MMTV-cre;Ccn6 knockout mice develop tumors recapitulating human metaplastic breast carcinomas
Metaplastic breast carcinoma is an aggressive form of invasive breast cancer with histological evidence of epithelial to mesenchymal transition (EMT). However, the defining molecular events are unknown. Here we show that CCN6 (WISP3), a secreted matricellular protein of the CCN (CYR61/CTGF/NOV) fami...
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| Veröffentlicht in: | Oncogene 2017-04, Vol.36 (16), p.2275-2285 |
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| creator | Martin, E E Huang, W Anwar, T Arellano-Garcia, C Burman, B Guan, J-L Gonzalez, M E Kleer, C G |
| description | Metaplastic breast carcinoma is an aggressive form of invasive breast cancer with histological evidence of epithelial to mesenchymal transition (EMT). However, the defining molecular events are unknown. Here we show that CCN6 (WISP3), a secreted matricellular protein of the CCN (CYR61/CTGF/NOV) family, is significantly downregulated in clinical samples of human spindle cell metaplastic breast carcinoma. We generated a mouse model of mammary epithelial-specific
Ccn6
deletion by developing a floxed
Ccn6
mouse which was bred with an MMTV-Cre mouse.
Ccn6
fl/fl
;MMTV-Cre mice displayed severe defects in ductal branching and abnormal age-related involution compared to littermate controls.
Ccn6
fl/fl
;MMTV-Cre mice developed invasive high grade mammary carcinomas with
bona fide
EMT, histologically similar to human metaplastic breast carcinomas. Global gene expression profiling of
Ccn6
fl/fl
mammary carcinomas and comparison of orthologous genes with a human metaplastic carcinoma signature revealed a significant overlap of 87 genes (
P
=5 × 10
−11
). Among the shared deregulated genes between mouse and human are important regulators of epithelial morphogenesis including
Cdh1, Ck19, Cldn3
and
4, Ddr1,
and
Wnt10a
. These results document a causal role for
Ccn6
deletion in the pathogenesis of metaplastic carcinomas with histological and molecular similarities with human disease. We provide a platform to study new targets in the diagnosis and treatment of human metaplastic carcinomas, and a new disease relevant model in which to test new treatment strategies. |
| doi_str_mv | 10.1038/onc.2016.381 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5398917</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1897390781</sourcerecordid><originalsourceid>FETCH-LOGICAL-c511t-3e93189ab776df9ad4e2dc077a78d1dd8ccb18015a98ccb66b0037125cda63953</originalsourceid><addsrcrecordid>eNqNkstrFTEUxoMo9lrduZaAGxfONY_JC0GQiy9ocVPdScgkubdpZ5Jpkin435vrraWKiKscOD--c86XD4CnGK0xovJVinZNEOZrKvE9sMK94B1jqr8PVkgx1ClCyRF4VMoFQkgoRB6CIyIkVlz0K_Dt9PTsa2ezf72xkcPLmOxlWiqcgvXQ-Ws_phnWZUq5wOytmUNdRlND3MHzZTIRTr6aeTSlBguH7FsBrck2xDSZ8hg82Jqx-Cc37zH48v7d2eZjd_L5w6fN25POMoxrR72iWCozCMHdVhnXe-IsEsII6bBz0toBS4SZUfuS8wEhKjBh1hlOFaPH4M1Bd16GyTvrY81m1HMOk8nfdTJB_96J4Vzv0rVmVEmFRRN4cSOQ09XiS9VTKNaPo4k-LUW37QRVqNn2HygViDRZ0tDnf6AXacmxOaEJx4xRipT8F4Vlm8sIZn2jXh4om1Mp2W9vr8NI74OgWxD0Pgia_tzy2V1HbuFfP9-A7gCU1oo7n-9M_ZvgD1ljvcs</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1889752154</pqid></control><display><type>article</type><title>MMTV-cre;Ccn6 knockout mice develop tumors recapitulating human metaplastic breast carcinomas</title><source>MEDLINE</source><source>Nature</source><source>SpringerLink Journals - AutoHoldings</source><creator>Martin, E E ; Huang, W ; Anwar, T ; Arellano-Garcia, C ; Burman, B ; Guan, J-L ; Gonzalez, M E ; Kleer, C G</creator><creatorcontrib>Martin, E E ; Huang, W ; Anwar, T ; Arellano-Garcia, C ; Burman, B ; Guan, J-L ; Gonzalez, M E ; Kleer, C G</creatorcontrib><description>Metaplastic breast carcinoma is an aggressive form of invasive breast cancer with histological evidence of epithelial to mesenchymal transition (EMT). However, the defining molecular events are unknown. Here we show that CCN6 (WISP3), a secreted matricellular protein of the CCN (CYR61/CTGF/NOV) family, is significantly downregulated in clinical samples of human spindle cell metaplastic breast carcinoma. We generated a mouse model of mammary epithelial-specific
Ccn6
deletion by developing a floxed
Ccn6
mouse which was bred with an MMTV-Cre mouse.
Ccn6
fl/fl
;MMTV-Cre mice displayed severe defects in ductal branching and abnormal age-related involution compared to littermate controls.
Ccn6
fl/fl
;MMTV-Cre mice developed invasive high grade mammary carcinomas with
bona fide
EMT, histologically similar to human metaplastic breast carcinomas. Global gene expression profiling of
Ccn6
fl/fl
mammary carcinomas and comparison of orthologous genes with a human metaplastic carcinoma signature revealed a significant overlap of 87 genes (
P
=5 × 10
−11
). Among the shared deregulated genes between mouse and human are important regulators of epithelial morphogenesis including
Cdh1, Ck19, Cldn3
and
4, Ddr1,
and
Wnt10a
. These results document a causal role for
Ccn6
deletion in the pathogenesis of metaplastic carcinomas with histological and molecular similarities with human disease. We provide a platform to study new targets in the diagnosis and treatment of human metaplastic carcinomas, and a new disease relevant model in which to test new treatment strategies.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/onc.2016.381</identifier><identifier>PMID: 27819674</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>42/41 ; 631/67/1347 ; 64/110 ; 692/53/2421 ; 82/51 ; Age ; Animals ; Apoptosis ; Breast - pathology ; Breast cancer ; Breast carcinoma ; Breast Neoplasms - genetics ; Breast Neoplasms - pathology ; CCN Intercellular Signaling Proteins - genetics ; Cell Biology ; Connective tissue growth factor ; CYR61 protein ; Disease Models, Animal ; E-cadherin ; Female ; Gene expression ; Genes, Tumor Suppressor ; Human Genetics ; Humans ; Internal Medicine ; Invasiveness ; Male ; Mammary gland ; Mammary Neoplasms, Animal - pathology ; Medicine ; Medicine & Public Health ; Mesenchyme ; Metaplasia - genetics ; Mice ; Mice, Inbred Strains ; Mice, Knockout ; Morphogenesis ; Oncology ; original-article ; Rodents ; Tumors</subject><ispartof>Oncogene, 2017-04, Vol.36 (16), p.2275-2285</ispartof><rights>Macmillan Publishers Limited, part of Springer Nature. 2017</rights><rights>Copyright Nature Publishing Group Apr 20, 2017</rights><rights>Macmillan Publishers Limited, part of Springer Nature. 2017.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c511t-3e93189ab776df9ad4e2dc077a78d1dd8ccb18015a98ccb66b0037125cda63953</citedby><cites>FETCH-LOGICAL-c511t-3e93189ab776df9ad4e2dc077a78d1dd8ccb18015a98ccb66b0037125cda63953</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/onc.2016.381$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/onc.2016.381$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,780,784,885,27922,27923,41486,42555,51317</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27819674$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Martin, E E</creatorcontrib><creatorcontrib>Huang, W</creatorcontrib><creatorcontrib>Anwar, T</creatorcontrib><creatorcontrib>Arellano-Garcia, C</creatorcontrib><creatorcontrib>Burman, B</creatorcontrib><creatorcontrib>Guan, J-L</creatorcontrib><creatorcontrib>Gonzalez, M E</creatorcontrib><creatorcontrib>Kleer, C G</creatorcontrib><title>MMTV-cre;Ccn6 knockout mice develop tumors recapitulating human metaplastic breast carcinomas</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Metaplastic breast carcinoma is an aggressive form of invasive breast cancer with histological evidence of epithelial to mesenchymal transition (EMT). However, the defining molecular events are unknown. Here we show that CCN6 (WISP3), a secreted matricellular protein of the CCN (CYR61/CTGF/NOV) family, is significantly downregulated in clinical samples of human spindle cell metaplastic breast carcinoma. We generated a mouse model of mammary epithelial-specific
Ccn6
deletion by developing a floxed
Ccn6
mouse which was bred with an MMTV-Cre mouse.
Ccn6
fl/fl
;MMTV-Cre mice displayed severe defects in ductal branching and abnormal age-related involution compared to littermate controls.
Ccn6
fl/fl
;MMTV-Cre mice developed invasive high grade mammary carcinomas with
bona fide
EMT, histologically similar to human metaplastic breast carcinomas. Global gene expression profiling of
Ccn6
fl/fl
mammary carcinomas and comparison of orthologous genes with a human metaplastic carcinoma signature revealed a significant overlap of 87 genes (
P
=5 × 10
−11
). Among the shared deregulated genes between mouse and human are important regulators of epithelial morphogenesis including
Cdh1, Ck19, Cldn3
and
4, Ddr1,
and
Wnt10a
. These results document a causal role for
Ccn6
deletion in the pathogenesis of metaplastic carcinomas with histological and molecular similarities with human disease. We provide a platform to study new targets in the diagnosis and treatment of human metaplastic carcinomas, and a new disease relevant model in which to test new treatment strategies.</description><subject>42/41</subject><subject>631/67/1347</subject><subject>64/110</subject><subject>692/53/2421</subject><subject>82/51</subject><subject>Age</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Breast - pathology</subject><subject>Breast cancer</subject><subject>Breast carcinoma</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - pathology</subject><subject>CCN Intercellular Signaling Proteins - genetics</subject><subject>Cell Biology</subject><subject>Connective tissue growth factor</subject><subject>CYR61 protein</subject><subject>Disease Models, Animal</subject><subject>E-cadherin</subject><subject>Female</subject><subject>Gene expression</subject><subject>Genes, Tumor Suppressor</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Invasiveness</subject><subject>Male</subject><subject>Mammary gland</subject><subject>Mammary Neoplasms, Animal - pathology</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mesenchyme</subject><subject>Metaplasia - genetics</subject><subject>Mice</subject><subject>Mice, Inbred Strains</subject><subject>Mice, Knockout</subject><subject>Morphogenesis</subject><subject>Oncology</subject><subject>original-article</subject><subject>Rodents</subject><subject>Tumors</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkstrFTEUxoMo9lrduZaAGxfONY_JC0GQiy9ocVPdScgkubdpZ5Jpkin435vrraWKiKscOD--c86XD4CnGK0xovJVinZNEOZrKvE9sMK94B1jqr8PVkgx1ClCyRF4VMoFQkgoRB6CIyIkVlz0K_Dt9PTsa2ezf72xkcPLmOxlWiqcgvXQ-Ws_phnWZUq5wOytmUNdRlND3MHzZTIRTr6aeTSlBguH7FsBrck2xDSZ8hg82Jqx-Cc37zH48v7d2eZjd_L5w6fN25POMoxrR72iWCozCMHdVhnXe-IsEsII6bBz0toBS4SZUfuS8wEhKjBh1hlOFaPH4M1Bd16GyTvrY81m1HMOk8nfdTJB_96J4Vzv0rVmVEmFRRN4cSOQ09XiS9VTKNaPo4k-LUW37QRVqNn2HygViDRZ0tDnf6AXacmxOaEJx4xRipT8F4Vlm8sIZn2jXh4om1Mp2W9vr8NI74OgWxD0Pgia_tzy2V1HbuFfP9-A7gCU1oo7n-9M_ZvgD1ljvcs</recordid><startdate>20170420</startdate><enddate>20170420</enddate><creator>Martin, E E</creator><creator>Huang, W</creator><creator>Anwar, T</creator><creator>Arellano-Garcia, C</creator><creator>Burman, B</creator><creator>Guan, J-L</creator><creator>Gonzalez, M E</creator><creator>Kleer, C G</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</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>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170420</creationdate><title>MMTV-cre;Ccn6 knockout mice develop tumors recapitulating human metaplastic breast carcinomas</title><author>Martin, E E ; Huang, W ; Anwar, T ; Arellano-Garcia, C ; Burman, B ; Guan, J-L ; Gonzalez, M E ; Kleer, C G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c511t-3e93189ab776df9ad4e2dc077a78d1dd8ccb18015a98ccb66b0037125cda63953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>42/41</topic><topic>631/67/1347</topic><topic>64/110</topic><topic>692/53/2421</topic><topic>82/51</topic><topic>Age</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Breast - pathology</topic><topic>Breast cancer</topic><topic>Breast carcinoma</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - pathology</topic><topic>CCN Intercellular Signaling Proteins - genetics</topic><topic>Cell Biology</topic><topic>Connective tissue growth factor</topic><topic>CYR61 protein</topic><topic>Disease Models, Animal</topic><topic>E-cadherin</topic><topic>Female</topic><topic>Gene expression</topic><topic>Genes, Tumor Suppressor</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Invasiveness</topic><topic>Male</topic><topic>Mammary gland</topic><topic>Mammary Neoplasms, Animal - pathology</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mesenchyme</topic><topic>Metaplasia - genetics</topic><topic>Mice</topic><topic>Mice, Inbred Strains</topic><topic>Mice, Knockout</topic><topic>Morphogenesis</topic><topic>Oncology</topic><topic>original-article</topic><topic>Rodents</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Martin, E E</creatorcontrib><creatorcontrib>Huang, W</creatorcontrib><creatorcontrib>Anwar, T</creatorcontrib><creatorcontrib>Arellano-Garcia, C</creatorcontrib><creatorcontrib>Burman, B</creatorcontrib><creatorcontrib>Guan, J-L</creatorcontrib><creatorcontrib>Gonzalez, M E</creatorcontrib><creatorcontrib>Kleer, C G</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>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS 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>ProQuest Pharma Collection</collection><collection>Public Health Database</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>Research Library (Alumni Edition)</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>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</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>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</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 China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Martin, E E</au><au>Huang, W</au><au>Anwar, T</au><au>Arellano-Garcia, C</au><au>Burman, B</au><au>Guan, J-L</au><au>Gonzalez, M E</au><au>Kleer, C G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MMTV-cre;Ccn6 knockout mice develop tumors recapitulating human metaplastic breast carcinomas</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2017-04-20</date><risdate>2017</risdate><volume>36</volume><issue>16</issue><spage>2275</spage><epage>2285</epage><pages>2275-2285</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>Metaplastic breast carcinoma is an aggressive form of invasive breast cancer with histological evidence of epithelial to mesenchymal transition (EMT). However, the defining molecular events are unknown. Here we show that CCN6 (WISP3), a secreted matricellular protein of the CCN (CYR61/CTGF/NOV) family, is significantly downregulated in clinical samples of human spindle cell metaplastic breast carcinoma. We generated a mouse model of mammary epithelial-specific
Ccn6
deletion by developing a floxed
Ccn6
mouse which was bred with an MMTV-Cre mouse.
Ccn6
fl/fl
;MMTV-Cre mice displayed severe defects in ductal branching and abnormal age-related involution compared to littermate controls.
Ccn6
fl/fl
;MMTV-Cre mice developed invasive high grade mammary carcinomas with
bona fide
EMT, histologically similar to human metaplastic breast carcinomas. Global gene expression profiling of
Ccn6
fl/fl
mammary carcinomas and comparison of orthologous genes with a human metaplastic carcinoma signature revealed a significant overlap of 87 genes (
P
=5 × 10
−11
). Among the shared deregulated genes between mouse and human are important regulators of epithelial morphogenesis including
Cdh1, Ck19, Cldn3
and
4, Ddr1,
and
Wnt10a
. These results document a causal role for
Ccn6
deletion in the pathogenesis of metaplastic carcinomas with histological and molecular similarities with human disease. We provide a platform to study new targets in the diagnosis and treatment of human metaplastic carcinomas, and a new disease relevant model in which to test new treatment strategies.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>27819674</pmid><doi>10.1038/onc.2016.381</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 0950-9232 1476-5594 |
| language | eng |
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| source | MEDLINE; Nature; SpringerLink Journals - AutoHoldings |
| subjects | 42/41 631/67/1347 64/110 692/53/2421 82/51 Age Animals Apoptosis Breast - pathology Breast cancer Breast carcinoma Breast Neoplasms - genetics Breast Neoplasms - pathology CCN Intercellular Signaling Proteins - genetics Cell Biology Connective tissue growth factor CYR61 protein Disease Models, Animal E-cadherin Female Gene expression Genes, Tumor Suppressor Human Genetics Humans Internal Medicine Invasiveness Male Mammary gland Mammary Neoplasms, Animal - pathology Medicine Medicine & Public Health Mesenchyme Metaplasia - genetics Mice Mice, Inbred Strains Mice, Knockout Morphogenesis Oncology original-article Rodents Tumors |
| title | MMTV-cre;Ccn6 knockout mice develop tumors recapitulating human metaplastic breast carcinomas |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-09T19%3A55%3A28IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=MMTV-cre;Ccn6%20knockout%20mice%20develop%20tumors%20recapitulating%20human%20metaplastic%20breast%20carcinomas&rft.jtitle=Oncogene&rft.au=Martin,%20E%20E&rft.date=2017-04-20&rft.volume=36&rft.issue=16&rft.spage=2275&rft.epage=2285&rft.pages=2275-2285&rft.issn=0950-9232&rft.eissn=1476-5594&rft.coden=ONCNES&rft_id=info:doi/10.1038/onc.2016.381&rft_dat=%3Cproquest_pubme%3E1897390781%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1889752154&rft_id=info:pmid/27819674&rfr_iscdi=true |