Simultaneously detection of genomic and expression alterations in prostate cancer using cDNA microarray

BACKGROUND Prostate cancer is a common disease among men but the knowledge of the prostate carcinogenesis is still limited. METHODS cDNA microarray‐based comparative genomic hybridization (CGH) and expression profiling were performed to screen the genomic and the expression changes in prostate cance...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:The Prostate 2008-10, Vol.68 (14), p.1496-1509
Hauptverfasser: Jiang, Mei, Li, Ming, Fu, Xuping, Huang, Yan, Qian, Hui, Sun, Ruping, Mao, Yumin, Xie, Yi, Li, Yao
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 1509
container_issue 14
container_start_page 1496
container_title The Prostate
container_volume 68
creator Jiang, Mei
Li, Ming
Fu, Xuping
Huang, Yan
Qian, Hui
Sun, Ruping
Mao, Yumin
Xie, Yi
Li, Yao
description BACKGROUND Prostate cancer is a common disease among men but the knowledge of the prostate carcinogenesis is still limited. METHODS cDNA microarray‐based comparative genomic hybridization (CGH) and expression profiling were performed to screen the genomic and the expression changes in prostate cancer respectively. The two data were integrated to study the influence of genomic aberrations on gene expression and seek for the genes with their expression affected by the genomic aberrations. Real‐time PCR was performed to evaluate the array data. RESULTS Array‐based CGH detected gains at 2q, 3p/q, 5q, 6q, 8q, 9p, 10p/q, 11q, 12p, 14q, and 19p/q and losses at 1p, 2p, 4q, 6p/q, 7p, 11p/q, 12q, 17p/q, 19p/q, and Xp/q in more than 20% prostate tumors and narrowed these aberrations. For example, the gain of 8q was mapped to five minimal regions. Novel aberrations were also identified, such as loss at Xq21.33‐q22.2. Expression profiling discovered the significant biological processes involved in the prostate carcinogenesis, such as exogenous antigen presentation via MHC class II and protein ubiquitination. Integration analysis revealed a weak positive correlation between genomic copy number and gene expression level. Fifty‐three genes showed their expression directly affected by the genomic aberrations possibly, including more than one member of Ras superfamily and major histocompatibility complex (MHC). These genes are involved in multiple biological processes. CONCLUSIONS Integration of the CGH and expression data provided more information than separate analysis. Although the direct influence of genomic aberrations on gene expression seems weak, the influence can be extended by indirect regulation through a few directly affected genes. Because the influence can be persistent, the genes directly affected by the genomic aberrations may play key roles in the prostate carcinogenesis and are worth further analysis. Prostate 68: 1496–1509, 2008. © 2008 Wiley‐Liss, Inc.
doi_str_mv 10.1002/pros.20756
format Article
fullrecord <record><control><sourceid>wiley_cross</sourceid><recordid>TN_cdi_crossref_primary_10_1002_pros_20756</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>PROS20756</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3956-b9642fd68b025f348223d79291f92865e1be2ef87590863a8267aed6669792b03</originalsourceid><addsrcrecordid>eNp90E9P2zAYBnBrGloL7LIPMPmyy6TAazvxnyOCDSYqQBTEbpaTvKm8pUllpxr99jhrKTdOPvj3-Hn9EvKFwQkD4Ker0McTDqqQH8iUgVEZQF58JFPgCrKcCTUhhzH-AUgc-CcyYVpICbyYksXcL9ft4Drs17Hd0BoHrAbfd7Rv6AK7fukr6rqa4vMqYIzjjWsHDG5EkfqOjvWDG5BWrqsw0HX03YJWFzdnNIVD70Jwm2Ny0Lg24ufdeUQef_54OL_KZreXv87PZlklTCGz0sicN7XUZZquEbnmXNTKcMMaw7UskJXIsdGqMKClcJpL5bCWUpqkShBH5Pv23VQcY8DGroJfurCxDOy4LTuOa_9vK-GvW7xal0us3-huPQl82wEXK9c2If3Qx73jIHOlmEmObd0_3-LmnUp7d387fy3PthkfB3zeZ1z4a6USqrBPN5c2Z_paFdfa_hYvvTaR2w</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Simultaneously detection of genomic and expression alterations in prostate cancer using cDNA microarray</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Jiang, Mei ; Li, Ming ; Fu, Xuping ; Huang, Yan ; Qian, Hui ; Sun, Ruping ; Mao, Yumin ; Xie, Yi ; Li, Yao</creator><creatorcontrib>Jiang, Mei ; Li, Ming ; Fu, Xuping ; Huang, Yan ; Qian, Hui ; Sun, Ruping ; Mao, Yumin ; Xie, Yi ; Li, Yao</creatorcontrib><description>BACKGROUND Prostate cancer is a common disease among men but the knowledge of the prostate carcinogenesis is still limited. METHODS cDNA microarray‐based comparative genomic hybridization (CGH) and expression profiling were performed to screen the genomic and the expression changes in prostate cancer respectively. The two data were integrated to study the influence of genomic aberrations on gene expression and seek for the genes with their expression affected by the genomic aberrations. Real‐time PCR was performed to evaluate the array data. RESULTS Array‐based CGH detected gains at 2q, 3p/q, 5q, 6q, 8q, 9p, 10p/q, 11q, 12p, 14q, and 19p/q and losses at 1p, 2p, 4q, 6p/q, 7p, 11p/q, 12q, 17p/q, 19p/q, and Xp/q in more than 20% prostate tumors and narrowed these aberrations. For example, the gain of 8q was mapped to five minimal regions. Novel aberrations were also identified, such as loss at Xq21.33‐q22.2. Expression profiling discovered the significant biological processes involved in the prostate carcinogenesis, such as exogenous antigen presentation via MHC class II and protein ubiquitination. Integration analysis revealed a weak positive correlation between genomic copy number and gene expression level. Fifty‐three genes showed their expression directly affected by the genomic aberrations possibly, including more than one member of Ras superfamily and major histocompatibility complex (MHC). These genes are involved in multiple biological processes. CONCLUSIONS Integration of the CGH and expression data provided more information than separate analysis. Although the direct influence of genomic aberrations on gene expression seems weak, the influence can be extended by indirect regulation through a few directly affected genes. Because the influence can be persistent, the genes directly affected by the genomic aberrations may play key roles in the prostate carcinogenesis and are worth further analysis. Prostate 68: 1496–1509, 2008. © 2008 Wiley‐Liss, Inc.</description><identifier>ISSN: 0270-4137</identifier><identifier>EISSN: 1097-0045</identifier><identifier>DOI: 10.1002/pros.20756</identifier><identifier>PMID: 18366025</identifier><identifier>CODEN: PRSTDS</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Biological and medical sciences ; cDNA microarray ; CGH ; Chromosome Aberrations ; data integration ; expression profiling ; Gene Dosage ; Gene Expression Profiling - methods ; Gene Expression Regulation, Neoplastic ; Genetic Variation ; Gynecology. Andrology. Obstetrics ; Humans ; Male ; Male genital diseases ; Medical sciences ; Nephrology. Urinary tract diseases ; Nucleic Acid Hybridization ; Oligonucleotide Array Sequence Analysis - methods ; prostate cancer ; Prostatic Neoplasms - genetics ; Reproducibility of Results ; RNA, Neoplasm - chemistry ; RNA, Neoplasm - genetics ; Statistics, Nonparametric ; Tumors ; Tumors of the urinary system ; Urinary tract. Prostate gland</subject><ispartof>The Prostate, 2008-10, Vol.68 (14), p.1496-1509</ispartof><rights>Copyright © 2008 Wiley‐Liss, Inc.</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3956-b9642fd68b025f348223d79291f92865e1be2ef87590863a8267aed6669792b03</citedby><cites>FETCH-LOGICAL-c3956-b9642fd68b025f348223d79291f92865e1be2ef87590863a8267aed6669792b03</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%2Fpros.20756$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fpros.20756$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=20647719$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18366025$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jiang, Mei</creatorcontrib><creatorcontrib>Li, Ming</creatorcontrib><creatorcontrib>Fu, Xuping</creatorcontrib><creatorcontrib>Huang, Yan</creatorcontrib><creatorcontrib>Qian, Hui</creatorcontrib><creatorcontrib>Sun, Ruping</creatorcontrib><creatorcontrib>Mao, Yumin</creatorcontrib><creatorcontrib>Xie, Yi</creatorcontrib><creatorcontrib>Li, Yao</creatorcontrib><title>Simultaneously detection of genomic and expression alterations in prostate cancer using cDNA microarray</title><title>The Prostate</title><addtitle>Prostate</addtitle><description>BACKGROUND Prostate cancer is a common disease among men but the knowledge of the prostate carcinogenesis is still limited. METHODS cDNA microarray‐based comparative genomic hybridization (CGH) and expression profiling were performed to screen the genomic and the expression changes in prostate cancer respectively. The two data were integrated to study the influence of genomic aberrations on gene expression and seek for the genes with their expression affected by the genomic aberrations. Real‐time PCR was performed to evaluate the array data. RESULTS Array‐based CGH detected gains at 2q, 3p/q, 5q, 6q, 8q, 9p, 10p/q, 11q, 12p, 14q, and 19p/q and losses at 1p, 2p, 4q, 6p/q, 7p, 11p/q, 12q, 17p/q, 19p/q, and Xp/q in more than 20% prostate tumors and narrowed these aberrations. For example, the gain of 8q was mapped to five minimal regions. Novel aberrations were also identified, such as loss at Xq21.33‐q22.2. Expression profiling discovered the significant biological processes involved in the prostate carcinogenesis, such as exogenous antigen presentation via MHC class II and protein ubiquitination. Integration analysis revealed a weak positive correlation between genomic copy number and gene expression level. Fifty‐three genes showed their expression directly affected by the genomic aberrations possibly, including more than one member of Ras superfamily and major histocompatibility complex (MHC). These genes are involved in multiple biological processes. CONCLUSIONS Integration of the CGH and expression data provided more information than separate analysis. Although the direct influence of genomic aberrations on gene expression seems weak, the influence can be extended by indirect regulation through a few directly affected genes. Because the influence can be persistent, the genes directly affected by the genomic aberrations may play key roles in the prostate carcinogenesis and are worth further analysis. Prostate 68: 1496–1509, 2008. © 2008 Wiley‐Liss, Inc.</description><subject>Biological and medical sciences</subject><subject>cDNA microarray</subject><subject>CGH</subject><subject>Chromosome Aberrations</subject><subject>data integration</subject><subject>expression profiling</subject><subject>Gene Dosage</subject><subject>Gene Expression Profiling - methods</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genetic Variation</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Male</subject><subject>Male genital diseases</subject><subject>Medical sciences</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nucleic Acid Hybridization</subject><subject>Oligonucleotide Array Sequence Analysis - methods</subject><subject>prostate cancer</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Reproducibility of Results</subject><subject>RNA, Neoplasm - chemistry</subject><subject>RNA, Neoplasm - genetics</subject><subject>Statistics, Nonparametric</subject><subject>Tumors</subject><subject>Tumors of the urinary system</subject><subject>Urinary tract. Prostate gland</subject><issn>0270-4137</issn><issn>1097-0045</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp90E9P2zAYBnBrGloL7LIPMPmyy6TAazvxnyOCDSYqQBTEbpaTvKm8pUllpxr99jhrKTdOPvj3-Hn9EvKFwQkD4Ker0McTDqqQH8iUgVEZQF58JFPgCrKcCTUhhzH-AUgc-CcyYVpICbyYksXcL9ft4Drs17Hd0BoHrAbfd7Rv6AK7fukr6rqa4vMqYIzjjWsHDG5EkfqOjvWDG5BWrqsw0HX03YJWFzdnNIVD70Jwm2Ny0Lg24ufdeUQef_54OL_KZreXv87PZlklTCGz0sicN7XUZZquEbnmXNTKcMMaw7UskJXIsdGqMKClcJpL5bCWUpqkShBH5Pv23VQcY8DGroJfurCxDOy4LTuOa_9vK-GvW7xal0us3-huPQl82wEXK9c2If3Qx73jIHOlmEmObd0_3-LmnUp7d387fy3PthkfB3zeZ1z4a6USqrBPN5c2Z_paFdfa_hYvvTaR2w</recordid><startdate>20081001</startdate><enddate>20081001</enddate><creator>Jiang, Mei</creator><creator>Li, Ming</creator><creator>Fu, Xuping</creator><creator>Huang, Yan</creator><creator>Qian, Hui</creator><creator>Sun, Ruping</creator><creator>Mao, Yumin</creator><creator>Xie, Yi</creator><creator>Li, Yao</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</general><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></search><sort><creationdate>20081001</creationdate><title>Simultaneously detection of genomic and expression alterations in prostate cancer using cDNA microarray</title><author>Jiang, Mei ; Li, Ming ; Fu, Xuping ; Huang, Yan ; Qian, Hui ; Sun, Ruping ; Mao, Yumin ; Xie, Yi ; Li, Yao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3956-b9642fd68b025f348223d79291f92865e1be2ef87590863a8267aed6669792b03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Biological and medical sciences</topic><topic>cDNA microarray</topic><topic>CGH</topic><topic>Chromosome Aberrations</topic><topic>data integration</topic><topic>expression profiling</topic><topic>Gene Dosage</topic><topic>Gene Expression Profiling - methods</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genetic Variation</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Male</topic><topic>Male genital diseases</topic><topic>Medical sciences</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nucleic Acid Hybridization</topic><topic>Oligonucleotide Array Sequence Analysis - methods</topic><topic>prostate cancer</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Reproducibility of Results</topic><topic>RNA, Neoplasm - chemistry</topic><topic>RNA, Neoplasm - genetics</topic><topic>Statistics, Nonparametric</topic><topic>Tumors</topic><topic>Tumors of the urinary system</topic><topic>Urinary tract. Prostate gland</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jiang, Mei</creatorcontrib><creatorcontrib>Li, Ming</creatorcontrib><creatorcontrib>Fu, Xuping</creatorcontrib><creatorcontrib>Huang, Yan</creatorcontrib><creatorcontrib>Qian, Hui</creatorcontrib><creatorcontrib>Sun, Ruping</creatorcontrib><creatorcontrib>Mao, Yumin</creatorcontrib><creatorcontrib>Xie, Yi</creatorcontrib><creatorcontrib>Li, Yao</creatorcontrib><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><jtitle>The Prostate</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiang, Mei</au><au>Li, Ming</au><au>Fu, Xuping</au><au>Huang, Yan</au><au>Qian, Hui</au><au>Sun, Ruping</au><au>Mao, Yumin</au><au>Xie, Yi</au><au>Li, Yao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Simultaneously detection of genomic and expression alterations in prostate cancer using cDNA microarray</atitle><jtitle>The Prostate</jtitle><addtitle>Prostate</addtitle><date>2008-10-01</date><risdate>2008</risdate><volume>68</volume><issue>14</issue><spage>1496</spage><epage>1509</epage><pages>1496-1509</pages><issn>0270-4137</issn><eissn>1097-0045</eissn><coden>PRSTDS</coden><abstract>BACKGROUND Prostate cancer is a common disease among men but the knowledge of the prostate carcinogenesis is still limited. METHODS cDNA microarray‐based comparative genomic hybridization (CGH) and expression profiling were performed to screen the genomic and the expression changes in prostate cancer respectively. The two data were integrated to study the influence of genomic aberrations on gene expression and seek for the genes with their expression affected by the genomic aberrations. Real‐time PCR was performed to evaluate the array data. RESULTS Array‐based CGH detected gains at 2q, 3p/q, 5q, 6q, 8q, 9p, 10p/q, 11q, 12p, 14q, and 19p/q and losses at 1p, 2p, 4q, 6p/q, 7p, 11p/q, 12q, 17p/q, 19p/q, and Xp/q in more than 20% prostate tumors and narrowed these aberrations. For example, the gain of 8q was mapped to five minimal regions. Novel aberrations were also identified, such as loss at Xq21.33‐q22.2. Expression profiling discovered the significant biological processes involved in the prostate carcinogenesis, such as exogenous antigen presentation via MHC class II and protein ubiquitination. Integration analysis revealed a weak positive correlation between genomic copy number and gene expression level. Fifty‐three genes showed their expression directly affected by the genomic aberrations possibly, including more than one member of Ras superfamily and major histocompatibility complex (MHC). These genes are involved in multiple biological processes. CONCLUSIONS Integration of the CGH and expression data provided more information than separate analysis. Although the direct influence of genomic aberrations on gene expression seems weak, the influence can be extended by indirect regulation through a few directly affected genes. Because the influence can be persistent, the genes directly affected by the genomic aberrations may play key roles in the prostate carcinogenesis and are worth further analysis. Prostate 68: 1496–1509, 2008. © 2008 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>18366025</pmid><doi>10.1002/pros.20756</doi><tpages>14</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0270-4137
ispartof The Prostate, 2008-10, Vol.68 (14), p.1496-1509
issn 0270-4137
1097-0045
language eng
recordid cdi_crossref_primary_10_1002_pros_20756
source MEDLINE; Wiley Online Library Journals Frontfile Complete
subjects Biological and medical sciences
cDNA microarray
CGH
Chromosome Aberrations
data integration
expression profiling
Gene Dosage
Gene Expression Profiling - methods
Gene Expression Regulation, Neoplastic
Genetic Variation
Gynecology. Andrology. Obstetrics
Humans
Male
Male genital diseases
Medical sciences
Nephrology. Urinary tract diseases
Nucleic Acid Hybridization
Oligonucleotide Array Sequence Analysis - methods
prostate cancer
Prostatic Neoplasms - genetics
Reproducibility of Results
RNA, Neoplasm - chemistry
RNA, Neoplasm - genetics
Statistics, Nonparametric
Tumors
Tumors of the urinary system
Urinary tract. Prostate gland
title Simultaneously detection of genomic and expression alterations in prostate cancer using cDNA microarray
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-20T19%3A08%3A36IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-wiley_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Simultaneously%20detection%20of%20genomic%20and%20expression%20alterations%20in%20prostate%20cancer%20using%20cDNA%20microarray&rft.jtitle=The%20Prostate&rft.au=Jiang,%20Mei&rft.date=2008-10-01&rft.volume=68&rft.issue=14&rft.spage=1496&rft.epage=1509&rft.pages=1496-1509&rft.issn=0270-4137&rft.eissn=1097-0045&rft.coden=PRSTDS&rft_id=info:doi/10.1002/pros.20756&rft_dat=%3Cwiley_cross%3EPROS20756%3C/wiley_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_id=info:pmid/18366025&rfr_iscdi=true