Epigenetic Deregulation Across Chromosome 2q14.2 Differentiates Normal from Prostate Cancer and Provides a Regional Panel of Novel DNA Methylation Cancer Biomarkers
Previously, we showed that gene suppression commonly occurs across chromosome 2q14.2 in colorectal cancer, through a process of long-range epigenetic silencing (LRES), involving a combination of DNA methylation and repressive histone modifications. We now investigate whether LRES also occurs in pros...
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| Veröffentlicht in: | Cancer epidemiology, biomarkers & prevention biomarkers & prevention, 2011, Vol.20 (1), p.148-159 |
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| creator | DEVANEY, James STIRZAKER, Clare KENCH, James G HENSHALL, Susan M PE BENITO, Ruth HAYNES, Anne-Maree MAYOR, Regina PEINADO, Miguel A SUTHERLAND, Robert L CLARK, Susan J WENJIA QU SONG, Jenny Z STATHAM, Aaron L PATTERSON, Kate I HORVATH, Lisa G TABOR, Bruce COOLEN, Marcel W HULF, Toby |
| description | Previously, we showed that gene suppression commonly occurs across chromosome 2q14.2 in colorectal cancer, through a process of long-range epigenetic silencing (LRES), involving a combination of DNA methylation and repressive histone modifications. We now investigate whether LRES also occurs in prostate cancer across this 4-Mb region and whether differential DNA methylation of 2q14.2 genes could provide a regional panel of prostate cancer biomarkers.
We used highly sensitive DNA methylation headloop PCR assays that can detect 10 to 25 pg of methylated DNA with a specificity of at least 1:1,000, and chromatin immunoprecipitation assays to investigate regional epigenetic remodeling across 2q14.2 in prostate cancer, in a cohort of 195 primary prostate tumors and 90 matched normal controls.
Prostate cancer cells exhibit concordant deacetylation and methylation of histone H3 Lysine 9 (H3K9Ac and H3K9me2, respectively), and localized DNA hypermethylation of EN1, SCTR, and INHBB and corresponding loss of H3K27me3. EN1 and SCTR were frequently methylated (65% and 53%, respectively), whereas INHBB was less frequently methylated.
Consistent with LRES in colorectal cancer, we found regional epigenetic remodeling across 2q14.2 in prostate cancer. Concordant methylation of EN1 and SCTR was able to differentiate cancer from normal (P < 0.0001) and improved the diagnostic specificity of GSTP1 methylation for prostate cancer detection by 26%.
For the first time we show that DNA methylation of EN1 and SCTR promoters provide potential novel biomarkers for prostate cancer detection and in combination with GSTP1 methylation can add increased specificity and sensitivity to improve diagnostic potential. |
| doi_str_mv | 10.1158/1055-9965.EPI-10-0719 |
| format | Article |
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We used highly sensitive DNA methylation headloop PCR assays that can detect 10 to 25 pg of methylated DNA with a specificity of at least 1:1,000, and chromatin immunoprecipitation assays to investigate regional epigenetic remodeling across 2q14.2 in prostate cancer, in a cohort of 195 primary prostate tumors and 90 matched normal controls.
Prostate cancer cells exhibit concordant deacetylation and methylation of histone H3 Lysine 9 (H3K9Ac and H3K9me2, respectively), and localized DNA hypermethylation of EN1, SCTR, and INHBB and corresponding loss of H3K27me3. EN1 and SCTR were frequently methylated (65% and 53%, respectively), whereas INHBB was less frequently methylated.
Consistent with LRES in colorectal cancer, we found regional epigenetic remodeling across 2q14.2 in prostate cancer. Concordant methylation of EN1 and SCTR was able to differentiate cancer from normal (P < 0.0001) and improved the diagnostic specificity of GSTP1 methylation for prostate cancer detection by 26%.
For the first time we show that DNA methylation of EN1 and SCTR promoters provide potential novel biomarkers for prostate cancer detection and in combination with GSTP1 methylation can add increased specificity and sensitivity to improve diagnostic potential.</description><identifier>ISSN: 1055-9965</identifier><identifier>EISSN: 1538-7755</identifier><identifier>DOI: 10.1158/1055-9965.EPI-10-0719</identifier><identifier>PMID: 21098650</identifier><identifier>CODEN: CEBPE4</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Biological and medical sciences ; Biomarkers, Tumor - genetics ; Cell Line, Tumor ; Chromatin Immunoprecipitation ; Chromosomes, Human, Pair 2 ; DNA Methylation ; Epigenesis, Genetic ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Glutathione S-Transferase pi - genetics ; Homeodomain Proteins - genetics ; Humans ; Inhibin-beta Subunits - genetics ; Male ; Medical sciences ; Nephrology. Urinary tract diseases ; Polymerase Chain Reaction - methods ; Prognosis ; Prostatic Neoplasms - diagnosis ; Prostatic Neoplasms - genetics ; Receptors, G-Protein-Coupled - genetics ; Receptors, Gastrointestinal Hormone - genetics ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; Tumors ; Tumors of the urinary system ; Urinary tract. Prostate gland</subject><ispartof>Cancer epidemiology, biomarkers & prevention, 2011, Vol.20 (1), p.148-159</ispartof><rights>2015 INIST-CNRS</rights><rights>2011 AACR.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c417t-6559e22893aaf0e6becd222538209cb59b6b4bb848214cdc49ad164d22da3f3</citedby><cites>FETCH-LOGICAL-c417t-6559e22893aaf0e6becd222538209cb59b6b4bb848214cdc49ad164d22da3f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,3357,4025,27928,27929,27930</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23757456$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21098650$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>DEVANEY, James</creatorcontrib><creatorcontrib>STIRZAKER, Clare</creatorcontrib><creatorcontrib>KENCH, James G</creatorcontrib><creatorcontrib>HENSHALL, Susan M</creatorcontrib><creatorcontrib>PE BENITO, Ruth</creatorcontrib><creatorcontrib>HAYNES, Anne-Maree</creatorcontrib><creatorcontrib>MAYOR, Regina</creatorcontrib><creatorcontrib>PEINADO, Miguel A</creatorcontrib><creatorcontrib>SUTHERLAND, Robert L</creatorcontrib><creatorcontrib>CLARK, Susan J</creatorcontrib><creatorcontrib>WENJIA QU</creatorcontrib><creatorcontrib>SONG, Jenny Z</creatorcontrib><creatorcontrib>STATHAM, Aaron L</creatorcontrib><creatorcontrib>PATTERSON, Kate I</creatorcontrib><creatorcontrib>HORVATH, Lisa G</creatorcontrib><creatorcontrib>TABOR, Bruce</creatorcontrib><creatorcontrib>COOLEN, Marcel W</creatorcontrib><creatorcontrib>HULF, Toby</creatorcontrib><title>Epigenetic Deregulation Across Chromosome 2q14.2 Differentiates Normal from Prostate Cancer and Provides a Regional Panel of Novel DNA Methylation Cancer Biomarkers</title><title>Cancer epidemiology, biomarkers & prevention</title><addtitle>Cancer Epidemiol Biomarkers Prev</addtitle><description>Previously, we showed that gene suppression commonly occurs across chromosome 2q14.2 in colorectal cancer, through a process of long-range epigenetic silencing (LRES), involving a combination of DNA methylation and repressive histone modifications. We now investigate whether LRES also occurs in prostate cancer across this 4-Mb region and whether differential DNA methylation of 2q14.2 genes could provide a regional panel of prostate cancer biomarkers.
We used highly sensitive DNA methylation headloop PCR assays that can detect 10 to 25 pg of methylated DNA with a specificity of at least 1:1,000, and chromatin immunoprecipitation assays to investigate regional epigenetic remodeling across 2q14.2 in prostate cancer, in a cohort of 195 primary prostate tumors and 90 matched normal controls.
Prostate cancer cells exhibit concordant deacetylation and methylation of histone H3 Lysine 9 (H3K9Ac and H3K9me2, respectively), and localized DNA hypermethylation of EN1, SCTR, and INHBB and corresponding loss of H3K27me3. EN1 and SCTR were frequently methylated (65% and 53%, respectively), whereas INHBB was less frequently methylated.
Consistent with LRES in colorectal cancer, we found regional epigenetic remodeling across 2q14.2 in prostate cancer. Concordant methylation of EN1 and SCTR was able to differentiate cancer from normal (P < 0.0001) and improved the diagnostic specificity of GSTP1 methylation for prostate cancer detection by 26%.
For the first time we show that DNA methylation of EN1 and SCTR promoters provide potential novel biomarkers for prostate cancer detection and in combination with GSTP1 methylation can add increased specificity and sensitivity to improve diagnostic potential.</description><subject>Biological and medical sciences</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Cell Line, Tumor</subject><subject>Chromatin Immunoprecipitation</subject><subject>Chromosomes, Human, Pair 2</subject><subject>DNA Methylation</subject><subject>Epigenesis, Genetic</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes, Tumor Suppressor</subject><subject>Glutathione S-Transferase pi - genetics</subject><subject>Homeodomain Proteins - genetics</subject><subject>Humans</subject><subject>Inhibin-beta Subunits - genetics</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Polymerase Chain Reaction - methods</subject><subject>Prognosis</subject><subject>Prostatic Neoplasms - diagnosis</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Receptors, G-Protein-Coupled - genetics</subject><subject>Receptors, Gastrointestinal Hormone - genetics</subject><subject>Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization</subject><subject>Tumors</subject><subject>Tumors of the urinary system</subject><subject>Urinary tract. Prostate gland</subject><issn>1055-9965</issn><issn>1538-7755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc9u1DAQxi0Eon_gEUC-oJ6ytR07iY_L7lIqtWUF3CPHGW8NSby1s5X6PjwoE5qWY08ejX7fzPj7CPnA2YJzVZ1zplSmdaEWm-1lxlnGSq5fkWOu8iorS6VeY_3EHJGTlH4xxkqt1FtyJDjTVaHYMfmz2fsdDDB6S9cQYXfozOjDQJc2hpTo6jaGPqTQAxV3XC4EXXvnEBxGb0ZI9CbE3nTUIUa3KBmxS1dmsBCpGdqpd-9bBA39DjucjPDWDNDR4FB8j8X6ZkmvYbx9mFfP6s8-9Cb-hpjekTfOdAnez-8p-fFl83P1Nbv6dnG5Wl5lVvJyzAqlNAhR6dwYx6BowLZCCDREMG0bpZuikU1TyUpwaVsrtWl5IZFpTe7yU3L2OHUfw90B0lj3PlnoOrw2HFKt0WElZZW_SFZCaCZkUSGpHsl_bkZw9T56_NVDzVk95VhPGdVTRjXmOHWnHFH3cd5waHpon1VPwSHwaQZMsqZzET3z6T-Xl6qUqsj_ApCjp4Q</recordid><startdate>2011</startdate><enddate>2011</enddate><creator>DEVANEY, James</creator><creator>STIRZAKER, Clare</creator><creator>KENCH, James G</creator><creator>HENSHALL, Susan M</creator><creator>PE BENITO, Ruth</creator><creator>HAYNES, Anne-Maree</creator><creator>MAYOR, Regina</creator><creator>PEINADO, Miguel A</creator><creator>SUTHERLAND, Robert L</creator><creator>CLARK, Susan J</creator><creator>WENJIA QU</creator><creator>SONG, Jenny Z</creator><creator>STATHAM, Aaron L</creator><creator>PATTERSON, Kate I</creator><creator>HORVATH, Lisa G</creator><creator>TABOR, Bruce</creator><creator>COOLEN, Marcel W</creator><creator>HULF, Toby</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>7X8</scope><scope>7TM</scope></search><sort><creationdate>2011</creationdate><title>Epigenetic Deregulation Across Chromosome 2q14.2 Differentiates Normal from Prostate Cancer and Provides a Regional Panel of Novel DNA Methylation Cancer Biomarkers</title><author>DEVANEY, James ; STIRZAKER, Clare ; KENCH, James G ; HENSHALL, Susan M ; PE BENITO, Ruth ; HAYNES, Anne-Maree ; MAYOR, Regina ; PEINADO, Miguel A ; SUTHERLAND, Robert L ; CLARK, Susan J ; WENJIA QU ; SONG, Jenny Z ; STATHAM, Aaron L ; PATTERSON, Kate I ; HORVATH, Lisa G ; TABOR, Bruce ; COOLEN, Marcel W ; HULF, Toby</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-6559e22893aaf0e6becd222538209cb59b6b4bb848214cdc49ad164d22da3f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Biological and medical sciences</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Cell Line, Tumor</topic><topic>Chromatin Immunoprecipitation</topic><topic>Chromosomes, Human, Pair 2</topic><topic>DNA Methylation</topic><topic>Epigenesis, Genetic</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes, Tumor Suppressor</topic><topic>Glutathione S-Transferase pi - genetics</topic><topic>Homeodomain Proteins - genetics</topic><topic>Humans</topic><topic>Inhibin-beta Subunits - genetics</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Polymerase Chain Reaction - methods</topic><topic>Prognosis</topic><topic>Prostatic Neoplasms - diagnosis</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Receptors, G-Protein-Coupled - genetics</topic><topic>Receptors, Gastrointestinal Hormone - genetics</topic><topic>Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization</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>DEVANEY, James</creatorcontrib><creatorcontrib>STIRZAKER, Clare</creatorcontrib><creatorcontrib>KENCH, James G</creatorcontrib><creatorcontrib>HENSHALL, Susan M</creatorcontrib><creatorcontrib>PE BENITO, Ruth</creatorcontrib><creatorcontrib>HAYNES, Anne-Maree</creatorcontrib><creatorcontrib>MAYOR, Regina</creatorcontrib><creatorcontrib>PEINADO, Miguel A</creatorcontrib><creatorcontrib>SUTHERLAND, Robert L</creatorcontrib><creatorcontrib>CLARK, Susan J</creatorcontrib><creatorcontrib>WENJIA QU</creatorcontrib><creatorcontrib>SONG, Jenny Z</creatorcontrib><creatorcontrib>STATHAM, Aaron L</creatorcontrib><creatorcontrib>PATTERSON, Kate I</creatorcontrib><creatorcontrib>HORVATH, Lisa G</creatorcontrib><creatorcontrib>TABOR, Bruce</creatorcontrib><creatorcontrib>COOLEN, Marcel W</creatorcontrib><creatorcontrib>HULF, Toby</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>MEDLINE - Academic</collection><collection>Nucleic Acids Abstracts</collection><jtitle>Cancer epidemiology, biomarkers & prevention</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>DEVANEY, James</au><au>STIRZAKER, Clare</au><au>KENCH, James G</au><au>HENSHALL, Susan M</au><au>PE BENITO, Ruth</au><au>HAYNES, Anne-Maree</au><au>MAYOR, Regina</au><au>PEINADO, Miguel A</au><au>SUTHERLAND, Robert L</au><au>CLARK, Susan J</au><au>WENJIA QU</au><au>SONG, Jenny Z</au><au>STATHAM, Aaron L</au><au>PATTERSON, Kate I</au><au>HORVATH, Lisa G</au><au>TABOR, Bruce</au><au>COOLEN, Marcel W</au><au>HULF, Toby</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Epigenetic Deregulation Across Chromosome 2q14.2 Differentiates Normal from Prostate Cancer and Provides a Regional Panel of Novel DNA Methylation Cancer Biomarkers</atitle><jtitle>Cancer epidemiology, biomarkers & prevention</jtitle><addtitle>Cancer Epidemiol Biomarkers Prev</addtitle><date>2011</date><risdate>2011</risdate><volume>20</volume><issue>1</issue><spage>148</spage><epage>159</epage><pages>148-159</pages><issn>1055-9965</issn><eissn>1538-7755</eissn><coden>CEBPE4</coden><abstract>Previously, we showed that gene suppression commonly occurs across chromosome 2q14.2 in colorectal cancer, through a process of long-range epigenetic silencing (LRES), involving a combination of DNA methylation and repressive histone modifications. We now investigate whether LRES also occurs in prostate cancer across this 4-Mb region and whether differential DNA methylation of 2q14.2 genes could provide a regional panel of prostate cancer biomarkers.
We used highly sensitive DNA methylation headloop PCR assays that can detect 10 to 25 pg of methylated DNA with a specificity of at least 1:1,000, and chromatin immunoprecipitation assays to investigate regional epigenetic remodeling across 2q14.2 in prostate cancer, in a cohort of 195 primary prostate tumors and 90 matched normal controls.
Prostate cancer cells exhibit concordant deacetylation and methylation of histone H3 Lysine 9 (H3K9Ac and H3K9me2, respectively), and localized DNA hypermethylation of EN1, SCTR, and INHBB and corresponding loss of H3K27me3. EN1 and SCTR were frequently methylated (65% and 53%, respectively), whereas INHBB was less frequently methylated.
Consistent with LRES in colorectal cancer, we found regional epigenetic remodeling across 2q14.2 in prostate cancer. Concordant methylation of EN1 and SCTR was able to differentiate cancer from normal (P < 0.0001) and improved the diagnostic specificity of GSTP1 methylation for prostate cancer detection by 26%.
For the first time we show that DNA methylation of EN1 and SCTR promoters provide potential novel biomarkers for prostate cancer detection and in combination with GSTP1 methylation can add increased specificity and sensitivity to improve diagnostic potential.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>21098650</pmid><doi>10.1158/1055-9965.EPI-10-0719</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
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| ispartof | Cancer epidemiology, biomarkers & prevention, 2011, Vol.20 (1), p.148-159 |
| issn | 1055-9965 1538-7755 |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; American Association for Cancer Research |
| subjects | Biological and medical sciences Biomarkers, Tumor - genetics Cell Line, Tumor Chromatin Immunoprecipitation Chromosomes, Human, Pair 2 DNA Methylation Epigenesis, Genetic Gene Expression Regulation, Neoplastic Genes, Tumor Suppressor Glutathione S-Transferase pi - genetics Homeodomain Proteins - genetics Humans Inhibin-beta Subunits - genetics Male Medical sciences Nephrology. Urinary tract diseases Polymerase Chain Reaction - methods Prognosis Prostatic Neoplasms - diagnosis Prostatic Neoplasms - genetics Receptors, G-Protein-Coupled - genetics Receptors, Gastrointestinal Hormone - genetics Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization Tumors Tumors of the urinary system Urinary tract. Prostate gland |
| title | Epigenetic Deregulation Across Chromosome 2q14.2 Differentiates Normal from Prostate Cancer and Provides a Regional Panel of Novel DNA Methylation Cancer Biomarkers |
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