 12q13-15 (<it<MDM2 </it<and <it<CDK4</it<). In order to identify the putative target genes of the amplifications, and to determine the changes in gene expression levels associated with copy number change events, we carried out parallel gene expression profiling analyses using the same cDNA microarrays. We detected overexpression of the novel amplified genes <it<SLA/LP </it<and <it<STIM2 </it<(4p15), and <it<TNFSF13B </it<and <it<COL4A2 </it<(13q32-34). Some of the candidate target genes of amplification (<it<EGFR, CDK6, MDM2</it<, <it<CDK4</it<, and <it<TNFSF13B</it<) were tested in an independent set of 111 primary GBMs by using FISH and immunohistological assays. The novel candidate 13q-amplification target <it<TNFSF13B </it<was amplified in 8% of the tumors, and showed protein expression in 20% of the GBMs.</p< <p<Conclusion</p< <p<This high-resolution analysis allowed us to propose novel candidate target genes such as <it<STIM2 </it<at 4p15, and <it<TNFSF13B </it<or <it<COL4A2 </it<at 13q32-34 that could potentially contribute to the pathogenesis of these tumors and which would require futher investigations. We showed that overexpression of the amplified genes could be attributable to gene dosage and speculate that deregulation of those genes could be important in the development and progression of GBM. Our findings highlight the important influence in GBM of signaling pathways such as the PI3K/AKT, consistent with the invasive features of this tumor.</p< Neoplasms. Tumors. Oncology. Including cancer and carcinogens de Lope Angel verfasserin aut Gómez Elena verfasserin aut Camacho Francisca I verfasserin aut Fiaño Concepción verfasserin aut Ribalta Teresa verfasserin aut Mollejo Manuela verfasserin aut Ruano Yolanda verfasserin aut Martínez Pedro verfasserin aut Meléndez Bárbara verfasserin aut In Molecular Cancer BMC, 2003 5(2006), 1, p 39 (DE-627)355987619 (DE-600)2091373-4 14764598 nnns volume:5 year:2006 number:1, p 39 https://doi.org/10.1186/1476-4598-5-39 kostenfrei https://doaj.org/article/7896976e49dd44c3849c20d5f2ee3a9d kostenfrei http://www.molecular-cancer.com/content/5/1/39 kostenfrei https://doaj.org/toc/1476-4598 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2006 1, p 39
spelling	10.1186/1476-4598-5-39 doi (DE-627)DOAJ043278345 (DE-599)DOAJ7896976e49dd44c3849c20d5f2ee3a9d DE-627 ger DE-627 rakwb eng RC254-282 Hernández-Moneo Jose-Luis verfasserin aut Identification of novel candidate target genes in amplicons of Glioblastoma multiforme tumors detected by expression and CGH microarray profiling 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<Conventional cytogenetic and comparative genomic hybridization (CGH) studies in brain malignancies have shown that glioblastoma multiforme (GBM) is characterized by complex structural and numerical alterations. However, the limited resolution of these techniques has precluded the precise identification of detailed specific gene copy number alterations.</p< <p<Results</p< <p<We performed a genome-wide survey of gene copy number changes in 20 primary GBMs by CGH on cDNA microarrays. A novel amplicon at 4p15, and previously uncharacterized amplicons at 13q32-34 and 1q32 were detected and are analyzed here. These amplicons contained amplified genes not previously reported. Other amplified regions containg well-known oncogenes in GBMs were also detected at 7p12 (<it<EGFR</it<), 7q21 (<it<CDK6</it<), 4q12 (<it<PDGFRA</it<), and 12q13-15 (<it<MDM2 </it<and <it<CDK4</it<). In order to identify the putative target genes of the amplifications, and to determine the changes in gene expression levels associated with copy number change events, we carried out parallel gene expression profiling analyses using the same cDNA microarrays. We detected overexpression of the novel amplified genes <it<SLA/LP </it<and <it<STIM2 </it<(4p15), and <it<TNFSF13B </it<and <it<COL4A2 </it<(13q32-34). Some of the candidate target genes of amplification (<it<EGFR, CDK6, MDM2</it<, <it<CDK4</it<, and <it<TNFSF13B</it<) were tested in an independent set of 111 primary GBMs by using FISH and immunohistological assays. The novel candidate 13q-amplification target <it<TNFSF13B </it<was amplified in 8% of the tumors, and showed protein expression in 20% of the GBMs.</p< <p<Conclusion</p< <p<This high-resolution analysis allowed us to propose novel candidate target genes such as <it<STIM2 </it<at 4p15, and <it<TNFSF13B </it<or <it<COL4A2 </it<at 13q32-34 that could potentially contribute to the pathogenesis of these tumors and which would require futher investigations. We showed that overexpression of the amplified genes could be attributable to gene dosage and speculate that deregulation of those genes could be important in the development and progression of GBM. Our findings highlight the important influence in GBM of signaling pathways such as the PI3K/AKT, consistent with the invasive features of this tumor.</p< Neoplasms. Tumors. Oncology. Including cancer and carcinogens de Lope Angel verfasserin aut Gómez Elena verfasserin aut Camacho Francisca I verfasserin aut Fiaño Concepción verfasserin aut Ribalta Teresa verfasserin aut Mollejo Manuela verfasserin aut Ruano Yolanda verfasserin aut Martínez Pedro verfasserin aut Meléndez Bárbara verfasserin aut In Molecular Cancer BMC, 2003 5(2006), 1, p 39 (DE-627)355987619 (DE-600)2091373-4 14764598 nnns volume:5 year:2006 number:1, p 39 https://doi.org/10.1186/1476-4598-5-39 kostenfrei https://doaj.org/article/7896976e49dd44c3849c20d5f2ee3a9d kostenfrei http://www.molecular-cancer.com/content/5/1/39 kostenfrei https://doaj.org/toc/1476-4598 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2006 1, p 39
allfields_unstemmed	10.1186/1476-4598-5-39 doi (DE-627)DOAJ043278345 (DE-599)DOAJ7896976e49dd44c3849c20d5f2ee3a9d DE-627 ger DE-627 rakwb eng RC254-282 Hernández-Moneo Jose-Luis verfasserin aut Identification of novel candidate target genes in amplicons of Glioblastoma multiforme tumors detected by expression and CGH microarray profiling 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<Conventional cytogenetic and comparative genomic hybridization (CGH) studies in brain malignancies have shown that glioblastoma multiforme (GBM) is characterized by complex structural and numerical alterations. However, the limited resolution of these techniques has precluded the precise identification of detailed specific gene copy number alterations.</p< <p<Results</p< <p<We performed a genome-wide survey of gene copy number changes in 20 primary GBMs by CGH on cDNA microarrays. A novel amplicon at 4p15, and previously uncharacterized amplicons at 13q32-34 and 1q32 were detected and are analyzed here. These amplicons contained amplified genes not previously reported. Other amplified regions containg well-known oncogenes in GBMs were also detected at 7p12 (<it<EGFR</it<), 7q21 (<it<CDK6</it<), 4q12 (<it<PDGFRA</it<), and 12q13-15 (<it<MDM2 </it<and <it<CDK4</it<). In order to identify the putative target genes of the amplifications, and to determine the changes in gene expression levels associated with copy number change events, we carried out parallel gene expression profiling analyses using the same cDNA microarrays. We detected overexpression of the novel amplified genes <it<SLA/LP </it<and <it<STIM2 </it<(4p15), and <it<TNFSF13B </it<and <it<COL4A2 </it<(13q32-34). Some of the candidate target genes of amplification (<it<EGFR, CDK6, MDM2</it<, <it<CDK4</it<, and <it<TNFSF13B</it<) were tested in an independent set of 111 primary GBMs by using FISH and immunohistological assays. The novel candidate 13q-amplification target <it<TNFSF13B </it<was amplified in 8% of the tumors, and showed protein expression in 20% of the GBMs.</p< <p<Conclusion</p< <p<This high-resolution analysis allowed us to propose novel candidate target genes such as <it<STIM2 </it<at 4p15, and <it<TNFSF13B </it<or <it<COL4A2 </it<at 13q32-34 that could potentially contribute to the pathogenesis of these tumors and which would require futher investigations. We showed that overexpression of the amplified genes could be attributable to gene dosage and speculate that deregulation of those genes could be important in the development and progression of GBM. Our findings highlight the important influence in GBM of signaling pathways such as the PI3K/AKT, consistent with the invasive features of this tumor.</p< Neoplasms. Tumors. Oncology. Including cancer and carcinogens de Lope Angel verfasserin aut Gómez Elena verfasserin aut Camacho Francisca I verfasserin aut Fiaño Concepción verfasserin aut Ribalta Teresa verfasserin aut Mollejo Manuela verfasserin aut Ruano Yolanda verfasserin aut Martínez Pedro verfasserin aut Meléndez Bárbara verfasserin aut In Molecular Cancer BMC, 2003 5(2006), 1, p 39 (DE-627)355987619 (DE-600)2091373-4 14764598 nnns volume:5 year:2006 number:1, p 39 https://doi.org/10.1186/1476-4598-5-39 kostenfrei https://doaj.org/article/7896976e49dd44c3849c20d5f2ee3a9d kostenfrei http://www.molecular-cancer.com/content/5/1/39 kostenfrei https://doaj.org/toc/1476-4598 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2006 1, p 39
allfieldsGer	10.1186/1476-4598-5-39 doi (DE-627)DOAJ043278345 (DE-599)DOAJ7896976e49dd44c3849c20d5f2ee3a9d DE-627 ger DE-627 rakwb eng RC254-282 Hernández-Moneo Jose-Luis verfasserin aut Identification of novel candidate target genes in amplicons of Glioblastoma multiforme tumors detected by expression and CGH microarray profiling 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<Conventional cytogenetic and comparative genomic hybridization (CGH) studies in brain malignancies have shown that glioblastoma multiforme (GBM) is characterized by complex structural and numerical alterations. However, the limited resolution of these techniques has precluded the precise identification of detailed specific gene copy number alterations.</p< <p<Results</p< <p<We performed a genome-wide survey of gene copy number changes in 20 primary GBMs by CGH on cDNA microarrays. A novel amplicon at 4p15, and previously uncharacterized amplicons at 13q32-34 and 1q32 were detected and are analyzed here. These amplicons contained amplified genes not previously reported. Other amplified regions containg well-known oncogenes in GBMs were also detected at 7p12 (<it<EGFR</it<), 7q21 (<it<CDK6</it<), 4q12 (<it<PDGFRA</it<), and 12q13-15 (<it<MDM2 </it<and <it<CDK4</it<). In order to identify the putative target genes of the amplifications, and to determine the changes in gene expression levels associated with copy number change events, we carried out parallel gene expression profiling analyses using the same cDNA microarrays. We detected overexpression of the novel amplified genes <it<SLA/LP </it<and <it<STIM2 </it<(4p15), and <it<TNFSF13B </it<and <it<COL4A2 </it<(13q32-34). Some of the candidate target genes of amplification (<it<EGFR, CDK6, MDM2</it<, <it<CDK4</it<, and <it<TNFSF13B</it<) were tested in an independent set of 111 primary GBMs by using FISH and immunohistological assays. The novel candidate 13q-amplification target <it<TNFSF13B </it<was amplified in 8% of the tumors, and showed protein expression in 20% of the GBMs.</p< <p<Conclusion</p< <p<This high-resolution analysis allowed us to propose novel candidate target genes such as <it<STIM2 </it<at 4p15, and <it<TNFSF13B </it<or <it<COL4A2 </it<at 13q32-34 that could potentially contribute to the pathogenesis of these tumors and which would require futher investigations. We showed that overexpression of the amplified genes could be attributable to gene dosage and speculate that deregulation of those genes could be important in the development and progression of GBM. Our findings highlight the important influence in GBM of signaling pathways such as the PI3K/AKT, consistent with the invasive features of this tumor.</p< Neoplasms. Tumors. Oncology. Including cancer and carcinogens de Lope Angel verfasserin aut Gómez Elena verfasserin aut Camacho Francisca I verfasserin aut Fiaño Concepción verfasserin aut Ribalta Teresa verfasserin aut Mollejo Manuela verfasserin aut Ruano Yolanda verfasserin aut Martínez Pedro verfasserin aut Meléndez Bárbara verfasserin aut In Molecular Cancer BMC, 2003 5(2006), 1, p 39 (DE-627)355987619 (DE-600)2091373-4 14764598 nnns volume:5 year:2006 number:1, p 39 https://doi.org/10.1186/1476-4598-5-39 kostenfrei https://doaj.org/article/7896976e49dd44c3849c20d5f2ee3a9d kostenfrei http://www.molecular-cancer.com/content/5/1/39 kostenfrei https://doaj.org/toc/1476-4598 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2006 1, p 39
allfieldsSound	10.1186/1476-4598-5-39 doi (DE-627)DOAJ043278345 (DE-599)DOAJ7896976e49dd44c3849c20d5f2ee3a9d DE-627 ger DE-627 rakwb eng RC254-282 Hernández-Moneo Jose-Luis verfasserin aut Identification of novel candidate target genes in amplicons of Glioblastoma multiforme tumors detected by expression and CGH microarray profiling 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<Conventional cytogenetic and comparative genomic hybridization (CGH) studies in brain malignancies have shown that glioblastoma multiforme (GBM) is characterized by complex structural and numerical alterations. However, the limited resolution of these techniques has precluded the precise identification of detailed specific gene copy number alterations.</p< <p<Results</p< <p<We performed a genome-wide survey of gene copy number changes in 20 primary GBMs by CGH on cDNA microarrays. A novel amplicon at 4p15, and previously uncharacterized amplicons at 13q32-34 and 1q32 were detected and are analyzed here. These amplicons contained amplified genes not previously reported. Other amplified regions containg well-known oncogenes in GBMs were also detected at 7p12 (<it<EGFR</it<), 7q21 (<it<CDK6</it<), 4q12 (<it<PDGFRA</it<), and 12q13-15 (<it<MDM2 </it<and <it<CDK4</it<). In order to identify the putative target genes of the amplifications, and to determine the changes in gene expression levels associated with copy number change events, we carried out parallel gene expression profiling analyses using the same cDNA microarrays. We detected overexpression of the novel amplified genes <it<SLA/LP </it<and <it<STIM2 </it<(4p15), and <it<TNFSF13B </it<and <it<COL4A2 </it<(13q32-34). Some of the candidate target genes of amplification (<it<EGFR, CDK6, MDM2</it<, <it<CDK4</it<, and <it<TNFSF13B</it<) were tested in an independent set of 111 primary GBMs by using FISH and immunohistological assays. The novel candidate 13q-amplification target <it<TNFSF13B </it<was amplified in 8% of the tumors, and showed protein expression in 20% of the GBMs.</p< <p<Conclusion</p< <p<This high-resolution analysis allowed us to propose novel candidate target genes such as <it<STIM2 </it<at 4p15, and <it<TNFSF13B </it<or <it<COL4A2 </it<at 13q32-34 that could potentially contribute to the pathogenesis of these tumors and which would require futher investigations. We showed that overexpression of the amplified genes could be attributable to gene dosage and speculate that deregulation of those genes could be important in the development and progression of GBM. Our findings highlight the important influence in GBM of signaling pathways such as the PI3K/AKT, consistent with the invasive features of this tumor.</p< Neoplasms. Tumors. Oncology. Including cancer and carcinogens de Lope Angel verfasserin aut Gómez Elena verfasserin aut Camacho Francisca I verfasserin aut Fiaño Concepción verfasserin aut Ribalta Teresa verfasserin aut Mollejo Manuela verfasserin aut Ruano Yolanda verfasserin aut Martínez Pedro verfasserin aut Meléndez Bárbara verfasserin aut In Molecular Cancer BMC, 2003 5(2006), 1, p 39 (DE-627)355987619 (DE-600)2091373-4 14764598 nnns volume:5 year:2006 number:1, p 39 https://doi.org/10.1186/1476-4598-5-39 kostenfrei https://doaj.org/article/7896976e49dd44c3849c20d5f2ee3a9d kostenfrei http://www.molecular-cancer.com/content/5/1/39 kostenfrei https://doaj.org/toc/1476-4598 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2006 1, p 39
language	English
source	In Molecular Cancer 5(2006), 1, p 39 volume:5 year:2006 number:1, p 39
sourceStr	In Molecular Cancer 5(2006), 1, p 39 volume:5 year:2006 number:1, p 39
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Neoplasms. Tumors. Oncology. Including cancer and carcinogens
isfreeaccess_bool	true
container_title	Molecular Cancer
authorswithroles_txt_mv	Hernández-Moneo Jose-Luis @@aut@@ de Lope Angel @@aut@@ Gómez Elena @@aut@@ Camacho Francisca I @@aut@@ Fiaño Concepción @@aut@@ Ribalta Teresa @@aut@@ Mollejo Manuela @@aut@@ Ruano Yolanda @@aut@@ Martínez Pedro @@aut@@ Meléndez Bárbara @@aut@@
publishDateDaySort_date	2006-01-01T00:00:00Z
hierarchy_top_id	355987619
id	DOAJ043278345
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ043278345</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230308071207.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230227s2006 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1186/1476-4598-5-39</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ043278345</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ7896976e49dd44c3849c20d5f2ee3a9d</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RC254-282</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Hernández-Moneo Jose-Luis</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Identification of novel candidate target genes in amplicons of Glioblastoma multiforme tumors detected by expression and CGH microarray profiling</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2006</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a"><p<Abstract</p< <p<Background</p< <p<Conventional cytogenetic and comparative genomic hybridization (CGH) studies in brain malignancies have shown that glioblastoma multiforme (GBM) is characterized by complex structural and numerical alterations. However, the limited resolution of these techniques has precluded the precise identification of detailed specific gene copy number alterations.</p< <p<Results</p< <p<We performed a genome-wide survey of gene copy number changes in 20 primary GBMs by CGH on cDNA microarrays. A novel amplicon at 4p15, and previously uncharacterized amplicons at 13q32-34 and 1q32 were detected and are analyzed here. These amplicons contained amplified genes not previously reported. Other amplified regions containg well-known oncogenes in GBMs were also detected at 7p12 (<it<EGFR</it<), 7q21 (<it<CDK6</it<), 4q12 (<it<PDGFRA</it<), and 12q13-15 (<it<MDM2 </it<and <it<CDK4</it<). In order to identify the putative target genes of the amplifications, and to determine the changes in gene expression levels associated with copy number change events, we carried out parallel gene expression profiling analyses using the same cDNA microarrays. 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callnumber-first	R - Medicine
author	Hernández-Moneo Jose-Luis
spellingShingle	Hernández-Moneo Jose-Luis misc RC254-282 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens Identification of novel candidate target genes in amplicons of Glioblastoma multiforme tumors detected by expression and CGH microarray profiling
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topic_title	RC254-282 Identification of novel candidate target genes in amplicons of Glioblastoma multiforme tumors detected by expression and CGH microarray profiling
topic	misc RC254-282 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
topic_unstemmed	misc RC254-282 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
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title	Identification of novel candidate target genes in amplicons of Glioblastoma multiforme tumors detected by expression and CGH microarray profiling
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title_full	Identification of novel candidate target genes in amplicons of Glioblastoma multiforme tumors detected by expression and CGH microarray profiling
author_sort	Hernández-Moneo Jose-Luis
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author_browse	Hernández-Moneo Jose-Luis de Lope Angel Gómez Elena Camacho Francisca I Fiaño Concepción Ribalta Teresa Mollejo Manuela Ruano Yolanda Martínez Pedro Meléndez Bárbara
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title_sort	identification of novel candidate target genes in amplicons of glioblastoma multiforme tumors detected by expression and cgh microarray profiling
callnumber	RC254-282
title_auth	Identification of novel candidate target genes in amplicons of Glioblastoma multiforme tumors detected by expression and CGH microarray profiling
abstract	<p<Abstract</p< <p<Background</p< <p<Conventional cytogenetic and comparative genomic hybridization (CGH) studies in brain malignancies have shown that glioblastoma multiforme (GBM) is characterized by complex structural and numerical alterations. However, the limited resolution of these techniques has precluded the precise identification of detailed specific gene copy number alterations.</p< <p<Results</p< <p<We performed a genome-wide survey of gene copy number changes in 20 primary GBMs by CGH on cDNA microarrays. A novel amplicon at 4p15, and previously uncharacterized amplicons at 13q32-34 and 1q32 were detected and are analyzed here. These amplicons contained amplified genes not previously reported. Other amplified regions containg well-known oncogenes in GBMs were also detected at 7p12 (<it<EGFR</it<), 7q21 (<it<CDK6</it<), 4q12 (<it<PDGFRA</it<), and 12q13-15 (<it<MDM2 </it<and <it<CDK4</it<). In order to identify the putative target genes of the amplifications, and to determine the changes in gene expression levels associated with copy number change events, we carried out parallel gene expression profiling analyses using the same cDNA microarrays. We detected overexpression of the novel amplified genes <it<SLA/LP </it<and <it<STIM2 </it<(4p15), and <it<TNFSF13B </it<and <it<COL4A2 </it<(13q32-34). Some of the candidate target genes of amplification (<it<EGFR, CDK6, MDM2</it<, <it<CDK4</it<, and <it<TNFSF13B</it<) were tested in an independent set of 111 primary GBMs by using FISH and immunohistological assays. The novel candidate 13q-amplification target <it<TNFSF13B </it<was amplified in 8% of the tumors, and showed protein expression in 20% of the GBMs.</p< <p<Conclusion</p< <p<This high-resolution analysis allowed us to propose novel candidate target genes such as <it<STIM2 </it<at 4p15, and <it<TNFSF13B </it<or <it<COL4A2 </it<at 13q32-34 that could potentially contribute to the pathogenesis of these tumors and which would require futher investigations. We showed that overexpression of the amplified genes could be attributable to gene dosage and speculate that deregulation of those genes could be important in the development and progression of GBM. Our findings highlight the important influence in GBM of signaling pathways such as the PI3K/AKT, consistent with the invasive features of this tumor.</p<
abstractGer	<p<Abstract</p< <p<Background</p< <p<Conventional cytogenetic and comparative genomic hybridization (CGH) studies in brain malignancies have shown that glioblastoma multiforme (GBM) is characterized by complex structural and numerical alterations. However, the limited resolution of these techniques has precluded the precise identification of detailed specific gene copy number alterations.</p< <p<Results</p< <p<We performed a genome-wide survey of gene copy number changes in 20 primary GBMs by CGH on cDNA microarrays. A novel amplicon at 4p15, and previously uncharacterized amplicons at 13q32-34 and 1q32 were detected and are analyzed here. These amplicons contained amplified genes not previously reported. Other amplified regions containg well-known oncogenes in GBMs were also detected at 7p12 (<it<EGFR</it<), 7q21 (<it<CDK6</it<), 4q12 (<it<PDGFRA</it<), and 12q13-15 (<it<MDM2 </it<and <it<CDK4</it<). In order to identify the putative target genes of the amplifications, and to determine the changes in gene expression levels associated with copy number change events, we carried out parallel gene expression profiling analyses using the same cDNA microarrays. We detected overexpression of the novel amplified genes <it<SLA/LP </it<and <it<STIM2 </it<(4p15), and <it<TNFSF13B </it<and <it<COL4A2 </it<(13q32-34). Some of the candidate target genes of amplification (<it<EGFR, CDK6, MDM2</it<, <it<CDK4</it<, and <it<TNFSF13B</it<) were tested in an independent set of 111 primary GBMs by using FISH and immunohistological assays. The novel candidate 13q-amplification target <it<TNFSF13B </it<was amplified in 8% of the tumors, and showed protein expression in 20% of the GBMs.</p< <p<Conclusion</p< <p<This high-resolution analysis allowed us to propose novel candidate target genes such as <it<STIM2 </it<at 4p15, and <it<TNFSF13B </it<or <it<COL4A2 </it<at 13q32-34 that could potentially contribute to the pathogenesis of these tumors and which would require futher investigations. We showed that overexpression of the amplified genes could be attributable to gene dosage and speculate that deregulation of those genes could be important in the development and progression of GBM. Our findings highlight the important influence in GBM of signaling pathways such as the PI3K/AKT, consistent with the invasive features of this tumor.</p<
abstract_unstemmed	<p<Abstract</p< <p<Background</p< <p<Conventional cytogenetic and comparative genomic hybridization (CGH) studies in brain malignancies have shown that glioblastoma multiforme (GBM) is characterized by complex structural and numerical alterations. However, the limited resolution of these techniques has precluded the precise identification of detailed specific gene copy number alterations.</p< <p<Results</p< <p<We performed a genome-wide survey of gene copy number changes in 20 primary GBMs by CGH on cDNA microarrays. A novel amplicon at 4p15, and previously uncharacterized amplicons at 13q32-34 and 1q32 were detected and are analyzed here. These amplicons contained amplified genes not previously reported. Other amplified regions containg well-known oncogenes in GBMs were also detected at 7p12 (<it<EGFR</it<), 7q21 (<it<CDK6</it<), 4q12 (<it<PDGFRA</it<), and 12q13-15 (<it<MDM2 </it<and <it<CDK4</it<). In order to identify the putative target genes of the amplifications, and to determine the changes in gene expression levels associated with copy number change events, we carried out parallel gene expression profiling analyses using the same cDNA microarrays. We detected overexpression of the novel amplified genes <it<SLA/LP </it<and <it<STIM2 </it<(4p15), and <it<TNFSF13B </it<and <it<COL4A2 </it<(13q32-34). Some of the candidate target genes of amplification (<it<EGFR, CDK6, MDM2</it<, <it<CDK4</it<, and <it<TNFSF13B</it<) were tested in an independent set of 111 primary GBMs by using FISH and immunohistological assays. The novel candidate 13q-amplification target <it<TNFSF13B </it<was amplified in 8% of the tumors, and showed protein expression in 20% of the GBMs.</p< <p<Conclusion</p< <p<This high-resolution analysis allowed us to propose novel candidate target genes such as <it<STIM2 </it<at 4p15, and <it<TNFSF13B </it<or <it<COL4A2 </it<at 13q32-34 that could potentially contribute to the pathogenesis of these tumors and which would require futher investigations. We showed that overexpression of the amplified genes could be attributable to gene dosage and speculate that deregulation of those genes could be important in the development and progression of GBM. Our findings highlight the important influence in GBM of signaling pathways such as the PI3K/AKT, consistent with the invasive features of this tumor.</p<
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title_short	Identification of novel candidate target genes in amplicons of Glioblastoma multiforme tumors detected by expression and CGH microarray profiling
url	https://doi.org/10.1186/1476-4598-5-39 https://doaj.org/article/7896976e49dd44c3849c20d5f2ee3a9d http://www.molecular-cancer.com/content/5/1/39 https://doaj.org/toc/1476-4598
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However, the limited resolution of these techniques has precluded the precise identification of detailed specific gene copy number alterations.</p< <p<Results</p< <p<We performed a genome-wide survey of gene copy number changes in 20 primary GBMs by CGH on cDNA microarrays. A novel amplicon at 4p15, and previously uncharacterized amplicons at 13q32-34 and 1q32 were detected and are analyzed here. These amplicons contained amplified genes not previously reported. Other amplified regions containg well-known oncogenes in GBMs were also detected at 7p12 (<it<EGFR</it<), 7q21 (<it<CDK6</it<), 4q12 (<it<PDGFRA</it<), and 12q13-15 (<it<MDM2 </it<and <it<CDK4</it<). In order to identify the putative target genes of the amplifications, and to determine the changes in gene expression levels associated with copy number change events, we carried out parallel gene expression profiling analyses using the same cDNA microarrays. We detected overexpression of the novel amplified genes <it<SLA/LP </it<and <it<STIM2 </it<(4p15), and <it<TNFSF13B </it<and <it<COL4A2 </it<(13q32-34). Some of the candidate target genes of amplification (<it<EGFR, CDK6, MDM2</it<, <it<CDK4</it<, and <it<TNFSF13B</it<) were tested in an independent set of 111 primary GBMs by using FISH and immunohistological assays. The novel candidate 13q-amplification target <it<TNFSF13B </it<was amplified in 8% of the tumors, and showed protein expression in 20% of the GBMs.</p< <p<Conclusion</p< <p<This high-resolution analysis allowed us to propose novel candidate target genes such as <it<STIM2 </it<at 4p15, and <it<TNFSF13B </it<or <it<COL4A2 </it<at 13q32-34 that could potentially contribute to the pathogenesis of these tumors and which would require futher investigations. We showed that overexpression of the amplified genes could be attributable to gene dosage and speculate that deregulation of those genes could be important in the development and progression of GBM. Our findings highlight the important influence in GBM of signaling pathways such as the PI3K/AKT, consistent with the invasive features of this tumor.</p<</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Neoplasms. Tumors. Oncology. 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Identification of novel candidate target genes in amplicons of Glioblastoma multiforme tumors detected by expression and CGH microarray profiling

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