Notch1-induced mammary tumor development is cyclin D1-dependent and correlates with expansion of pre-malignant multipotent duct-limited progenitors
Members of the Notch family are involved in the development of breast cancer in animal models and in humans. In young transgenic mice, expressing intracellular activated Notch1 (N1 IC ) in mammary cells, we found that CD24 + CD29 high progenitor cells had enhanced survival, and were expanded through...
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| Veröffentlicht in: | Oncogene 2010-08, Vol.29 (32), p.4543-4554 |
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| creator | Ling, H Sylvestre, J-R Jolicoeur, P |
| description | Members of the Notch family are involved in the development of breast cancer in animal models and in humans. In young transgenic mice, expressing intracellular activated Notch1 (N1
IC
) in mammary cells, we found that CD24
+
CD29
high
progenitor cells had enhanced survival, and were expanded through a cyclin D1-dependent pathway. This expansion positively correlated with the later cyclin D1-dependent formation of basal-like ductal tumors. This expanded population exhibited abnormal differentiation skewed toward the basal cells, showed signs of pre-malignancy (low PTEN/p53 and high c-myc) and contained stem cells with impaired self-renewal
in vivo
, and more numerous multipotent, ductal-restricted progenitors. Our data suggest that N1
IC
can favor transformation of progenitor cells early in life through a cyclin D1-dependent pathway. |
| doi_str_mv | 10.1038/onc.2010.186 |
| format | Article |
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IC
) in mammary cells, we found that CD24
+
CD29
high
progenitor cells had enhanced survival, and were expanded through a cyclin D1-dependent pathway. This expansion positively correlated with the later cyclin D1-dependent formation of basal-like ductal tumors. This expanded population exhibited abnormal differentiation skewed toward the basal cells, showed signs of pre-malignancy (low PTEN/p53 and high c-myc) and contained stem cells with impaired self-renewal
in vivo
, and more numerous multipotent, ductal-restricted progenitors. Our data suggest that N1
IC
can favor transformation of progenitor cells early in life through a cyclin D1-dependent pathway.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/onc.2010.186</identifier><identifier>PMID: 20562911</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/67/1347 ; 631/67/71 ; 631/80/86 ; Animal models ; Animals ; Apoptosis ; Basal cells ; Breast cancer ; c-Myc protein ; CD24 Antigen - metabolism ; Cell Biology ; Cell Culture Techniques ; Cell Differentiation ; Cell Proliferation ; Cell self-renewal ; Cell Transformation, Neoplastic ; Cellular biology ; Cyclin D1 ; Cyclin D1 - deficiency ; Cyclin D1 - metabolism ; Cyclins ; Female ; Gene Expression Regulation, Neoplastic ; Genetic aspects ; Genetic transformation ; Genetics ; Health aspects ; Human Genetics ; Integrin beta1 - metabolism ; Internal Medicine ; Malignancy ; Mammary gland ; Mammary Glands, Animal - growth & development ; Mammary Glands, Animal - pathology ; Mammary Neoplasms, Experimental - genetics ; Mammary Neoplasms, Experimental - metabolism ; Mammary Neoplasms, Experimental - pathology ; Mammary Tumor Virus, Mouse - genetics ; Medicine ; Medicine & Public Health ; Mice ; Mice, Transgenic ; Multipotent Stem Cells - metabolism ; Multipotent Stem Cells - pathology ; Myc protein ; Notch1 protein ; Oncology ; original-article ; Physiological aspects ; Progenitor cells ; PTEN Phosphohydrolase - genetics ; PTEN protein ; Receptor, Notch1 - genetics ; Receptor, Notch1 - metabolism ; Risk factors ; Stem cell transplantation ; Stem cells ; Transgenic animals ; Transgenic mice ; Tumor Suppressor Protein p53 - genetics ; Tumors</subject><ispartof>Oncogene, 2010-08, Vol.29 (32), p.4543-4554</ispartof><rights>Macmillan Publishers Limited 2010</rights><rights>COPYRIGHT 2010 Nature Publishing Group</rights><rights>Macmillan Publishers Limited 2010.</rights><rights>Copyright Nature Publishing Group Aug 12, 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c482t-612184c63bd957b098cd560d786dc55b908e2876dde0cb6982597d032e4c6a543</citedby><cites>FETCH-LOGICAL-c482t-612184c63bd957b098cd560d786dc55b908e2876dde0cb6982597d032e4c6a543</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.2010.186$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/onc.2010.186$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20562911$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ling, H</creatorcontrib><creatorcontrib>Sylvestre, J-R</creatorcontrib><creatorcontrib>Jolicoeur, P</creatorcontrib><title>Notch1-induced mammary tumor development is cyclin D1-dependent and correlates with expansion of pre-malignant multipotent duct-limited progenitors</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Members of the Notch family are involved in the development of breast cancer in animal models and in humans. In young transgenic mice, expressing intracellular activated Notch1 (N1
IC
) in mammary cells, we found that CD24
+
CD29
high
progenitor cells had enhanced survival, and were expanded through a cyclin D1-dependent pathway. This expansion positively correlated with the later cyclin D1-dependent formation of basal-like ductal tumors. This expanded population exhibited abnormal differentiation skewed toward the basal cells, showed signs of pre-malignancy (low PTEN/p53 and high c-myc) and contained stem cells with impaired self-renewal
in vivo
, and more numerous multipotent, ductal-restricted progenitors. Our data suggest that N1
IC
can favor transformation of progenitor cells early in life through a cyclin D1-dependent pathway.</description><subject>631/67/1347</subject><subject>631/67/71</subject><subject>631/80/86</subject><subject>Animal models</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Basal cells</subject><subject>Breast cancer</subject><subject>c-Myc protein</subject><subject>CD24 Antigen - metabolism</subject><subject>Cell Biology</subject><subject>Cell Culture Techniques</subject><subject>Cell Differentiation</subject><subject>Cell Proliferation</subject><subject>Cell self-renewal</subject><subject>Cell Transformation, Neoplastic</subject><subject>Cellular biology</subject><subject>Cyclin D1</subject><subject>Cyclin D1 - deficiency</subject><subject>Cyclin D1 - metabolism</subject><subject>Cyclins</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genetic aspects</subject><subject>Genetic transformation</subject><subject>Genetics</subject><subject>Health aspects</subject><subject>Human Genetics</subject><subject>Integrin beta1 - metabolism</subject><subject>Internal Medicine</subject><subject>Malignancy</subject><subject>Mammary gland</subject><subject>Mammary Glands, Animal - growth & development</subject><subject>Mammary Glands, Animal - pathology</subject><subject>Mammary Neoplasms, Experimental - genetics</subject><subject>Mammary Neoplasms, Experimental - metabolism</subject><subject>Mammary Neoplasms, Experimental - pathology</subject><subject>Mammary Tumor Virus, Mouse - genetics</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Multipotent Stem Cells - metabolism</subject><subject>Multipotent Stem Cells - pathology</subject><subject>Myc protein</subject><subject>Notch1 protein</subject><subject>Oncology</subject><subject>original-article</subject><subject>Physiological aspects</subject><subject>Progenitor cells</subject><subject>PTEN Phosphohydrolase - genetics</subject><subject>PTEN protein</subject><subject>Receptor, Notch1 - genetics</subject><subject>Receptor, Notch1 - metabolism</subject><subject>Risk factors</subject><subject>Stem cell transplantation</subject><subject>Stem cells</subject><subject>Transgenic animals</subject><subject>Transgenic mice</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumors</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkk9vFSEUxSdGY5_VnWtDdOHGeQIDDCyb1n9JoxtdTxi475VmgBEYtZ-jX1gmr9poagwLwuV37uGG0zRPCd4S3MnXMZgtxetJinvNhrBetJwrdr_ZYMVxq2hHj5pHOV9ijHuF6cPmiGIuqCJk01x_jMVckNYFuxiwyGvvdbpCZfExIQvfYIqzh1CQy8hcmckFdEZaCzMEu5Z1sMjElGDSBTL67soFgh-zDtnFgOIOzQlarye3D7rifpmKm2NZpdWxtJPzrlTjOcU9BFdiyo-bBzs9ZXhysx83X96--Xz6vj3_9O7D6cl5a5ikpRWEEsmM6EareD9iJY3lAtteCms4HxWWQGUvrAVsRqEk5aq3uKNQRZqz7rh5eehbvb8ukMvgXTYwTTpAXPLQcyZlr1j3f5JJxahgopLP_yIv45JCHaNCleCcru1e_AuqCGG4_g27pfZ6gsGFXSxJm9V4OKEdJ6rayUpt76DqsuCdiQF2rtb_ELw6CEyKOSfYDXNy658PBA9rooaaqGFN1FATVfFnN29dRg_2N_wrQhVoD0CuV2EP6XaYOxv-BCeT1Po</recordid><startdate>20100812</startdate><enddate>20100812</enddate><creator>Ling, H</creator><creator>Sylvestre, J-R</creator><creator>Jolicoeur, P</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></search><sort><creationdate>20100812</creationdate><title>Notch1-induced mammary tumor development is cyclin D1-dependent and correlates with expansion of pre-malignant multipotent duct-limited progenitors</title><author>Ling, H ; Sylvestre, J-R ; Jolicoeur, P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c482t-612184c63bd957b098cd560d786dc55b908e2876dde0cb6982597d032e4c6a543</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>631/67/1347</topic><topic>631/67/71</topic><topic>631/80/86</topic><topic>Animal models</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Basal cells</topic><topic>Breast cancer</topic><topic>c-Myc protein</topic><topic>CD24 Antigen - metabolism</topic><topic>Cell Biology</topic><topic>Cell Culture Techniques</topic><topic>Cell Differentiation</topic><topic>Cell Proliferation</topic><topic>Cell self-renewal</topic><topic>Cell Transformation, Neoplastic</topic><topic>Cellular biology</topic><topic>Cyclin D1</topic><topic>Cyclin D1 - deficiency</topic><topic>Cyclin D1 - metabolism</topic><topic>Cyclins</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genetic aspects</topic><topic>Genetic transformation</topic><topic>Genetics</topic><topic>Health aspects</topic><topic>Human Genetics</topic><topic>Integrin beta1 - metabolism</topic><topic>Internal Medicine</topic><topic>Malignancy</topic><topic>Mammary gland</topic><topic>Mammary Glands, Animal - growth & development</topic><topic>Mammary Glands, Animal - pathology</topic><topic>Mammary Neoplasms, Experimental - genetics</topic><topic>Mammary Neoplasms, Experimental - metabolism</topic><topic>Mammary Neoplasms, Experimental - pathology</topic><topic>Mammary Tumor Virus, Mouse - 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Academic</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ling, H</au><au>Sylvestre, J-R</au><au>Jolicoeur, P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Notch1-induced mammary tumor development is cyclin D1-dependent and correlates with expansion of pre-malignant multipotent duct-limited progenitors</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2010-08-12</date><risdate>2010</risdate><volume>29</volume><issue>32</issue><spage>4543</spage><epage>4554</epage><pages>4543-4554</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>Members of the Notch family are involved in the development of breast cancer in animal models and in humans. In young transgenic mice, expressing intracellular activated Notch1 (N1
IC
) in mammary cells, we found that CD24
+
CD29
high
progenitor cells had enhanced survival, and were expanded through a cyclin D1-dependent pathway. This expansion positively correlated with the later cyclin D1-dependent formation of basal-like ductal tumors. This expanded population exhibited abnormal differentiation skewed toward the basal cells, showed signs of pre-malignancy (low PTEN/p53 and high c-myc) and contained stem cells with impaired self-renewal
in vivo
, and more numerous multipotent, ductal-restricted progenitors. Our data suggest that N1
IC
can favor transformation of progenitor cells early in life through a cyclin D1-dependent pathway.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>20562911</pmid><doi>10.1038/onc.2010.186</doi><tpages>12</tpages></addata></record> |
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| ispartof | Oncogene, 2010-08, Vol.29 (32), p.4543-4554 |
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| language | eng |
| recordid | cdi_proquest_miscellaneous_754887943 |
| source | MEDLINE; Springer Nature - Complete Springer Journals; Nature Journals Online; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | 631/67/1347 631/67/71 631/80/86 Animal models Animals Apoptosis Basal cells Breast cancer c-Myc protein CD24 Antigen - metabolism Cell Biology Cell Culture Techniques Cell Differentiation Cell Proliferation Cell self-renewal Cell Transformation, Neoplastic Cellular biology Cyclin D1 Cyclin D1 - deficiency Cyclin D1 - metabolism Cyclins Female Gene Expression Regulation, Neoplastic Genetic aspects Genetic transformation Genetics Health aspects Human Genetics Integrin beta1 - metabolism Internal Medicine Malignancy Mammary gland Mammary Glands, Animal - growth & development Mammary Glands, Animal - pathology Mammary Neoplasms, Experimental - genetics Mammary Neoplasms, Experimental - metabolism Mammary Neoplasms, Experimental - pathology Mammary Tumor Virus, Mouse - genetics Medicine Medicine & Public Health Mice Mice, Transgenic Multipotent Stem Cells - metabolism Multipotent Stem Cells - pathology Myc protein Notch1 protein Oncology original-article Physiological aspects Progenitor cells PTEN Phosphohydrolase - genetics PTEN protein Receptor, Notch1 - genetics Receptor, Notch1 - metabolism Risk factors Stem cell transplantation Stem cells Transgenic animals Transgenic mice Tumor Suppressor Protein p53 - genetics Tumors |
| title | Notch1-induced mammary tumor development is cyclin D1-dependent and correlates with expansion of pre-malignant multipotent duct-limited progenitors |
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