Integrative analysis of genomic aberrations associated with prostate cancer progression
Integrative analysis of genomic aberrations in the context of trancriptomic alterations will lead to a more comprehensive perspective on prostate cancer progression. Genome-wide copy number changes were monitored using array comparative genomic hybridization of laser-capture microdissected prostate...
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| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 2007-09, Vol.67 (17), p.8229-8239 |
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| creator | KIM, Jung H DHANASEKARAN, Saravana M GHOSH, Debashis SHEDDEN, Kerby MONTIE, James E RUBIN, Mark A PIENTA, Kenneth J SHAH, Rajal B CHINNAIYAN, Arul M MEHRA, Rohit TOMLINS, Scott A WENJUAN GU JIANJUN YU KUMAR-SINHA, Chandan XUHONG CAO DASH, Atreya LEI WANG |
| description | Integrative analysis of genomic aberrations in the context of trancriptomic alterations will lead to a more comprehensive perspective on prostate cancer progression. Genome-wide copy number changes were monitored using array comparative genomic hybridization of laser-capture microdissected prostate cancer samples spanning stages of prostate cancer progression, including precursor lesions, clinically localized disease, and metastatic disease. A total of 62 specific cell populations from 38 patients were profiled. Minimal common regions (MCR) of alterations were defined for each sample type, and metastatic samples displayed the most number of alterations. Clinically localized prostate cancer samples with high Gleason grade resembled metastatic samples with respect to the size of altered regions and number of affected genes. A total of 9 out of 13 MCRs in the putative precursor lesion, high-grade prostatic intraepithelial neoplasia (PIN), showed an overlap with prostate cancer cases (amplifications in 3q29, 5q31.3-q32, 6q27, and 8q24.3 and deletions in 6q22.31, 16p12.2, 17q21.2, and 17q21.31), whereas postatrophic hyperplasia (PAH) did not exhibit this overlap. Interestingly, prostate cancers that do not overexpress ETS family members (i.e., gene fusion-negative prostate cancers) harbor differential aberrations in 1q23, 6q16, 6q21, 10q23, and 10q24. Integrative analysis with matched mRNA profiles identified genetic alterations in several proposed candidate genes implicated in prostate cancer progression. |
| doi_str_mv | 10.1158/0008-5472.CAN-07-1297 |
| format | Article |
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Genome-wide copy number changes were monitored using array comparative genomic hybridization of laser-capture microdissected prostate cancer samples spanning stages of prostate cancer progression, including precursor lesions, clinically localized disease, and metastatic disease. A total of 62 specific cell populations from 38 patients were profiled. Minimal common regions (MCR) of alterations were defined for each sample type, and metastatic samples displayed the most number of alterations. Clinically localized prostate cancer samples with high Gleason grade resembled metastatic samples with respect to the size of altered regions and number of affected genes. A total of 9 out of 13 MCRs in the putative precursor lesion, high-grade prostatic intraepithelial neoplasia (PIN), showed an overlap with prostate cancer cases (amplifications in 3q29, 5q31.3-q32, 6q27, and 8q24.3 and deletions in 6q22.31, 16p12.2, 17q21.2, and 17q21.31), whereas postatrophic hyperplasia (PAH) did not exhibit this overlap. Interestingly, prostate cancers that do not overexpress ETS family members (i.e., gene fusion-negative prostate cancers) harbor differential aberrations in 1q23, 6q16, 6q21, 10q23, and 10q24. Integrative analysis with matched mRNA profiles identified genetic alterations in several proposed candidate genes implicated in prostate cancer progression.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>DOI: 10.1158/0008-5472.CAN-07-1297</identifier><identifier>PMID: 17804737</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Antineoplastic agents ; Biological and medical sciences ; Chromosome Aberrations ; Chromosomes, Human, 16-18 ; Chromosomes, Human, 6-12 and X ; Chromosomes, Human, Pair 3 ; Chromosomes, Human, Pair 5 ; Disease Progression ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Gene Regulatory Networks - physiology ; Genes, Neoplasm ; Genome, Human ; Gynecology. Andrology. Obstetrics ; Humans ; Male ; Male genital diseases ; Medical sciences ; Neoplasm Metastasis ; Nephrology. Urinary tract diseases ; Pharmacology. Drug treatments ; Prostatic Intraepithelial Neoplasia - genetics ; Prostatic Intraepithelial Neoplasia - pathology ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - pathology ; Tissue Array Analysis ; Tumors ; Tumors of the urinary system ; Urinary tract. Prostate gland</subject><ispartof>Cancer research (Chicago, Ill.), 2007-09, Vol.67 (17), p.8229-8239</ispartof><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c449t-abd329dd9d938b90d258bd528ff5996f550d89018a89caa71b689cb36e0c6af63</citedby><cites>FETCH-LOGICAL-c449t-abd329dd9d938b90d258bd528ff5996f550d89018a89caa71b689cb36e0c6af63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3343,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19168919$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17804737$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KIM, Jung H</creatorcontrib><creatorcontrib>DHANASEKARAN, Saravana M</creatorcontrib><creatorcontrib>GHOSH, Debashis</creatorcontrib><creatorcontrib>SHEDDEN, Kerby</creatorcontrib><creatorcontrib>MONTIE, James E</creatorcontrib><creatorcontrib>RUBIN, Mark A</creatorcontrib><creatorcontrib>PIENTA, Kenneth J</creatorcontrib><creatorcontrib>SHAH, Rajal B</creatorcontrib><creatorcontrib>CHINNAIYAN, Arul M</creatorcontrib><creatorcontrib>MEHRA, Rohit</creatorcontrib><creatorcontrib>TOMLINS, Scott A</creatorcontrib><creatorcontrib>WENJUAN GU</creatorcontrib><creatorcontrib>JIANJUN YU</creatorcontrib><creatorcontrib>KUMAR-SINHA, Chandan</creatorcontrib><creatorcontrib>XUHONG CAO</creatorcontrib><creatorcontrib>DASH, Atreya</creatorcontrib><creatorcontrib>LEI WANG</creatorcontrib><title>Integrative analysis of genomic aberrations associated with prostate cancer progression</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Integrative analysis of genomic aberrations in the context of trancriptomic alterations will lead to a more comprehensive perspective on prostate cancer progression. Genome-wide copy number changes were monitored using array comparative genomic hybridization of laser-capture microdissected prostate cancer samples spanning stages of prostate cancer progression, including precursor lesions, clinically localized disease, and metastatic disease. A total of 62 specific cell populations from 38 patients were profiled. Minimal common regions (MCR) of alterations were defined for each sample type, and metastatic samples displayed the most number of alterations. Clinically localized prostate cancer samples with high Gleason grade resembled metastatic samples with respect to the size of altered regions and number of affected genes. A total of 9 out of 13 MCRs in the putative precursor lesion, high-grade prostatic intraepithelial neoplasia (PIN), showed an overlap with prostate cancer cases (amplifications in 3q29, 5q31.3-q32, 6q27, and 8q24.3 and deletions in 6q22.31, 16p12.2, 17q21.2, and 17q21.31), whereas postatrophic hyperplasia (PAH) did not exhibit this overlap. Interestingly, prostate cancers that do not overexpress ETS family members (i.e., gene fusion-negative prostate cancers) harbor differential aberrations in 1q23, 6q16, 6q21, 10q23, and 10q24. Integrative analysis with matched mRNA profiles identified genetic alterations in several proposed candidate genes implicated in prostate cancer progression.</description><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Chromosome Aberrations</subject><subject>Chromosomes, Human, 16-18</subject><subject>Chromosomes, Human, 6-12 and X</subject><subject>Chromosomes, Human, Pair 3</subject><subject>Chromosomes, Human, Pair 5</subject><subject>Disease Progression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Regulatory Networks - physiology</subject><subject>Genes, Neoplasm</subject><subject>Genome, Human</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Male</subject><subject>Male genital diseases</subject><subject>Medical sciences</subject><subject>Neoplasm Metastasis</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Pharmacology. Drug treatments</subject><subject>Prostatic Intraepithelial Neoplasia - genetics</subject><subject>Prostatic Intraepithelial Neoplasia - pathology</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Tissue Array Analysis</subject><subject>Tumors</subject><subject>Tumors of the urinary system</subject><subject>Urinary tract. Prostate gland</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1PwzAMhiMEYmPwE0C9wK0jaZomOU4TH5MQXEAcIzdJR1HXjrgD7d-TahM7cnJe5bEtP4RcMjplTKhbSqlKRS6z6Xz2nFKZskzLIzJmgqtU5rk4JuM_ZkTOED9jFIyKUzJiUtFccjkm74u298sAff3tE2ih2WKNSVclS992q9omUPowfHctJoDY2Rp675Kfuv9I1qHDPsbEQmt9GPIyeMQIn5OTChr0F_s6IW_3d6_zx_Tp5WExnz2lNs91n0LpeKad005zVWrqMqFKJzJVVULrohKCOqUpU6C0BZCsLOKj5IWntoCq4BNys5sbd39tPPZmVaP1TQOt7zZoCpXljFL5L5hRzjOe6wiKHWjjdRh8ZdahXkHYGkbNoN4MWs2g1UT1hkozqI99V_sFm3Ll3aFr7zoC13sA0EJThSitxgOnWbyNaf4Lu_SNzw</recordid><startdate>20070901</startdate><enddate>20070901</enddate><creator>KIM, Jung H</creator><creator>DHANASEKARAN, Saravana M</creator><creator>GHOSH, Debashis</creator><creator>SHEDDEN, Kerby</creator><creator>MONTIE, James E</creator><creator>RUBIN, Mark A</creator><creator>PIENTA, Kenneth J</creator><creator>SHAH, Rajal B</creator><creator>CHINNAIYAN, Arul M</creator><creator>MEHRA, Rohit</creator><creator>TOMLINS, Scott A</creator><creator>WENJUAN GU</creator><creator>JIANJUN YU</creator><creator>KUMAR-SINHA, Chandan</creator><creator>XUHONG CAO</creator><creator>DASH, Atreya</creator><creator>LEI WANG</creator><general>American Association for Cancer Research</general><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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20070901</creationdate><title>Integrative analysis of genomic aberrations associated with prostate cancer progression</title><author>KIM, Jung H ; DHANASEKARAN, Saravana M ; GHOSH, Debashis ; SHEDDEN, Kerby ; MONTIE, James E ; RUBIN, Mark A ; PIENTA, Kenneth J ; SHAH, Rajal B ; CHINNAIYAN, Arul M ; MEHRA, Rohit ; TOMLINS, Scott A ; WENJUAN GU ; JIANJUN YU ; KUMAR-SINHA, Chandan ; XUHONG CAO ; DASH, Atreya ; LEI WANG</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c449t-abd329dd9d938b90d258bd528ff5996f550d89018a89caa71b689cb36e0c6af63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Antineoplastic agents</topic><topic>Biological and medical sciences</topic><topic>Chromosome Aberrations</topic><topic>Chromosomes, Human, 16-18</topic><topic>Chromosomes, Human, 6-12 and X</topic><topic>Chromosomes, Human, Pair 3</topic><topic>Chromosomes, Human, Pair 5</topic><topic>Disease Progression</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene Regulatory Networks - physiology</topic><topic>Genes, Neoplasm</topic><topic>Genome, Human</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Male</topic><topic>Male genital diseases</topic><topic>Medical sciences</topic><topic>Neoplasm Metastasis</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Pharmacology. Drug treatments</topic><topic>Prostatic Intraepithelial Neoplasia - genetics</topic><topic>Prostatic Intraepithelial Neoplasia - pathology</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Tissue Array Analysis</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>KIM, Jung H</creatorcontrib><creatorcontrib>DHANASEKARAN, Saravana M</creatorcontrib><creatorcontrib>GHOSH, Debashis</creatorcontrib><creatorcontrib>SHEDDEN, Kerby</creatorcontrib><creatorcontrib>MONTIE, James E</creatorcontrib><creatorcontrib>RUBIN, Mark A</creatorcontrib><creatorcontrib>PIENTA, Kenneth J</creatorcontrib><creatorcontrib>SHAH, Rajal B</creatorcontrib><creatorcontrib>CHINNAIYAN, Arul M</creatorcontrib><creatorcontrib>MEHRA, Rohit</creatorcontrib><creatorcontrib>TOMLINS, Scott A</creatorcontrib><creatorcontrib>WENJUAN GU</creatorcontrib><creatorcontrib>JIANJUN YU</creatorcontrib><creatorcontrib>KUMAR-SINHA, Chandan</creatorcontrib><creatorcontrib>XUHONG CAO</creatorcontrib><creatorcontrib>DASH, Atreya</creatorcontrib><creatorcontrib>LEI WANG</creatorcontrib><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>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>KIM, Jung H</au><au>DHANASEKARAN, Saravana M</au><au>GHOSH, Debashis</au><au>SHEDDEN, Kerby</au><au>MONTIE, James E</au><au>RUBIN, Mark A</au><au>PIENTA, Kenneth J</au><au>SHAH, Rajal B</au><au>CHINNAIYAN, Arul M</au><au>MEHRA, Rohit</au><au>TOMLINS, Scott A</au><au>WENJUAN GU</au><au>JIANJUN YU</au><au>KUMAR-SINHA, Chandan</au><au>XUHONG CAO</au><au>DASH, Atreya</au><au>LEI WANG</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Integrative analysis of genomic aberrations associated with prostate cancer progression</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>2007-09-01</date><risdate>2007</risdate><volume>67</volume><issue>17</issue><spage>8229</spage><epage>8239</epage><pages>8229-8239</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><abstract>Integrative analysis of genomic aberrations in the context of trancriptomic alterations will lead to a more comprehensive perspective on prostate cancer progression. Genome-wide copy number changes were monitored using array comparative genomic hybridization of laser-capture microdissected prostate cancer samples spanning stages of prostate cancer progression, including precursor lesions, clinically localized disease, and metastatic disease. A total of 62 specific cell populations from 38 patients were profiled. Minimal common regions (MCR) of alterations were defined for each sample type, and metastatic samples displayed the most number of alterations. Clinically localized prostate cancer samples with high Gleason grade resembled metastatic samples with respect to the size of altered regions and number of affected genes. A total of 9 out of 13 MCRs in the putative precursor lesion, high-grade prostatic intraepithelial neoplasia (PIN), showed an overlap with prostate cancer cases (amplifications in 3q29, 5q31.3-q32, 6q27, and 8q24.3 and deletions in 6q22.31, 16p12.2, 17q21.2, and 17q21.31), whereas postatrophic hyperplasia (PAH) did not exhibit this overlap. Interestingly, prostate cancers that do not overexpress ETS family members (i.e., gene fusion-negative prostate cancers) harbor differential aberrations in 1q23, 6q16, 6q21, 10q23, and 10q24. Integrative analysis with matched mRNA profiles identified genetic alterations in several proposed candidate genes implicated in prostate cancer progression.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>17804737</pmid><doi>10.1158/0008-5472.CAN-07-1297</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Antineoplastic agents Biological and medical sciences Chromosome Aberrations Chromosomes, Human, 16-18 Chromosomes, Human, 6-12 and X Chromosomes, Human, Pair 3 Chromosomes, Human, Pair 5 Disease Progression Gene Expression Profiling Gene Expression Regulation, Neoplastic Gene Regulatory Networks - physiology Genes, Neoplasm Genome, Human Gynecology. Andrology. Obstetrics Humans Male Male genital diseases Medical sciences Neoplasm Metastasis Nephrology. Urinary tract diseases Pharmacology. Drug treatments Prostatic Intraepithelial Neoplasia - genetics Prostatic Intraepithelial Neoplasia - pathology Prostatic Neoplasms - genetics Prostatic Neoplasms - pathology Tissue Array Analysis Tumors Tumors of the urinary system Urinary tract. Prostate gland |
| title | Integrative analysis of genomic aberrations associated with prostate cancer progression |
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