Bile Acid and Inflammation Activate Gastric Cardia Stem Cells in a Mouse Model of Barrett-Like Metaplasia
Esophageal adenocarcinoma (EAC) arises from Barrett esophagus (BE), intestinal-like columnar metaplasia linked to reflux esophagitis. In a transgenic mouse model of BE, esophageal overexpression of interleukin-1β phenocopies human pathology with evolution of esophagitis, Barrett-like metaplasia and...
Gespeichert in:
| Veröffentlicht in: | Cancer cell 2012-01, Vol.21 (1), p.36-51 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 51 |
|---|---|
| container_issue | 1 |
| container_start_page | 36 |
| container_title | Cancer cell |
| container_volume | 21 |
| creator | Quante, Michael Bhagat, Govind Abrams, Julian A. Marache, Frederic Good, Pamela Lee, Michele D. Lee, Yoomi Friedman, Richard Asfaha, Samuel Dubeykovskaya, Zinaida Mahmood, Umar Figueiredo, Jose-Luiz Kitajewski, Jan Shawber, Carrie Lightdale, Charles J. Rustgi, Anil K. Wang, Timothy C. |
| description | Esophageal adenocarcinoma (EAC) arises from Barrett esophagus (BE), intestinal-like columnar metaplasia linked to reflux esophagitis. In a transgenic mouse model of BE, esophageal overexpression of interleukin-1β phenocopies human pathology with evolution of esophagitis, Barrett-like metaplasia and EAC. Histopathology and gene signatures closely resembled human BE, with upregulation of TFF2, Bmp4, Cdx2, Notch1, and IL-6. The development of BE and EAC was accelerated by exposure to bile acids and/or nitrosamines, and inhibited by IL-6 deficiency. Lgr5+ gastric cardia stem cells present in BE were able to lineage trace the early BE lesion. Our data suggest that BE and EAC arise from gastric progenitors due to a tumor-promoting IL-1β-IL-6 signaling cascade and Dll1-dependent Notch signaling.
► IL-1β overexpression in the mouse esophagus induces IL-6 dependent BE and EAC ► Bile acids accelerate intestinal metaplasia and dysplasia in this mouse model of BE ► Notch signaling in columnar cells, not goblet cells is associated with carcinogenesis ► BE and EAC likely arise from gastric cardia progenitor cells |
| doi_str_mv | 10.1016/j.ccr.2011.12.004 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_917575816</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S1535610811004740</els_id><sourcerecordid>917575816</sourcerecordid><originalsourceid>FETCH-LOGICAL-c461t-ad1fbeca1f763604acd9436aeed045cb969446328e842d35a4fa01aa9347621d3</originalsourceid><addsrcrecordid>eNp9kE9v2zAMxYWhRdt1_QC7FLr1ZE-UZdnGTkmwZQEy9LDtLDASDSj1n0xSAvTbT0W6HnshCeK9B_LH2GcQJQjQX_altaGUAqAEWQqhPrAbaJu2qHSrL_JcV3WhQbTX7GOMe5E90HRX7FpKqVXTNjfML_1AfGG94zg5vpn6AccRk5-nvE3-hIn4GmMK3vIVBueR_0o08hUNQ-R-4sh_zsdIuToa-NzzJYZAKRVb_5S3lPAwYPT4iV32OES6e-237M_3b79XP4rt43qzWmwLqzSkAh30O7IIfaMrLRRa16lKI5ETqra7TndK6Uq21CrpqhpVjwIQu0o1WoKrbtnDOfcQ5r9HismMPtp8LU6UDzUdNHVTt6CzEs5KG-YYA_XmEPyI4dmAMC-Azd5kwOYFsAFpMuDsuX9NP-5Gcm-O_0Sz4OtZQPnHk6dgovU0WXI-kE3Gzf6d-H9CR4qn</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>917575816</pqid></control><display><type>article</type><title>Bile Acid and Inflammation Activate Gastric Cardia Stem Cells in a Mouse Model of Barrett-Like Metaplasia</title><source>MEDLINE</source><source>Cell Press Free Archives</source><source>Elsevier ScienceDirect Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>Quante, Michael ; Bhagat, Govind ; Abrams, Julian A. ; Marache, Frederic ; Good, Pamela ; Lee, Michele D. ; Lee, Yoomi ; Friedman, Richard ; Asfaha, Samuel ; Dubeykovskaya, Zinaida ; Mahmood, Umar ; Figueiredo, Jose-Luiz ; Kitajewski, Jan ; Shawber, Carrie ; Lightdale, Charles J. ; Rustgi, Anil K. ; Wang, Timothy C.</creator><creatorcontrib>Quante, Michael ; Bhagat, Govind ; Abrams, Julian A. ; Marache, Frederic ; Good, Pamela ; Lee, Michele D. ; Lee, Yoomi ; Friedman, Richard ; Asfaha, Samuel ; Dubeykovskaya, Zinaida ; Mahmood, Umar ; Figueiredo, Jose-Luiz ; Kitajewski, Jan ; Shawber, Carrie ; Lightdale, Charles J. ; Rustgi, Anil K. ; Wang, Timothy C.</creatorcontrib><description>Esophageal adenocarcinoma (EAC) arises from Barrett esophagus (BE), intestinal-like columnar metaplasia linked to reflux esophagitis. In a transgenic mouse model of BE, esophageal overexpression of interleukin-1β phenocopies human pathology with evolution of esophagitis, Barrett-like metaplasia and EAC. Histopathology and gene signatures closely resembled human BE, with upregulation of TFF2, Bmp4, Cdx2, Notch1, and IL-6. The development of BE and EAC was accelerated by exposure to bile acids and/or nitrosamines, and inhibited by IL-6 deficiency. Lgr5+ gastric cardia stem cells present in BE were able to lineage trace the early BE lesion. Our data suggest that BE and EAC arise from gastric progenitors due to a tumor-promoting IL-1β-IL-6 signaling cascade and Dll1-dependent Notch signaling.
► IL-1β overexpression in the mouse esophagus induces IL-6 dependent BE and EAC ► Bile acids accelerate intestinal metaplasia and dysplasia in this mouse model of BE ► Notch signaling in columnar cells, not goblet cells is associated with carcinogenesis ► BE and EAC likely arise from gastric cardia progenitor cells</description><identifier>ISSN: 1535-6108</identifier><identifier>EISSN: 1878-3686</identifier><identifier>DOI: 10.1016/j.ccr.2011.12.004</identifier><identifier>PMID: 22264787</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adenocarcinoma - pathology ; Animals ; Barrett Esophagus - etiology ; Barrett Esophagus - pathology ; Bile Acids and Salts - pharmacology ; Bone Morphogenetic Protein 4 - genetics ; Bone Morphogenetic Protein 4 - metabolism ; Cardia - pathology ; CDX2 Transcription Factor ; Esophageal Neoplasms - pathology ; Esophagitis - pathology ; Homeodomain Proteins - genetics ; Homeodomain Proteins - metabolism ; Interleukin-1beta - genetics ; Interleukin-1beta - metabolism ; Interleukin-6 - genetics ; Interleukin-6 - metabolism ; Metaplasia - pathology ; Mice ; Mice, Transgenic ; Mucins - genetics ; Mucins - metabolism ; Muscle Proteins - genetics ; Muscle Proteins - metabolism ; Peptides - genetics ; Peptides - metabolism ; Receptor, Notch1 - genetics ; Receptor, Notch1 - metabolism ; Signal Transduction ; Stem Cells - pathology ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Trefoil Factor-2 ; Up-Regulation</subject><ispartof>Cancer cell, 2012-01, Vol.21 (1), p.36-51</ispartof><rights>2012 Elsevier Inc.</rights><rights>Copyright © 2012 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c461t-ad1fbeca1f763604acd9436aeed045cb969446328e842d35a4fa01aa9347621d3</citedby><cites>FETCH-LOGICAL-c461t-ad1fbeca1f763604acd9436aeed045cb969446328e842d35a4fa01aa9347621d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1535610811004740$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22264787$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Quante, Michael</creatorcontrib><creatorcontrib>Bhagat, Govind</creatorcontrib><creatorcontrib>Abrams, Julian A.</creatorcontrib><creatorcontrib>Marache, Frederic</creatorcontrib><creatorcontrib>Good, Pamela</creatorcontrib><creatorcontrib>Lee, Michele D.</creatorcontrib><creatorcontrib>Lee, Yoomi</creatorcontrib><creatorcontrib>Friedman, Richard</creatorcontrib><creatorcontrib>Asfaha, Samuel</creatorcontrib><creatorcontrib>Dubeykovskaya, Zinaida</creatorcontrib><creatorcontrib>Mahmood, Umar</creatorcontrib><creatorcontrib>Figueiredo, Jose-Luiz</creatorcontrib><creatorcontrib>Kitajewski, Jan</creatorcontrib><creatorcontrib>Shawber, Carrie</creatorcontrib><creatorcontrib>Lightdale, Charles J.</creatorcontrib><creatorcontrib>Rustgi, Anil K.</creatorcontrib><creatorcontrib>Wang, Timothy C.</creatorcontrib><title>Bile Acid and Inflammation Activate Gastric Cardia Stem Cells in a Mouse Model of Barrett-Like Metaplasia</title><title>Cancer cell</title><addtitle>Cancer Cell</addtitle><description>Esophageal adenocarcinoma (EAC) arises from Barrett esophagus (BE), intestinal-like columnar metaplasia linked to reflux esophagitis. In a transgenic mouse model of BE, esophageal overexpression of interleukin-1β phenocopies human pathology with evolution of esophagitis, Barrett-like metaplasia and EAC. Histopathology and gene signatures closely resembled human BE, with upregulation of TFF2, Bmp4, Cdx2, Notch1, and IL-6. The development of BE and EAC was accelerated by exposure to bile acids and/or nitrosamines, and inhibited by IL-6 deficiency. Lgr5+ gastric cardia stem cells present in BE were able to lineage trace the early BE lesion. Our data suggest that BE and EAC arise from gastric progenitors due to a tumor-promoting IL-1β-IL-6 signaling cascade and Dll1-dependent Notch signaling.
► IL-1β overexpression in the mouse esophagus induces IL-6 dependent BE and EAC ► Bile acids accelerate intestinal metaplasia and dysplasia in this mouse model of BE ► Notch signaling in columnar cells, not goblet cells is associated with carcinogenesis ► BE and EAC likely arise from gastric cardia progenitor cells</description><subject>Adenocarcinoma - pathology</subject><subject>Animals</subject><subject>Barrett Esophagus - etiology</subject><subject>Barrett Esophagus - pathology</subject><subject>Bile Acids and Salts - pharmacology</subject><subject>Bone Morphogenetic Protein 4 - genetics</subject><subject>Bone Morphogenetic Protein 4 - metabolism</subject><subject>Cardia - pathology</subject><subject>CDX2 Transcription Factor</subject><subject>Esophageal Neoplasms - pathology</subject><subject>Esophagitis - pathology</subject><subject>Homeodomain Proteins - genetics</subject><subject>Homeodomain Proteins - metabolism</subject><subject>Interleukin-1beta - genetics</subject><subject>Interleukin-1beta - metabolism</subject><subject>Interleukin-6 - genetics</subject><subject>Interleukin-6 - metabolism</subject><subject>Metaplasia - pathology</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Mucins - genetics</subject><subject>Mucins - metabolism</subject><subject>Muscle Proteins - genetics</subject><subject>Muscle Proteins - metabolism</subject><subject>Peptides - genetics</subject><subject>Peptides - metabolism</subject><subject>Receptor, Notch1 - genetics</subject><subject>Receptor, Notch1 - metabolism</subject><subject>Signal Transduction</subject><subject>Stem Cells - pathology</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Trefoil Factor-2</subject><subject>Up-Regulation</subject><issn>1535-6108</issn><issn>1878-3686</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE9v2zAMxYWhRdt1_QC7FLr1ZE-UZdnGTkmwZQEy9LDtLDASDSj1n0xSAvTbT0W6HnshCeK9B_LH2GcQJQjQX_altaGUAqAEWQqhPrAbaJu2qHSrL_JcV3WhQbTX7GOMe5E90HRX7FpKqVXTNjfML_1AfGG94zg5vpn6AccRk5-nvE3-hIn4GmMK3vIVBueR_0o08hUNQ-R-4sh_zsdIuToa-NzzJYZAKRVb_5S3lPAwYPT4iV32OES6e-237M_3b79XP4rt43qzWmwLqzSkAh30O7IIfaMrLRRa16lKI5ETqra7TndK6Uq21CrpqhpVjwIQu0o1WoKrbtnDOfcQ5r9HismMPtp8LU6UDzUdNHVTt6CzEs5KG-YYA_XmEPyI4dmAMC-Azd5kwOYFsAFpMuDsuX9NP-5Gcm-O_0Sz4OtZQPnHk6dgovU0WXI-kE3Gzf6d-H9CR4qn</recordid><startdate>20120117</startdate><enddate>20120117</enddate><creator>Quante, Michael</creator><creator>Bhagat, Govind</creator><creator>Abrams, Julian A.</creator><creator>Marache, Frederic</creator><creator>Good, Pamela</creator><creator>Lee, Michele D.</creator><creator>Lee, Yoomi</creator><creator>Friedman, Richard</creator><creator>Asfaha, Samuel</creator><creator>Dubeykovskaya, Zinaida</creator><creator>Mahmood, Umar</creator><creator>Figueiredo, Jose-Luiz</creator><creator>Kitajewski, Jan</creator><creator>Shawber, Carrie</creator><creator>Lightdale, Charles J.</creator><creator>Rustgi, Anil K.</creator><creator>Wang, Timothy C.</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</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>7X8</scope></search><sort><creationdate>20120117</creationdate><title>Bile Acid and Inflammation Activate Gastric Cardia Stem Cells in a Mouse Model of Barrett-Like Metaplasia</title><author>Quante, Michael ; Bhagat, Govind ; Abrams, Julian A. ; Marache, Frederic ; Good, Pamela ; Lee, Michele D. ; Lee, Yoomi ; Friedman, Richard ; Asfaha, Samuel ; Dubeykovskaya, Zinaida ; Mahmood, Umar ; Figueiredo, Jose-Luiz ; Kitajewski, Jan ; Shawber, Carrie ; Lightdale, Charles J. ; Rustgi, Anil K. ; Wang, Timothy C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c461t-ad1fbeca1f763604acd9436aeed045cb969446328e842d35a4fa01aa9347621d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adenocarcinoma - pathology</topic><topic>Animals</topic><topic>Barrett Esophagus - etiology</topic><topic>Barrett Esophagus - pathology</topic><topic>Bile Acids and Salts - pharmacology</topic><topic>Bone Morphogenetic Protein 4 - genetics</topic><topic>Bone Morphogenetic Protein 4 - metabolism</topic><topic>Cardia - pathology</topic><topic>CDX2 Transcription Factor</topic><topic>Esophageal Neoplasms - pathology</topic><topic>Esophagitis - pathology</topic><topic>Homeodomain Proteins - genetics</topic><topic>Homeodomain Proteins - metabolism</topic><topic>Interleukin-1beta - genetics</topic><topic>Interleukin-1beta - metabolism</topic><topic>Interleukin-6 - genetics</topic><topic>Interleukin-6 - metabolism</topic><topic>Metaplasia - pathology</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Mucins - genetics</topic><topic>Mucins - metabolism</topic><topic>Muscle Proteins - genetics</topic><topic>Muscle Proteins - metabolism</topic><topic>Peptides - genetics</topic><topic>Peptides - metabolism</topic><topic>Receptor, Notch1 - genetics</topic><topic>Receptor, Notch1 - metabolism</topic><topic>Signal Transduction</topic><topic>Stem Cells - pathology</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><topic>Trefoil Factor-2</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Quante, Michael</creatorcontrib><creatorcontrib>Bhagat, Govind</creatorcontrib><creatorcontrib>Abrams, Julian A.</creatorcontrib><creatorcontrib>Marache, Frederic</creatorcontrib><creatorcontrib>Good, Pamela</creatorcontrib><creatorcontrib>Lee, Michele D.</creatorcontrib><creatorcontrib>Lee, Yoomi</creatorcontrib><creatorcontrib>Friedman, Richard</creatorcontrib><creatorcontrib>Asfaha, Samuel</creatorcontrib><creatorcontrib>Dubeykovskaya, Zinaida</creatorcontrib><creatorcontrib>Mahmood, Umar</creatorcontrib><creatorcontrib>Figueiredo, Jose-Luiz</creatorcontrib><creatorcontrib>Kitajewski, Jan</creatorcontrib><creatorcontrib>Shawber, Carrie</creatorcontrib><creatorcontrib>Lightdale, Charles J.</creatorcontrib><creatorcontrib>Rustgi, Anil K.</creatorcontrib><creatorcontrib>Wang, Timothy C.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Quante, Michael</au><au>Bhagat, Govind</au><au>Abrams, Julian A.</au><au>Marache, Frederic</au><au>Good, Pamela</au><au>Lee, Michele D.</au><au>Lee, Yoomi</au><au>Friedman, Richard</au><au>Asfaha, Samuel</au><au>Dubeykovskaya, Zinaida</au><au>Mahmood, Umar</au><au>Figueiredo, Jose-Luiz</au><au>Kitajewski, Jan</au><au>Shawber, Carrie</au><au>Lightdale, Charles J.</au><au>Rustgi, Anil K.</au><au>Wang, Timothy C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bile Acid and Inflammation Activate Gastric Cardia Stem Cells in a Mouse Model of Barrett-Like Metaplasia</atitle><jtitle>Cancer cell</jtitle><addtitle>Cancer Cell</addtitle><date>2012-01-17</date><risdate>2012</risdate><volume>21</volume><issue>1</issue><spage>36</spage><epage>51</epage><pages>36-51</pages><issn>1535-6108</issn><eissn>1878-3686</eissn><abstract>Esophageal adenocarcinoma (EAC) arises from Barrett esophagus (BE), intestinal-like columnar metaplasia linked to reflux esophagitis. In a transgenic mouse model of BE, esophageal overexpression of interleukin-1β phenocopies human pathology with evolution of esophagitis, Barrett-like metaplasia and EAC. Histopathology and gene signatures closely resembled human BE, with upregulation of TFF2, Bmp4, Cdx2, Notch1, and IL-6. The development of BE and EAC was accelerated by exposure to bile acids and/or nitrosamines, and inhibited by IL-6 deficiency. Lgr5+ gastric cardia stem cells present in BE were able to lineage trace the early BE lesion. Our data suggest that BE and EAC arise from gastric progenitors due to a tumor-promoting IL-1β-IL-6 signaling cascade and Dll1-dependent Notch signaling.
► IL-1β overexpression in the mouse esophagus induces IL-6 dependent BE and EAC ► Bile acids accelerate intestinal metaplasia and dysplasia in this mouse model of BE ► Notch signaling in columnar cells, not goblet cells is associated with carcinogenesis ► BE and EAC likely arise from gastric cardia progenitor cells</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>22264787</pmid><doi>10.1016/j.ccr.2011.12.004</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1535-6108 |
| ispartof | Cancer cell, 2012-01, Vol.21 (1), p.36-51 |
| issn | 1535-6108 1878-3686 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_917575816 |
| source | MEDLINE; Cell Press Free Archives; Elsevier ScienceDirect Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Adenocarcinoma - pathology Animals Barrett Esophagus - etiology Barrett Esophagus - pathology Bile Acids and Salts - pharmacology Bone Morphogenetic Protein 4 - genetics Bone Morphogenetic Protein 4 - metabolism Cardia - pathology CDX2 Transcription Factor Esophageal Neoplasms - pathology Esophagitis - pathology Homeodomain Proteins - genetics Homeodomain Proteins - metabolism Interleukin-1beta - genetics Interleukin-1beta - metabolism Interleukin-6 - genetics Interleukin-6 - metabolism Metaplasia - pathology Mice Mice, Transgenic Mucins - genetics Mucins - metabolism Muscle Proteins - genetics Muscle Proteins - metabolism Peptides - genetics Peptides - metabolism Receptor, Notch1 - genetics Receptor, Notch1 - metabolism Signal Transduction Stem Cells - pathology Transcription Factors - genetics Transcription Factors - metabolism Trefoil Factor-2 Up-Regulation |
| title | Bile Acid and Inflammation Activate Gastric Cardia Stem Cells in a Mouse Model of Barrett-Like Metaplasia |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-06T21%3A24%3A22IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Bile%20Acid%20and%20Inflammation%20Activate%20Gastric%20Cardia%20Stem%20Cells%20in%20a%20Mouse%20Model%20of%20Barrett-Like%20Metaplasia&rft.jtitle=Cancer%20cell&rft.au=Quante,%20Michael&rft.date=2012-01-17&rft.volume=21&rft.issue=1&rft.spage=36&rft.epage=51&rft.pages=36-51&rft.issn=1535-6108&rft.eissn=1878-3686&rft_id=info:doi/10.1016/j.ccr.2011.12.004&rft_dat=%3Cproquest_cross%3E917575816%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=917575816&rft_id=info:pmid/22264787&rft_els_id=S1535610811004740&rfr_iscdi=true |