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...
Gespeichert in:
Veröffentlicht in: | The Prostate 2008-10, Vol.68 (14), p.1496-1509 |
---|---|
Hauptverfasser: | , , , , , , , , |
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&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 |