DNA methylation and hormone receptor status in breast cancer
We examined whether differences in tumor DNA methylation were associated with more aggressive hormone receptor-negative breast cancer in an ethnically diverse group of patients in the Breast Cancer Care in Chicago (BCCC) study and using data from The Cancer Genome Atlas (TCGA). DNA was extracted fro...
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| Veröffentlicht in: | Clinical epigenetics 2016-02, Vol.8 (17), p.17-17, Article 17 |
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| creator | Benevolenskaya, Elizaveta V Islam, Abul B M M K Ahsan, Habibul Kibriya, Muhammad G Jasmine, Farzana Wolff, Ben Al-Alem, Umaima Wiley, Elizabeth Kajdacsy-Balla, Andre Macias, Virgilia Rauscher, Garth H |
| description | We examined whether differences in tumor DNA methylation were associated with more aggressive hormone receptor-negative breast cancer in an ethnically diverse group of patients in the Breast Cancer Care in Chicago (BCCC) study and using data from The Cancer Genome Atlas (TCGA).
DNA was extracted from formalin-fixed, paraffin-embedded samples on 75 patients (21 White, 31 African-American, and 23 Hispanic) (training dataset) enrolled in the BCCC. Hormone receptor status was defined as negative if tumors were negative for both estrogen and progesterone (ER/PR) receptors (N = 22/75). DNA methylation was analyzed at 1505 CpG sites within 807 gene promoters using the Illumina GoldenGate assay. Differential DNA methylation as a predictor of hormone receptor status was tested while controlling for false discovery rate and assigned to the gene closest to the respective CpG site. Next, those genes that predicted ER/PR status were validated using TCGA data with respect to DNA methylation (validation dataset), and correlations between CpG methylation and gene expression were examined. In the training dataset, 5.7 % of promoter mean methylation values (46/807) were associated with receptor status at P |
| doi_str_mv | 10.1186/s13148-016-0184-7 |
| format | Article |
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DNA was extracted from formalin-fixed, paraffin-embedded samples on 75 patients (21 White, 31 African-American, and 23 Hispanic) (training dataset) enrolled in the BCCC. Hormone receptor status was defined as negative if tumors were negative for both estrogen and progesterone (ER/PR) receptors (N = 22/75). DNA methylation was analyzed at 1505 CpG sites within 807 gene promoters using the Illumina GoldenGate assay. Differential DNA methylation as a predictor of hormone receptor status was tested while controlling for false discovery rate and assigned to the gene closest to the respective CpG site. Next, those genes that predicted ER/PR status were validated using TCGA data with respect to DNA methylation (validation dataset), and correlations between CpG methylation and gene expression were examined. In the training dataset, 5.7 % of promoter mean methylation values (46/807) were associated with receptor status at P < 0.05; for 88 % of these (38/46), hypermethylation was associated with receptor-positive disease. Hypermethylation for FZD9, MME, BCAP31, HDAC9, PAX6, SCGB3A1, PDGFRA, IGFBP3, and PTGS2 genes most strongly predicted receptor-positive disease. Twenty-one of 24 predictor genes from the training dataset were confirmed in the validation dataset. The level of DNA methylation at 19 out 22 genes, for which gene expression data were available, was associated with gene activity.
Higher levels of promoter methylation strongly correlate with hormone receptor positive status of breast tumors. For most of the genes identified in our training dataset as ER/PR receptor status predictors, DNA methylation correlated with stable gene expression level. The predictors performed well when evaluated on independent set of samples, with different racioethnic distribution, thus providing evidence that this set of DNA methylation biomarkers will likely generalize to prospective patient samples.</description><identifier>ISSN: 1868-7075</identifier><identifier>ISSN: 1868-7083</identifier><identifier>EISSN: 1868-7083</identifier><identifier>EISSN: 1868-7075</identifier><identifier>DOI: 10.1186/s13148-016-0184-7</identifier><identifier>PMID: 26884818</identifier><language>eng</language><publisher>Germany: BioMed Central Ltd</publisher><subject>Aged ; Breast cancer ; Breast Neoplasms - genetics ; Breast Neoplasms - physiopathology ; Cancer ; CpG Islands - genetics ; DNA ; DNA Methylation ; Epigenesis, Genetic ; Female ; Gene expression ; Genetic aspects ; Genetic Markers ; Genomes ; Genomics ; Hormones ; Humans ; Methylation ; Middle Aged ; Receptors, Estrogen - genetics ; Receptors, Estrogen - physiology ; Receptors, Progesterone - genetics ; Receptors, Progesterone - physiology</subject><ispartof>Clinical epigenetics, 2016-02, Vol.8 (17), p.17-17, Article 17</ispartof><rights>COPYRIGHT 2016 BioMed Central Ltd.</rights><rights>Copyright BioMed Central 2016</rights><rights>Benevolenskaya et al. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c494t-10cfacd125b57c47a3fc9a07b3c81e0ebd448fa521e070bf0a97519c73e1380e3</citedby><cites>FETCH-LOGICAL-c494t-10cfacd125b57c47a3fc9a07b3c81e0ebd448fa521e070bf0a97519c73e1380e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4754852/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4754852/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27915,27916,53782,53784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26884818$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Benevolenskaya, Elizaveta V</creatorcontrib><creatorcontrib>Islam, Abul B M M K</creatorcontrib><creatorcontrib>Ahsan, Habibul</creatorcontrib><creatorcontrib>Kibriya, Muhammad G</creatorcontrib><creatorcontrib>Jasmine, Farzana</creatorcontrib><creatorcontrib>Wolff, Ben</creatorcontrib><creatorcontrib>Al-Alem, Umaima</creatorcontrib><creatorcontrib>Wiley, Elizabeth</creatorcontrib><creatorcontrib>Kajdacsy-Balla, Andre</creatorcontrib><creatorcontrib>Macias, Virgilia</creatorcontrib><creatorcontrib>Rauscher, Garth H</creatorcontrib><title>DNA methylation and hormone receptor status in breast cancer</title><title>Clinical epigenetics</title><addtitle>Clin Epigenetics</addtitle><description>We examined whether differences in tumor DNA methylation were associated with more aggressive hormone receptor-negative breast cancer in an ethnically diverse group of patients in the Breast Cancer Care in Chicago (BCCC) study and using data from The Cancer Genome Atlas (TCGA).
DNA was extracted from formalin-fixed, paraffin-embedded samples on 75 patients (21 White, 31 African-American, and 23 Hispanic) (training dataset) enrolled in the BCCC. Hormone receptor status was defined as negative if tumors were negative for both estrogen and progesterone (ER/PR) receptors (N = 22/75). DNA methylation was analyzed at 1505 CpG sites within 807 gene promoters using the Illumina GoldenGate assay. Differential DNA methylation as a predictor of hormone receptor status was tested while controlling for false discovery rate and assigned to the gene closest to the respective CpG site. Next, those genes that predicted ER/PR status were validated using TCGA data with respect to DNA methylation (validation dataset), and correlations between CpG methylation and gene expression were examined. In the training dataset, 5.7 % of promoter mean methylation values (46/807) were associated with receptor status at P < 0.05; for 88 % of these (38/46), hypermethylation was associated with receptor-positive disease. Hypermethylation for FZD9, MME, BCAP31, HDAC9, PAX6, SCGB3A1, PDGFRA, IGFBP3, and PTGS2 genes most strongly predicted receptor-positive disease. Twenty-one of 24 predictor genes from the training dataset were confirmed in the validation dataset. The level of DNA methylation at 19 out 22 genes, for which gene expression data were available, was associated with gene activity.
Higher levels of promoter methylation strongly correlate with hormone receptor positive status of breast tumors. For most of the genes identified in our training dataset as ER/PR receptor status predictors, DNA methylation correlated with stable gene expression level. The predictors performed well when evaluated on independent set of samples, with different racioethnic distribution, thus providing evidence that this set of DNA methylation biomarkers will likely generalize to prospective patient samples.</description><subject>Aged</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - physiopathology</subject><subject>Cancer</subject><subject>CpG Islands - genetics</subject><subject>DNA</subject><subject>DNA Methylation</subject><subject>Epigenesis, Genetic</subject><subject>Female</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Genetic Markers</subject><subject>Genomes</subject><subject>Genomics</subject><subject>Hormones</subject><subject>Humans</subject><subject>Methylation</subject><subject>Middle Aged</subject><subject>Receptors, Estrogen - genetics</subject><subject>Receptors, Estrogen - physiology</subject><subject>Receptors, Progesterone - genetics</subject><subject>Receptors, Progesterone - physiology</subject><issn>1868-7075</issn><issn>1868-7083</issn><issn>1868-7083</issn><issn>1868-7075</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptUV1L5DAUDbKiov6AfZGCL_tSzW3SJgVZGPxckN2X3eeQprdOpE3GJBX892YYd9RlE0KSe885yb2HkK9AzwBkcx6BAZclhSYvyUuxQw5yXJaCSvZlexb1PjmO8ZHmwdq2BbpH9qtGSi5BHpCLq5-LYsK0fBl1st4V2vXF0ofJOywCGlwlH4qYdJpjYV3RBdQxFUY7g-GI7A56jHj8th-SPzfXvy_vyvtftz8uF_el4S1PJVAzaNNDVXe1MFxoNphWU9ExIwEpdj3nctB1lS-CdgPVraihNYIhMEmRHZLvG93V3E3YG3Qp6FGtgp10eFFeW_U54-xSPfhnxUXNZV1lgW9vAsE_zRiTmmw0OI7aoZ-jAtE0VcOaCjL09B_oo5-Dy-VllABayQbEO-pBj6isG3x-16xF1YJzxiXN3mTU2X9QefY4WZM7PNgc_0SADcEEH2PAYVsjULV2XW1cV9l1tXZdrb9y8rE5W8Zfj9krxNel9Q</recordid><startdate>20160216</startdate><enddate>20160216</enddate><creator>Benevolenskaya, Elizaveta V</creator><creator>Islam, Abul B M M K</creator><creator>Ahsan, Habibul</creator><creator>Kibriya, Muhammad G</creator><creator>Jasmine, Farzana</creator><creator>Wolff, Ben</creator><creator>Al-Alem, Umaima</creator><creator>Wiley, Elizabeth</creator><creator>Kajdacsy-Balla, Andre</creator><creator>Macias, Virgilia</creator><creator>Rauscher, Garth H</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160216</creationdate><title>DNA methylation and hormone receptor status in breast cancer</title><author>Benevolenskaya, Elizaveta V ; Islam, Abul B M M K ; Ahsan, Habibul ; Kibriya, Muhammad G ; Jasmine, Farzana ; Wolff, Ben ; Al-Alem, Umaima ; Wiley, Elizabeth ; Kajdacsy-Balla, Andre ; Macias, Virgilia ; Rauscher, Garth H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c494t-10cfacd125b57c47a3fc9a07b3c81e0ebd448fa521e070bf0a97519c73e1380e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Aged</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - physiopathology</topic><topic>Cancer</topic><topic>CpG Islands - genetics</topic><topic>DNA</topic><topic>DNA Methylation</topic><topic>Epigenesis, Genetic</topic><topic>Female</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Genetic Markers</topic><topic>Genomes</topic><topic>Genomics</topic><topic>Hormones</topic><topic>Humans</topic><topic>Methylation</topic><topic>Middle Aged</topic><topic>Receptors, Estrogen - genetics</topic><topic>Receptors, Estrogen - physiology</topic><topic>Receptors, Progesterone - genetics</topic><topic>Receptors, Progesterone - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Benevolenskaya, Elizaveta V</creatorcontrib><creatorcontrib>Islam, Abul B M M K</creatorcontrib><creatorcontrib>Ahsan, Habibul</creatorcontrib><creatorcontrib>Kibriya, Muhammad G</creatorcontrib><creatorcontrib>Jasmine, Farzana</creatorcontrib><creatorcontrib>Wolff, Ben</creatorcontrib><creatorcontrib>Al-Alem, Umaima</creatorcontrib><creatorcontrib>Wiley, Elizabeth</creatorcontrib><creatorcontrib>Kajdacsy-Balla, Andre</creatorcontrib><creatorcontrib>Macias, Virgilia</creatorcontrib><creatorcontrib>Rauscher, Garth H</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Clinical epigenetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Benevolenskaya, Elizaveta V</au><au>Islam, Abul B M M K</au><au>Ahsan, Habibul</au><au>Kibriya, Muhammad G</au><au>Jasmine, Farzana</au><au>Wolff, Ben</au><au>Al-Alem, Umaima</au><au>Wiley, Elizabeth</au><au>Kajdacsy-Balla, Andre</au><au>Macias, Virgilia</au><au>Rauscher, Garth H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>DNA methylation and hormone receptor status in breast cancer</atitle><jtitle>Clinical epigenetics</jtitle><addtitle>Clin Epigenetics</addtitle><date>2016-02-16</date><risdate>2016</risdate><volume>8</volume><issue>17</issue><spage>17</spage><epage>17</epage><pages>17-17</pages><artnum>17</artnum><issn>1868-7075</issn><issn>1868-7083</issn><eissn>1868-7083</eissn><eissn>1868-7075</eissn><abstract>We examined whether differences in tumor DNA methylation were associated with more aggressive hormone receptor-negative breast cancer in an ethnically diverse group of patients in the Breast Cancer Care in Chicago (BCCC) study and using data from The Cancer Genome Atlas (TCGA).
DNA was extracted from formalin-fixed, paraffin-embedded samples on 75 patients (21 White, 31 African-American, and 23 Hispanic) (training dataset) enrolled in the BCCC. Hormone receptor status was defined as negative if tumors were negative for both estrogen and progesterone (ER/PR) receptors (N = 22/75). DNA methylation was analyzed at 1505 CpG sites within 807 gene promoters using the Illumina GoldenGate assay. Differential DNA methylation as a predictor of hormone receptor status was tested while controlling for false discovery rate and assigned to the gene closest to the respective CpG site. Next, those genes that predicted ER/PR status were validated using TCGA data with respect to DNA methylation (validation dataset), and correlations between CpG methylation and gene expression were examined. In the training dataset, 5.7 % of promoter mean methylation values (46/807) were associated with receptor status at P < 0.05; for 88 % of these (38/46), hypermethylation was associated with receptor-positive disease. Hypermethylation for FZD9, MME, BCAP31, HDAC9, PAX6, SCGB3A1, PDGFRA, IGFBP3, and PTGS2 genes most strongly predicted receptor-positive disease. Twenty-one of 24 predictor genes from the training dataset were confirmed in the validation dataset. The level of DNA methylation at 19 out 22 genes, for which gene expression data were available, was associated with gene activity.
Higher levels of promoter methylation strongly correlate with hormone receptor positive status of breast tumors. For most of the genes identified in our training dataset as ER/PR receptor status predictors, DNA methylation correlated with stable gene expression level. The predictors performed well when evaluated on independent set of samples, with different racioethnic distribution, thus providing evidence that this set of DNA methylation biomarkers will likely generalize to prospective patient samples.</abstract><cop>Germany</cop><pub>BioMed Central Ltd</pub><pmid>26884818</pmid><doi>10.1186/s13148-016-0184-7</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aged Breast cancer Breast Neoplasms - genetics Breast Neoplasms - physiopathology Cancer CpG Islands - genetics DNA DNA Methylation Epigenesis, Genetic Female Gene expression Genetic aspects Genetic Markers Genomes Genomics Hormones Humans Methylation Middle Aged Receptors, Estrogen - genetics Receptors, Estrogen - physiology Receptors, Progesterone - genetics Receptors, Progesterone - physiology |
| title | DNA methylation and hormone receptor status in breast cancer |
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