Methodology to analyze gene expression patterns of early mammary development in pig models
In mammary gland development, normal stem cell activity occurs in the embryonic stage and postnatally. Research supports that certain breast cancers contain a small sub-population of cells that mimic stem-like activity. It is believed stem cell activation in the mutated mature human mammary tissue i...
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description | In mammary gland development, normal stem cell activity occurs in the embryonic stage and postnatally. Research supports that certain breast cancers contain a small sub-population of cells that mimic stem-like activity. It is believed stem cell activation in the mutated mature human mammary tissue is what drives quiescent epithelial cells to convert to mesenchymal states initiating migration, invasion, and metastasis in breast cancer. The goal of the work reported herein was to investigate early mammary development gene expression in the postnatal pig using fine needle biopsy methods in order to establish a reliable model for human breast cancer detection. Tissue samples were collected from pig mammary glands beginning at Day 11 of age through Day 39 in order to capture early postnatal-growth gene expression. Based on the initial clustering analysis, two distinct clusters of gene expression profiles occurred before and after Day 25 of mammary development. Gene set enrichment analysis (GSEA) ontology indicated the cellular processes that changed after Day 25, and many of these processes were implicated in epithelial–mesenchymal transition (EMT) signaling events. Gene expression in the postnatal pig was compared with the Epithelial–Mesenchymal Transition gene database (dbEMT) confirming the presence of EMT activity in this early developmental program. Information from this study will provide insight into early postnatal mammary gland development. In addition, mechanisms exploited by mutated mammary epithelial cells leading to cancer initiation and growth may be detected considering that mutated mammary epithelial cells can reactivate early developmental signals. |
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Research supports that certain breast cancers contain a small sub-population of cells that mimic stem-like activity. It is believed stem cell activation in the mutated mature human mammary tissue is what drives quiescent epithelial cells to convert to mesenchymal states initiating migration, invasion, and metastasis in breast cancer. The goal of the work reported herein was to investigate early mammary development gene expression in the postnatal pig using fine needle biopsy methods in order to establish a reliable model for human breast cancer detection. Tissue samples were collected from pig mammary glands beginning at Day 11 of age through Day 39 in order to capture early postnatal-growth gene expression. Based on the initial clustering analysis, two distinct clusters of gene expression profiles occurred before and after Day 25 of mammary development. Gene set enrichment analysis (GSEA) ontology indicated the cellular processes that changed after Day 25, and many of these processes were implicated in epithelial–mesenchymal transition (EMT) signaling events. Gene expression in the postnatal pig was compared with the Epithelial–Mesenchymal Transition gene database (dbEMT) confirming the presence of EMT activity in this early developmental program. Information from this study will provide insight into early postnatal mammary gland development. In addition, mechanisms exploited by mutated mammary epithelial cells leading to cancer initiation and growth may be detected considering that mutated mammary epithelial cells can reactivate early developmental signals.</description><identifier>ISSN: 0301-4851</identifier><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-020-05362-1</identifier><identifier>PMID: 32219771</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Animal Anatomy ; Animal Biochemistry ; Animal models ; Animals ; Biomedical and Life Sciences ; Biopsy ; Breast cancer ; Breast Neoplasms - metabolism ; Cell activation ; Embryogenesis ; Epithelial cells ; Epithelial Cells - metabolism ; Epithelial-Mesenchymal Transition - genetics ; Female ; Gene expression ; Gene Expression - genetics ; Gene Expression Profiling - methods ; Gene Expression Regulation, Neoplastic - genetics ; Gene set enrichment analysis ; Histology ; Life Sciences ; Mammary gland ; Mammary Glands, Animal - growth & development ; Mammary Glands, Animal - metabolism ; Mesenchyme ; Metastases ; Methods Paper ; Morphology ; Organogenesis - genetics ; Signal Transduction - physiology ; Stem cells ; Stem Cells - metabolism ; Swine - genetics ; Transcriptome - genetics</subject><ispartof>Molecular biology reports, 2020-04, Vol.47 (4), p.3241-3248</ispartof><rights>The Author(s) 2020</rights><rights>The Author(s) 2020. 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Research supports that certain breast cancers contain a small sub-population of cells that mimic stem-like activity. It is believed stem cell activation in the mutated mature human mammary tissue is what drives quiescent epithelial cells to convert to mesenchymal states initiating migration, invasion, and metastasis in breast cancer. The goal of the work reported herein was to investigate early mammary development gene expression in the postnatal pig using fine needle biopsy methods in order to establish a reliable model for human breast cancer detection. Tissue samples were collected from pig mammary glands beginning at Day 11 of age through Day 39 in order to capture early postnatal-growth gene expression. Based on the initial clustering analysis, two distinct clusters of gene expression profiles occurred before and after Day 25 of mammary development. Gene set enrichment analysis (GSEA) ontology indicated the cellular processes that changed after Day 25, and many of these processes were implicated in epithelial–mesenchymal transition (EMT) signaling events. Gene expression in the postnatal pig was compared with the Epithelial–Mesenchymal Transition gene database (dbEMT) confirming the presence of EMT activity in this early developmental program. Information from this study will provide insight into early postnatal mammary gland development. In addition, mechanisms exploited by mutated mammary epithelial cells leading to cancer initiation and growth may be detected considering that mutated mammary epithelial cells can reactivate early developmental signals.</description><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Animal models</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biopsy</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - metabolism</subject><subject>Cell activation</subject><subject>Embryogenesis</subject><subject>Epithelial cells</subject><subject>Epithelial Cells - metabolism</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression - genetics</subject><subject>Gene Expression Profiling - methods</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Gene set enrichment analysis</subject><subject>Histology</subject><subject>Life Sciences</subject><subject>Mammary gland</subject><subject>Mammary Glands, Animal - growth & development</subject><subject>Mammary Glands, Animal - metabolism</subject><subject>Mesenchyme</subject><subject>Metastases</subject><subject>Methods Paper</subject><subject>Morphology</subject><subject>Organogenesis - genetics</subject><subject>Signal Transduction - physiology</subject><subject>Stem cells</subject><subject>Stem Cells - metabolism</subject><subject>Swine - genetics</subject><subject>Transcriptome - genetics</subject><issn>0301-4851</issn><issn>1573-4978</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><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>eNp9kE1P3DAQhq2qqCwLf6CHylIvvYR6_BE7R7RqSyVQL3DhYjnx7JJVEgc7i7r8egy7gMSB0xzmed_RPIR8BXYKjOmfCYAJUTDOCqZEyQv4RGagtChkpc1nMmOCQSGNgkNylNKaMSZBqy_kUHAOldYwIzeXON0GH7qw2tIpUDe4bvuAdIUDUvw_RkypDQMd3TRhHBINS4oudlvau753cUs93mMXxh6HibYZbFe0Dx67dEwOlq5LeLKfc3L9-9fV4ry4-Pfn7-LsomgkVFNhvKpMjY1hXqpKQCk1Go1QctV40KWUTDUOwSgtaxDoS14vQZa1MHWtnBdz8mPXO8Zwt8E02b5NDXadGzBskuXCSA5SKZXR7-_QddjE_HKmlNZaltLwTPEd1cSQUsSlHWP79KsFZp_M2515m83bZ_MWcujbvnpT9-hfIy-qMyB2QMqrYYXx7fYHtY8YV44Z</recordid><startdate>20200401</startdate><enddate>20200401</enddate><creator>Moss, Matthew A.</creator><creator>Williams, Breanne</creator><creator>Ferdous, Farzana</creator><creator>Scott, Tom</creator><creator>Dunn, Heather W.</creator><general>Springer Netherlands</general><general>Springer Nature B.V</general><scope>C6C</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>3V.</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</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>FR3</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>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-3657-452X</orcidid><orcidid>https://orcid.org/0000-0002-3468-6608</orcidid><orcidid>https://orcid.org/0000-0001-6816-3453</orcidid></search><sort><creationdate>20200401</creationdate><title>Methodology to analyze gene expression patterns of early mammary development in pig models</title><author>Moss, Matthew A. ; Williams, Breanne ; Ferdous, Farzana ; Scott, Tom ; Dunn, Heather W.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c419t-8d598bec80d45931647e87e1625cd1764405cae18574b13ed62bf146b38bb5ad3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animal Anatomy</topic><topic>Animal Biochemistry</topic><topic>Animal models</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biopsy</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - metabolism</topic><topic>Cell activation</topic><topic>Embryogenesis</topic><topic>Epithelial cells</topic><topic>Epithelial Cells - metabolism</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression - genetics</topic><topic>Gene Expression Profiling - methods</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Gene set enrichment analysis</topic><topic>Histology</topic><topic>Life Sciences</topic><topic>Mammary gland</topic><topic>Mammary Glands, Animal - growth & development</topic><topic>Mammary Glands, Animal - metabolism</topic><topic>Mesenchyme</topic><topic>Metastases</topic><topic>Methods Paper</topic><topic>Morphology</topic><topic>Organogenesis - genetics</topic><topic>Signal Transduction - physiology</topic><topic>Stem cells</topic><topic>Stem Cells - metabolism</topic><topic>Swine - genetics</topic><topic>Transcriptome - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Moss, Matthew A.</creatorcontrib><creatorcontrib>Williams, Breanne</creatorcontrib><creatorcontrib>Ferdous, Farzana</creatorcontrib><creatorcontrib>Scott, Tom</creatorcontrib><creatorcontrib>Dunn, Heather W.</creatorcontrib><collection>Springer Nature OA Free Journals</collection><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>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</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>Engineering Research Database</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>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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 Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular biology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Moss, Matthew A.</au><au>Williams, Breanne</au><au>Ferdous, Farzana</au><au>Scott, Tom</au><au>Dunn, Heather W.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Methodology to analyze gene expression patterns of early mammary development in pig models</atitle><jtitle>Molecular biology reports</jtitle><stitle>Mol Biol Rep</stitle><addtitle>Mol Biol Rep</addtitle><date>2020-04-01</date><risdate>2020</risdate><volume>47</volume><issue>4</issue><spage>3241</spage><epage>3248</epage><pages>3241-3248</pages><issn>0301-4851</issn><eissn>1573-4978</eissn><abstract>In mammary gland development, normal stem cell activity occurs in the embryonic stage and postnatally. Research supports that certain breast cancers contain a small sub-population of cells that mimic stem-like activity. It is believed stem cell activation in the mutated mature human mammary tissue is what drives quiescent epithelial cells to convert to mesenchymal states initiating migration, invasion, and metastasis in breast cancer. The goal of the work reported herein was to investigate early mammary development gene expression in the postnatal pig using fine needle biopsy methods in order to establish a reliable model for human breast cancer detection. Tissue samples were collected from pig mammary glands beginning at Day 11 of age through Day 39 in order to capture early postnatal-growth gene expression. Based on the initial clustering analysis, two distinct clusters of gene expression profiles occurred before and after Day 25 of mammary development. Gene set enrichment analysis (GSEA) ontology indicated the cellular processes that changed after Day 25, and many of these processes were implicated in epithelial–mesenchymal transition (EMT) signaling events. Gene expression in the postnatal pig was compared with the Epithelial–Mesenchymal Transition gene database (dbEMT) confirming the presence of EMT activity in this early developmental program. Information from this study will provide insight into early postnatal mammary gland development. In addition, mechanisms exploited by mutated mammary epithelial cells leading to cancer initiation and growth may be detected considering that mutated mammary epithelial cells can reactivate early developmental signals.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>32219771</pmid><doi>10.1007/s11033-020-05362-1</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-3657-452X</orcidid><orcidid>https://orcid.org/0000-0002-3468-6608</orcidid><orcidid>https://orcid.org/0000-0001-6816-3453</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Animal Anatomy Animal Biochemistry Animal models Animals Biomedical and Life Sciences Biopsy Breast cancer Breast Neoplasms - metabolism Cell activation Embryogenesis Epithelial cells Epithelial Cells - metabolism Epithelial-Mesenchymal Transition - genetics Female Gene expression Gene Expression - genetics Gene Expression Profiling - methods Gene Expression Regulation, Neoplastic - genetics Gene set enrichment analysis Histology Life Sciences Mammary gland Mammary Glands, Animal - growth & development Mammary Glands, Animal - metabolism Mesenchyme Metastases Methods Paper Morphology Organogenesis - genetics Signal Transduction - physiology Stem cells Stem Cells - metabolism Swine - genetics Transcriptome - genetics |
title | Methodology to analyze gene expression patterns of early mammary development in pig models |
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