High-resolution analysis of DNA copy number alterations and gene expression in renal clear cell carcinoma
We analysed chromosomal copy number aberrations (CNAs) in renal cell carcinomas by array-based comparative genomic hybridization, using a genome-wide scanning array with 2304 BAC and PAC clones covering the whole human genome at a resolution of roughly 1.3 Mb. A total of 30 samples of renal cell car...
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| Veröffentlicht in: | The Journal of pathology 2007-12, Vol.213 (4), p.392-401 |
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| creator | Yoshimoto, T Matsuura, K Karnan, S Tagawa, H Nakada, C Tanigawa, M Tsukamoto, Y Uchida, T Kashima, K Akizuki, S Takeuchi, I Sato, F Mimata, H Seto, M Moriyama, M |
| description | We analysed chromosomal copy number aberrations (CNAs) in renal cell carcinomas by array-based comparative genomic hybridization, using a genome-wide scanning array with 2304 BAC and PAC clones covering the whole human genome at a resolution of roughly 1.3 Mb. A total of 30 samples of renal cell carcinoma were analysed, including 26 cases of clear cell carcinoma (CCC) and four cases of chromophobe renal cell carcinoma (ChCC). In CCCs, gains of chromosomes 5q33.1-qter (58%), 7q11.22-q35 (35%) and 16p12.3-p13.12 (19%), and losses of chromosomes 3p25.1-p25.3 (77%), 3p21.31-p22.3 (81%), 3p14.1-p14.2 (77%), 8p23.3 (31%), 9q21.13-qter (19%) and 14q32.32-qter (38%) were detected. On the other hand, the patterns of CNAs differed markedly between CCCs and ChCCs. Next, we examined the correlation of CNAs with expression profiles in the same tumour samples in 22/26 cases of CCC, using oligonucleotide microarray. We extracted genes that were differentially expressed between cases with and without CNAs, and found that significantly more up-regulated genes were localized on chromosomes 5 and 7, where recurrent genomic gains have been detected. Conversely, significantly more down-regulated genes were localized on chromosomes 14 and 3, where recurrent genomic losses have been detected. These results revealed that CNAs were correlated with deregulation of gene expression in CCCs. Furthermore, we compared the patterns of genomic imbalance with histopathological features, and found that loss of 14q appeared to be a specific and additional genetic abnormality in high-grade CCC. When we compared the expression profiles of low-grade CCCs with those of high-grade CCCs, differentially down-regulated genes tended to be localized on chromosomes 14 and 9. Thus, it is suggested that copy number loss at 14q in high-grade CCC may be involved in the down-regulation of genes located in this region. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. |
| doi_str_mv | 10.1002/path.2239 |
| format | Article |
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A total of 30 samples of renal cell carcinoma were analysed, including 26 cases of clear cell carcinoma (CCC) and four cases of chromophobe renal cell carcinoma (ChCC). In CCCs, gains of chromosomes 5q33.1-qter (58%), 7q11.22-q35 (35%) and 16p12.3-p13.12 (19%), and losses of chromosomes 3p25.1-p25.3 (77%), 3p21.31-p22.3 (81%), 3p14.1-p14.2 (77%), 8p23.3 (31%), 9q21.13-qter (19%) and 14q32.32-qter (38%) were detected. On the other hand, the patterns of CNAs differed markedly between CCCs and ChCCs. Next, we examined the correlation of CNAs with expression profiles in the same tumour samples in 22/26 cases of CCC, using oligonucleotide microarray. We extracted genes that were differentially expressed between cases with and without CNAs, and found that significantly more up-regulated genes were localized on chromosomes 5 and 7, where recurrent genomic gains have been detected. Conversely, significantly more down-regulated genes were localized on chromosomes 14 and 3, where recurrent genomic losses have been detected. These results revealed that CNAs were correlated with deregulation of gene expression in CCCs. Furthermore, we compared the patterns of genomic imbalance with histopathological features, and found that loss of 14q appeared to be a specific and additional genetic abnormality in high-grade CCC. When we compared the expression profiles of low-grade CCCs with those of high-grade CCCs, differentially down-regulated genes tended to be localized on chromosomes 14 and 9. Thus, it is suggested that copy number loss at 14q in high-grade CCC may be involved in the down-regulation of genes located in this region. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</description><identifier>ISSN: 0022-3417</identifier><identifier>EISSN: 1096-9896</identifier><identifier>DOI: 10.1002/path.2239</identifier><identifier>PMID: 17922474</identifier><identifier>CODEN: JPTLAS</identifier><language>eng</language><publisher>Chichester, UK: John Wiley & Sons, Ltd</publisher><subject>Aged ; Aged, 80 and over ; array CGH ; Biological and medical sciences ; Carcinoma, Renal Cell - genetics ; Carcinoma, Renal Cell - pathology ; Chromosome Aberrations ; Chromosomes, Human, Pair 14 - genetics ; clear cell carcinoma ; DNA, Neoplasm - genetics ; Down-Regulation - genetics ; Female ; Gene Dosage - genetics ; gene expression ; Gene Expression Profiling - methods ; Gene Expression Regulation, Neoplastic ; Humans ; Investigative techniques, diagnostic techniques (general aspects) ; Kidney Neoplasms - genetics ; Kidney Neoplasms - pathology ; Kidneys ; Male ; Medical sciences ; Middle Aged ; Nephrology. Urinary tract diseases ; Nucleic Acid Hybridization - methods ; Oligonucleotide Array Sequence Analysis - methods ; oligonucleotide microarray ; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques ; renal cell carcinoma ; Sequence Analysis, DNA - methods ; Tumors of the urinary system</subject><ispartof>The Journal of pathology, 2007-12, Vol.213 (4), p.392-401</ispartof><rights>Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</rights><rights>2008 INIST-CNRS</rights><rights>(c) 2007 Pathological Society of Great Britain and Ireland</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4819-6d74d7740d9482e27f0f4439257a690eea0e508ea684a598228d582cb084f8353</citedby><cites>FETCH-LOGICAL-c4819-6d74d7740d9482e27f0f4439257a690eea0e508ea684a598228d582cb084f8353</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fpath.2239$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fpath.2239$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,27923,27924,45573,45574</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19438621$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17922474$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yoshimoto, T</creatorcontrib><creatorcontrib>Matsuura, K</creatorcontrib><creatorcontrib>Karnan, S</creatorcontrib><creatorcontrib>Tagawa, H</creatorcontrib><creatorcontrib>Nakada, C</creatorcontrib><creatorcontrib>Tanigawa, M</creatorcontrib><creatorcontrib>Tsukamoto, Y</creatorcontrib><creatorcontrib>Uchida, T</creatorcontrib><creatorcontrib>Kashima, K</creatorcontrib><creatorcontrib>Akizuki, S</creatorcontrib><creatorcontrib>Takeuchi, I</creatorcontrib><creatorcontrib>Sato, F</creatorcontrib><creatorcontrib>Mimata, H</creatorcontrib><creatorcontrib>Seto, M</creatorcontrib><creatorcontrib>Moriyama, M</creatorcontrib><title>High-resolution analysis of DNA copy number alterations and gene expression in renal clear cell carcinoma</title><title>The Journal of pathology</title><addtitle>J. Pathol</addtitle><description>We analysed chromosomal copy number aberrations (CNAs) in renal cell carcinomas by array-based comparative genomic hybridization, using a genome-wide scanning array with 2304 BAC and PAC clones covering the whole human genome at a resolution of roughly 1.3 Mb. A total of 30 samples of renal cell carcinoma were analysed, including 26 cases of clear cell carcinoma (CCC) and four cases of chromophobe renal cell carcinoma (ChCC). In CCCs, gains of chromosomes 5q33.1-qter (58%), 7q11.22-q35 (35%) and 16p12.3-p13.12 (19%), and losses of chromosomes 3p25.1-p25.3 (77%), 3p21.31-p22.3 (81%), 3p14.1-p14.2 (77%), 8p23.3 (31%), 9q21.13-qter (19%) and 14q32.32-qter (38%) were detected. On the other hand, the patterns of CNAs differed markedly between CCCs and ChCCs. Next, we examined the correlation of CNAs with expression profiles in the same tumour samples in 22/26 cases of CCC, using oligonucleotide microarray. We extracted genes that were differentially expressed between cases with and without CNAs, and found that significantly more up-regulated genes were localized on chromosomes 5 and 7, where recurrent genomic gains have been detected. Conversely, significantly more down-regulated genes were localized on chromosomes 14 and 3, where recurrent genomic losses have been detected. These results revealed that CNAs were correlated with deregulation of gene expression in CCCs. Furthermore, we compared the patterns of genomic imbalance with histopathological features, and found that loss of 14q appeared to be a specific and additional genetic abnormality in high-grade CCC. When we compared the expression profiles of low-grade CCCs with those of high-grade CCCs, differentially down-regulated genes tended to be localized on chromosomes 14 and 9. Thus, it is suggested that copy number loss at 14q in high-grade CCC may be involved in the down-regulation of genes located in this region. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>array CGH</subject><subject>Biological and medical sciences</subject><subject>Carcinoma, Renal Cell - genetics</subject><subject>Carcinoma, Renal Cell - pathology</subject><subject>Chromosome Aberrations</subject><subject>Chromosomes, Human, Pair 14 - genetics</subject><subject>clear cell carcinoma</subject><subject>DNA, Neoplasm - genetics</subject><subject>Down-Regulation - genetics</subject><subject>Female</subject><subject>Gene Dosage - genetics</subject><subject>gene expression</subject><subject>Gene Expression Profiling - methods</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>Kidney Neoplasms - genetics</subject><subject>Kidney Neoplasms - pathology</subject><subject>Kidneys</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nucleic Acid Hybridization - methods</subject><subject>Oligonucleotide Array Sequence Analysis - methods</subject><subject>oligonucleotide microarray</subject><subject>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</subject><subject>renal cell carcinoma</subject><subject>Sequence Analysis, DNA - methods</subject><subject>Tumors of the urinary system</subject><issn>0022-3417</issn><issn>1096-9896</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10Mtu1DAUBmALgehQWPAC4A1ILNL6lthejgp0QKUgMQWJjXUmOZkacsNOROftcZQRXbGyJX__8dFPyHPOzjhj4nyA8fZMCGkfkBVntsisscVDskpvIpOK6xPyJMafjDFr8_wxOeHaCqG0WhG_8fvbLGDsm2n0fUehg-YQfaR9Td9er2nZDwfaTe0OA4VmxAAzi8lVdI8dUrwbUjzOWd_RgClPywYh0BKbdIVQ-q5v4Sl5VEMT8dnxPCU3799tLzbZ1efLDxfrq6xUhtusqLSqtFasssoIFLpmtVLSilxDYRkiMMyZQSiMgtwaIUyVG1HumFG1kbk8Ja-XuUPof08YR9f6OK8CHfZTdIXJmeJGJvhmgWXoYwxYuyH4FsLBcebmXt3cq5t7TfbFcei0a7G6l8ciE3h1BBBLaOoAXenjvbNKmkLw5M4X98c3ePj_j-7Lers5fp0tCR9HvPuXgPDLFVrq3H2_vnQ_Pn7abjnn7lvyLxdfQ-9gH9IWN18F45IxI9K6Wv4FPk6ndQ</recordid><startdate>200712</startdate><enddate>200712</enddate><creator>Yoshimoto, T</creator><creator>Matsuura, K</creator><creator>Karnan, S</creator><creator>Tagawa, H</creator><creator>Nakada, C</creator><creator>Tanigawa, M</creator><creator>Tsukamoto, Y</creator><creator>Uchida, T</creator><creator>Kashima, K</creator><creator>Akizuki, S</creator><creator>Takeuchi, I</creator><creator>Sato, F</creator><creator>Mimata, H</creator><creator>Seto, M</creator><creator>Moriyama, M</creator><general>John Wiley & Sons, Ltd</general><general>Wiley</general><scope>FBQ</scope><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>200712</creationdate><title>High-resolution analysis of DNA copy number alterations and gene expression in renal clear cell carcinoma</title><author>Yoshimoto, T ; Matsuura, K ; Karnan, S ; Tagawa, H ; Nakada, C ; Tanigawa, M ; Tsukamoto, Y ; Uchida, T ; Kashima, K ; Akizuki, S ; Takeuchi, I ; Sato, F ; Mimata, H ; Seto, M ; Moriyama, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4819-6d74d7740d9482e27f0f4439257a690eea0e508ea684a598228d582cb084f8353</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>array CGH</topic><topic>Biological and medical sciences</topic><topic>Carcinoma, Renal Cell - genetics</topic><topic>Carcinoma, Renal Cell - pathology</topic><topic>Chromosome Aberrations</topic><topic>Chromosomes, Human, Pair 14 - genetics</topic><topic>clear cell carcinoma</topic><topic>DNA, Neoplasm - genetics</topic><topic>Down-Regulation - genetics</topic><topic>Female</topic><topic>Gene Dosage - genetics</topic><topic>gene expression</topic><topic>Gene Expression Profiling - methods</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Investigative techniques, diagnostic techniques (general aspects)</topic><topic>Kidney Neoplasms - genetics</topic><topic>Kidney Neoplasms - pathology</topic><topic>Kidneys</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nucleic Acid Hybridization - methods</topic><topic>Oligonucleotide Array Sequence Analysis - methods</topic><topic>oligonucleotide microarray</topic><topic>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</topic><topic>renal cell carcinoma</topic><topic>Sequence Analysis, DNA - methods</topic><topic>Tumors of the urinary system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yoshimoto, T</creatorcontrib><creatorcontrib>Matsuura, K</creatorcontrib><creatorcontrib>Karnan, S</creatorcontrib><creatorcontrib>Tagawa, H</creatorcontrib><creatorcontrib>Nakada, C</creatorcontrib><creatorcontrib>Tanigawa, M</creatorcontrib><creatorcontrib>Tsukamoto, Y</creatorcontrib><creatorcontrib>Uchida, T</creatorcontrib><creatorcontrib>Kashima, K</creatorcontrib><creatorcontrib>Akizuki, S</creatorcontrib><creatorcontrib>Takeuchi, I</creatorcontrib><creatorcontrib>Sato, F</creatorcontrib><creatorcontrib>Mimata, H</creatorcontrib><creatorcontrib>Seto, M</creatorcontrib><creatorcontrib>Moriyama, M</creatorcontrib><collection>AGRIS</collection><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yoshimoto, T</au><au>Matsuura, K</au><au>Karnan, S</au><au>Tagawa, H</au><au>Nakada, C</au><au>Tanigawa, M</au><au>Tsukamoto, Y</au><au>Uchida, T</au><au>Kashima, K</au><au>Akizuki, S</au><au>Takeuchi, I</au><au>Sato, F</au><au>Mimata, H</au><au>Seto, M</au><au>Moriyama, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>High-resolution analysis of DNA copy number alterations and gene expression in renal clear cell carcinoma</atitle><jtitle>The Journal of pathology</jtitle><addtitle>J. Pathol</addtitle><date>2007-12</date><risdate>2007</risdate><volume>213</volume><issue>4</issue><spage>392</spage><epage>401</epage><pages>392-401</pages><issn>0022-3417</issn><eissn>1096-9896</eissn><coden>JPTLAS</coden><abstract>We analysed chromosomal copy number aberrations (CNAs) in renal cell carcinomas by array-based comparative genomic hybridization, using a genome-wide scanning array with 2304 BAC and PAC clones covering the whole human genome at a resolution of roughly 1.3 Mb. A total of 30 samples of renal cell carcinoma were analysed, including 26 cases of clear cell carcinoma (CCC) and four cases of chromophobe renal cell carcinoma (ChCC). In CCCs, gains of chromosomes 5q33.1-qter (58%), 7q11.22-q35 (35%) and 16p12.3-p13.12 (19%), and losses of chromosomes 3p25.1-p25.3 (77%), 3p21.31-p22.3 (81%), 3p14.1-p14.2 (77%), 8p23.3 (31%), 9q21.13-qter (19%) and 14q32.32-qter (38%) were detected. On the other hand, the patterns of CNAs differed markedly between CCCs and ChCCs. Next, we examined the correlation of CNAs with expression profiles in the same tumour samples in 22/26 cases of CCC, using oligonucleotide microarray. We extracted genes that were differentially expressed between cases with and without CNAs, and found that significantly more up-regulated genes were localized on chromosomes 5 and 7, where recurrent genomic gains have been detected. Conversely, significantly more down-regulated genes were localized on chromosomes 14 and 3, where recurrent genomic losses have been detected. These results revealed that CNAs were correlated with deregulation of gene expression in CCCs. Furthermore, we compared the patterns of genomic imbalance with histopathological features, and found that loss of 14q appeared to be a specific and additional genetic abnormality in high-grade CCC. When we compared the expression profiles of low-grade CCCs with those of high-grade CCCs, differentially down-regulated genes tended to be localized on chromosomes 14 and 9. Thus, it is suggested that copy number loss at 14q in high-grade CCC may be involved in the down-regulation of genes located in this region. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</abstract><cop>Chichester, UK</cop><pub>John Wiley & Sons, Ltd</pub><pmid>17922474</pmid><doi>10.1002/path.2239</doi><tpages>10</tpages></addata></record> |
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| subjects | Aged Aged, 80 and over array CGH Biological and medical sciences Carcinoma, Renal Cell - genetics Carcinoma, Renal Cell - pathology Chromosome Aberrations Chromosomes, Human, Pair 14 - genetics clear cell carcinoma DNA, Neoplasm - genetics Down-Regulation - genetics Female Gene Dosage - genetics gene expression Gene Expression Profiling - methods Gene Expression Regulation, Neoplastic Humans Investigative techniques, diagnostic techniques (general aspects) Kidney Neoplasms - genetics Kidney Neoplasms - pathology Kidneys Male Medical sciences Middle Aged Nephrology. Urinary tract diseases Nucleic Acid Hybridization - methods Oligonucleotide Array Sequence Analysis - methods oligonucleotide microarray Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques renal cell carcinoma Sequence Analysis, DNA - methods Tumors of the urinary system |
| title | High-resolution analysis of DNA copy number alterations and gene expression in renal clear cell carcinoma |
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