Prolactin induces ERalpha-positive and ERalpha-negative mammary cancer in transgenic mice
The role of prolactin in human breast cancer has been controversial. However, it is now apparent that human mammary epithelial cells can synthesize prolactin endogenously, permitting autocrine/paracrine actions within the mammary gland that are independent of pituitary prolactin. To model this local...
Gespeichert in:
| Veröffentlicht in: | Oncogene 2003-07, Vol.22 (30), p.4664-4674 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 4674 |
|---|---|
| container_issue | 30 |
| container_start_page | 4664 |
| container_title | Oncogene |
| container_volume | 22 |
| creator | Rose-Hellekant, Teresa A Arendt, Lisa M Schroeder, Matthew D Gilchrist, Kennedy Sandgren, Eric P Schuler, Linda A |
| description | The role of prolactin in human breast cancer has been controversial. However, it is now apparent that human mammary epithelial cells can synthesize prolactin endogenously, permitting autocrine/paracrine actions within the mammary gland that are independent of pituitary prolactin. To model this local mammary production of prolactin (PRL), we have generated mice that overexpress prolactin within mammary epithelial cells under the control of a hormonally nonresponsive promoter, neu-related lipocalin (NRL). In each of the two examined NRL-PRL transgenic mouse lineages, female virgin mice display mammary developmental abnormalities, mammary intraepithelial neoplasias, and invasive neoplasms. Prolactin increases proliferation in morphologically normal alveoli and ducts, as well as in lesions. The tumors are of varied histotype, but papillary adenocarcinomas and adenosquamous neoplasms predominate. Neoplasms can be separated into two populations: one is estrogen receptor alpha (ERalpha) positive (greater than 15% of the cells stain for ERalpha), and the other is ERalpha- ( |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_73507510</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>73507510</sourcerecordid><originalsourceid>FETCH-LOGICAL-p541-6fc1f79878cbe524de1963681d1ae456601128fddf16dd61b773f384c70600383</originalsourceid><addsrcrecordid>eNo9kEtPwzAQhH0A0VL4C8gnbpH8iB85oqo8pEog1AunyLXXxSh2gp0g8e8JUDjt6tPsaGdO0JI0glQN42yBzkt5I4SohrAztKBMzxulS_TylPvO2DEkHJKbLBS8eTbd8GqqoS9hDB-ATXL_MMHB_MBoYjT5E1uTLOT5GI_ZpHKAFCyOwcIFOvWmK3B5nCu0u93s1vfV9vHuYX2zrQZR00p6S71qtNJ2D4LVDmgjudTUUQO1kHL-kmnvnKfSOUn3SnHPdW0VkYRwzVfo-td2yP37BGVsYygWus4k6KfSKi6IEpTMwqujcNpHcO2Qw3eA9q8L_gXX7Vmk</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>73507510</pqid></control><display><type>article</type><title>Prolactin induces ERalpha-positive and ERalpha-negative mammary cancer in transgenic mice</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Nature Journals Online</source><source>SpringerLink Journals - AutoHoldings</source><creator>Rose-Hellekant, Teresa A ; Arendt, Lisa M ; Schroeder, Matthew D ; Gilchrist, Kennedy ; Sandgren, Eric P ; Schuler, Linda A</creator><creatorcontrib>Rose-Hellekant, Teresa A ; Arendt, Lisa M ; Schroeder, Matthew D ; Gilchrist, Kennedy ; Sandgren, Eric P ; Schuler, Linda A</creatorcontrib><description>The role of prolactin in human breast cancer has been controversial. However, it is now apparent that human mammary epithelial cells can synthesize prolactin endogenously, permitting autocrine/paracrine actions within the mammary gland that are independent of pituitary prolactin. To model this local mammary production of prolactin (PRL), we have generated mice that overexpress prolactin within mammary epithelial cells under the control of a hormonally nonresponsive promoter, neu-related lipocalin (NRL). In each of the two examined NRL-PRL transgenic mouse lineages, female virgin mice display mammary developmental abnormalities, mammary intraepithelial neoplasias, and invasive neoplasms. Prolactin increases proliferation in morphologically normal alveoli and ducts, as well as in lesions. The tumors are of varied histotype, but papillary adenocarcinomas and adenosquamous neoplasms predominate. Neoplasms can be separated into two populations: one is estrogen receptor alpha (ERalpha) positive (greater than 15% of the cells stain for ERalpha), and the other is ERalpha- (<3%). ERalpha expression does not correlate with tumor histotype, or proliferative or apoptotic indices. These studies provide a mouse model of hormonally dependent breast cancer, and, perhaps most strikingly, a model in which some neoplasms retain ERalpha, as occurs in the human disease.</description><identifier>ISSN: 0950-9232</identifier><identifier>PMID: 12879011</identifier><language>eng</language><publisher>England</publisher><subject>Animals ; Apoptosis ; Bromodeoxyuridine - pharmacology ; Carrier Proteins - genetics ; Cell Division ; Cell Lineage ; Estrogen Receptor alpha ; Female ; Lipocalin-2 ; Lipocalins ; Mammary Neoplasms, Animal - etiology ; Mammary Neoplasms, Animal - metabolism ; Mice ; Mice, Transgenic ; Mitosis ; Phenotype ; Prolactin - physiology ; Promoter Regions, Genetic ; Rats ; Receptors, Estrogen - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Time Factors ; Transgenes</subject><ispartof>Oncogene, 2003-07, Vol.22 (30), p.4664-4674</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12879011$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rose-Hellekant, Teresa A</creatorcontrib><creatorcontrib>Arendt, Lisa M</creatorcontrib><creatorcontrib>Schroeder, Matthew D</creatorcontrib><creatorcontrib>Gilchrist, Kennedy</creatorcontrib><creatorcontrib>Sandgren, Eric P</creatorcontrib><creatorcontrib>Schuler, Linda A</creatorcontrib><title>Prolactin induces ERalpha-positive and ERalpha-negative mammary cancer in transgenic mice</title><title>Oncogene</title><addtitle>Oncogene</addtitle><description>The role of prolactin in human breast cancer has been controversial. However, it is now apparent that human mammary epithelial cells can synthesize prolactin endogenously, permitting autocrine/paracrine actions within the mammary gland that are independent of pituitary prolactin. To model this local mammary production of prolactin (PRL), we have generated mice that overexpress prolactin within mammary epithelial cells under the control of a hormonally nonresponsive promoter, neu-related lipocalin (NRL). In each of the two examined NRL-PRL transgenic mouse lineages, female virgin mice display mammary developmental abnormalities, mammary intraepithelial neoplasias, and invasive neoplasms. Prolactin increases proliferation in morphologically normal alveoli and ducts, as well as in lesions. The tumors are of varied histotype, but papillary adenocarcinomas and adenosquamous neoplasms predominate. Neoplasms can be separated into two populations: one is estrogen receptor alpha (ERalpha) positive (greater than 15% of the cells stain for ERalpha), and the other is ERalpha- (<3%). ERalpha expression does not correlate with tumor histotype, or proliferative or apoptotic indices. These studies provide a mouse model of hormonally dependent breast cancer, and, perhaps most strikingly, a model in which some neoplasms retain ERalpha, as occurs in the human disease.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Bromodeoxyuridine - pharmacology</subject><subject>Carrier Proteins - genetics</subject><subject>Cell Division</subject><subject>Cell Lineage</subject><subject>Estrogen Receptor alpha</subject><subject>Female</subject><subject>Lipocalin-2</subject><subject>Lipocalins</subject><subject>Mammary Neoplasms, Animal - etiology</subject><subject>Mammary Neoplasms, Animal - metabolism</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Mitosis</subject><subject>Phenotype</subject><subject>Prolactin - physiology</subject><subject>Promoter Regions, Genetic</subject><subject>Rats</subject><subject>Receptors, Estrogen - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Time Factors</subject><subject>Transgenes</subject><issn>0950-9232</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kEtPwzAQhH0A0VL4C8gnbpH8iB85oqo8pEog1AunyLXXxSh2gp0g8e8JUDjt6tPsaGdO0JI0glQN42yBzkt5I4SohrAztKBMzxulS_TylPvO2DEkHJKbLBS8eTbd8GqqoS9hDB-ATXL_MMHB_MBoYjT5E1uTLOT5GI_ZpHKAFCyOwcIFOvWmK3B5nCu0u93s1vfV9vHuYX2zrQZR00p6S71qtNJ2D4LVDmgjudTUUQO1kHL-kmnvnKfSOUn3SnHPdW0VkYRwzVfo-td2yP37BGVsYygWus4k6KfSKi6IEpTMwqujcNpHcO2Qw3eA9q8L_gXX7Vmk</recordid><startdate>20030724</startdate><enddate>20030724</enddate><creator>Rose-Hellekant, Teresa A</creator><creator>Arendt, Lisa M</creator><creator>Schroeder, Matthew D</creator><creator>Gilchrist, Kennedy</creator><creator>Sandgren, Eric P</creator><creator>Schuler, Linda A</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20030724</creationdate><title>Prolactin induces ERalpha-positive and ERalpha-negative mammary cancer in transgenic mice</title><author>Rose-Hellekant, Teresa A ; Arendt, Lisa M ; Schroeder, Matthew D ; Gilchrist, Kennedy ; Sandgren, Eric P ; Schuler, Linda A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p541-6fc1f79878cbe524de1963681d1ae456601128fddf16dd61b773f384c70600383</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Bromodeoxyuridine - pharmacology</topic><topic>Carrier Proteins - genetics</topic><topic>Cell Division</topic><topic>Cell Lineage</topic><topic>Estrogen Receptor alpha</topic><topic>Female</topic><topic>Lipocalin-2</topic><topic>Lipocalins</topic><topic>Mammary Neoplasms, Animal - etiology</topic><topic>Mammary Neoplasms, Animal - metabolism</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Mitosis</topic><topic>Phenotype</topic><topic>Prolactin - physiology</topic><topic>Promoter Regions, Genetic</topic><topic>Rats</topic><topic>Receptors, Estrogen - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Time Factors</topic><topic>Transgenes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rose-Hellekant, Teresa A</creatorcontrib><creatorcontrib>Arendt, Lisa M</creatorcontrib><creatorcontrib>Schroeder, Matthew D</creatorcontrib><creatorcontrib>Gilchrist, Kennedy</creatorcontrib><creatorcontrib>Sandgren, Eric P</creatorcontrib><creatorcontrib>Schuler, Linda A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rose-Hellekant, Teresa A</au><au>Arendt, Lisa M</au><au>Schroeder, Matthew D</au><au>Gilchrist, Kennedy</au><au>Sandgren, Eric P</au><au>Schuler, Linda A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Prolactin induces ERalpha-positive and ERalpha-negative mammary cancer in transgenic mice</atitle><jtitle>Oncogene</jtitle><addtitle>Oncogene</addtitle><date>2003-07-24</date><risdate>2003</risdate><volume>22</volume><issue>30</issue><spage>4664</spage><epage>4674</epage><pages>4664-4674</pages><issn>0950-9232</issn><abstract>The role of prolactin in human breast cancer has been controversial. However, it is now apparent that human mammary epithelial cells can synthesize prolactin endogenously, permitting autocrine/paracrine actions within the mammary gland that are independent of pituitary prolactin. To model this local mammary production of prolactin (PRL), we have generated mice that overexpress prolactin within mammary epithelial cells under the control of a hormonally nonresponsive promoter, neu-related lipocalin (NRL). In each of the two examined NRL-PRL transgenic mouse lineages, female virgin mice display mammary developmental abnormalities, mammary intraepithelial neoplasias, and invasive neoplasms. Prolactin increases proliferation in morphologically normal alveoli and ducts, as well as in lesions. The tumors are of varied histotype, but papillary adenocarcinomas and adenosquamous neoplasms predominate. Neoplasms can be separated into two populations: one is estrogen receptor alpha (ERalpha) positive (greater than 15% of the cells stain for ERalpha), and the other is ERalpha- (<3%). ERalpha expression does not correlate with tumor histotype, or proliferative or apoptotic indices. These studies provide a mouse model of hormonally dependent breast cancer, and, perhaps most strikingly, a model in which some neoplasms retain ERalpha, as occurs in the human disease.</abstract><cop>England</cop><pmid>12879011</pmid><tpages>11</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0950-9232 |
| ispartof | Oncogene, 2003-07, Vol.22 (30), p.4664-4674 |
| issn | 0950-9232 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_73507510 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Nature Journals Online; SpringerLink Journals - AutoHoldings |
| subjects | Animals Apoptosis Bromodeoxyuridine - pharmacology Carrier Proteins - genetics Cell Division Cell Lineage Estrogen Receptor alpha Female Lipocalin-2 Lipocalins Mammary Neoplasms, Animal - etiology Mammary Neoplasms, Animal - metabolism Mice Mice, Transgenic Mitosis Phenotype Prolactin - physiology Promoter Regions, Genetic Rats Receptors, Estrogen - metabolism Reverse Transcriptase Polymerase Chain Reaction Time Factors Transgenes |
| title | Prolactin induces ERalpha-positive and ERalpha-negative mammary cancer in transgenic mice |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-11T20%3A09%3A36IST&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=Prolactin%20induces%20ERalpha-positive%20and%20ERalpha-negative%20mammary%20cancer%20in%20transgenic%20mice&rft.jtitle=Oncogene&rft.au=Rose-Hellekant,%20Teresa%20A&rft.date=2003-07-24&rft.volume=22&rft.issue=30&rft.spage=4664&rft.epage=4674&rft.pages=4664-4674&rft.issn=0950-9232&rft_id=info:doi/&rft_dat=%3Cproquest_pubme%3E73507510%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=73507510&rft_id=info:pmid/12879011&rfr_iscdi=true |