Pancreatic neoplasia induced by ras expression in acinar cells of transgenic mice
Expression of an activated human c-H- ras oncogene under control of rat elastase I regulating elements leads to neoplasia of the fetal exocrine pancreas. In most transgenic mice bearing this gene construct, massive tumors involving all the pancreatic acinar cells develop within a few days of pancrea...
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Veröffentlicht in: | Cell 1987-03, Vol.48 (6), p.1023-1034 |
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creator | Quaife, Carol J. Pinkert, Carl A. Ornitz, David M. Palmiter, Richard D. Brinster, Ralph L. |
description | Expression of an activated human c-H-
ras oncogene under control of rat elastase I regulating elements leads to neoplasia of the fetal exocrine pancreas. In most transgenic mice bearing this gene construct, massive tumors involving all the pancreatic acinar cells develop within a few days of pancreatic differentiation. Expression of the normal c-H-
ras proto-oncogene in acinar cells leads to more subtle anomalies, but no tumors develop. Thus modest amounts of the mutant
ras proteins are sufficient, in an otherwise normal genetic background, to lead to neoplastic transformation of differentiating pancreatic acinar cells. In contrast, a comparable elastase-
myc construct produces no pancreatic tumors in transgenic mice. |
doi_str_mv | 10.1016/0092-8674(87)90710-0 |
format | Article |
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ras oncogene under control of rat elastase I regulating elements leads to neoplasia of the fetal exocrine pancreas. In most transgenic mice bearing this gene construct, massive tumors involving all the pancreatic acinar cells develop within a few days of pancreatic differentiation. Expression of the normal c-H-
ras proto-oncogene in acinar cells leads to more subtle anomalies, but no tumors develop. Thus modest amounts of the mutant
ras proteins are sufficient, in an otherwise normal genetic background, to lead to neoplastic transformation of differentiating pancreatic acinar cells. In contrast, a comparable elastase-
myc construct produces no pancreatic tumors in transgenic mice.</description><identifier>ISSN: 0092-8674</identifier><identifier>EISSN: 1097-4172</identifier><identifier>DOI: 10.1016/0092-8674(87)90710-0</identifier><identifier>PMID: 3470144</identifier><identifier>CODEN: CELLB5</identifier><language>eng</language><publisher>Cambridge, MA: Elsevier Inc</publisher><subject>Animals ; Biological and medical sciences ; Cell Differentiation ; Cell physiology ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Cell Transformation, Neoplastic ; Fetus ; Flow Cytometry ; Fundamental and applied biological sciences. Psychology ; Genetic Engineering ; Mice ; Molecular and cellular biology ; Pancreas - cytology ; Pancreas - embryology ; Pancreas - pathology ; Pancreatic Neoplasms - genetics ; Pancreatic Neoplasms - pathology ; Proto-Oncogenes</subject><ispartof>Cell, 1987-03, Vol.48 (6), p.1023-1034</ispartof><rights>1987</rights><rights>1988 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c452t-d81a9bc41872ee73e98e07dbaab2be4b3f33b0854b503f59664b0b06935ceca53</citedby><cites>FETCH-LOGICAL-c452t-d81a9bc41872ee73e98e07dbaab2be4b3f33b0854b503f59664b0b06935ceca53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/0092867487907100$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=7447302$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/3470144$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Quaife, Carol J.</creatorcontrib><creatorcontrib>Pinkert, Carl A.</creatorcontrib><creatorcontrib>Ornitz, David M.</creatorcontrib><creatorcontrib>Palmiter, Richard D.</creatorcontrib><creatorcontrib>Brinster, Ralph L.</creatorcontrib><title>Pancreatic neoplasia induced by ras expression in acinar cells of transgenic mice</title><title>Cell</title><addtitle>Cell</addtitle><description>Expression of an activated human c-H-
ras oncogene under control of rat elastase I regulating elements leads to neoplasia of the fetal exocrine pancreas. In most transgenic mice bearing this gene construct, massive tumors involving all the pancreatic acinar cells develop within a few days of pancreatic differentiation. Expression of the normal c-H-
ras proto-oncogene in acinar cells leads to more subtle anomalies, but no tumors develop. Thus modest amounts of the mutant
ras proteins are sufficient, in an otherwise normal genetic background, to lead to neoplastic transformation of differentiating pancreatic acinar cells. In contrast, a comparable elastase-
myc construct produces no pancreatic tumors in transgenic mice.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell Differentiation</subject><subject>Cell physiology</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Cell Transformation, Neoplastic</subject><subject>Fetus</subject><subject>Flow Cytometry</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genetic Engineering</subject><subject>Mice</subject><subject>Molecular and cellular biology</subject><subject>Pancreas - cytology</subject><subject>Pancreas - embryology</subject><subject>Pancreas - pathology</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Proto-Oncogenes</subject><issn>0092-8674</issn><issn>1097-4172</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1987</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1r3DAURUVISSdp_0EKWoSQLtw-WZJlbwIh9AsCbaFdiyf5Oah47KmepzT_vprMMMuutLjnXa6OEJcK3ilQzXuArq7axpmb1r3twCmo4ESsFHSuMsrVp2J1RF6Kc-ZfANBaa8_EmTYOlDEr8f0bTjETLinKiebNiJxQpqnfRupleJIZWdLfTSbmNE8lkRjThFlGGkeW8yCXjBM_0lQa1inSK_FiwJHp9eG9ED8_fvhx_7l6-Prpy_3dQxWNrZeqbxV2IRrVuprIaepaAtcHxFAHMkEPWocy1wQLerBd05gAAZpO20gRrb4Q1_veTZ5_b4kXv068G4XlH1v2zhndgDUFNHsw5pk50-A3Oa0xP3kFfmfS7zT5nSbfOv9s0kM5e3Po34Y19cejg7qSXx1y5IjjUCzExEfMGeM01AW73WNUXPxJlD3HRFOxmzLFxfdz-v-Ofzabj04</recordid><startdate>19870327</startdate><enddate>19870327</enddate><creator>Quaife, Carol J.</creator><creator>Pinkert, Carl A.</creator><creator>Ornitz, David M.</creator><creator>Palmiter, Richard D.</creator><creator>Brinster, Ralph L.</creator><general>Elsevier Inc</general><general>Cell Press</general><scope>IQODW</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>19870327</creationdate><title>Pancreatic neoplasia induced by ras expression in acinar cells of transgenic mice</title><author>Quaife, Carol J. ; Pinkert, Carl A. ; Ornitz, David M. ; Palmiter, Richard D. ; Brinster, Ralph L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c452t-d81a9bc41872ee73e98e07dbaab2be4b3f33b0854b503f59664b0b06935ceca53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1987</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell Differentiation</topic><topic>Cell physiology</topic><topic>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</topic><topic>Cell Transformation, Neoplastic</topic><topic>Fetus</topic><topic>Flow Cytometry</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Genetic Engineering</topic><topic>Mice</topic><topic>Molecular and cellular biology</topic><topic>Pancreas - cytology</topic><topic>Pancreas - embryology</topic><topic>Pancreas - pathology</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Proto-Oncogenes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Quaife, Carol J.</creatorcontrib><creatorcontrib>Pinkert, Carl A.</creatorcontrib><creatorcontrib>Ornitz, David M.</creatorcontrib><creatorcontrib>Palmiter, Richard D.</creatorcontrib><creatorcontrib>Brinster, Ralph L.</creatorcontrib><collection>Pascal-Francis</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>Cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Quaife, Carol J.</au><au>Pinkert, Carl A.</au><au>Ornitz, David M.</au><au>Palmiter, Richard D.</au><au>Brinster, Ralph L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pancreatic neoplasia induced by ras expression in acinar cells of transgenic mice</atitle><jtitle>Cell</jtitle><addtitle>Cell</addtitle><date>1987-03-27</date><risdate>1987</risdate><volume>48</volume><issue>6</issue><spage>1023</spage><epage>1034</epage><pages>1023-1034</pages><issn>0092-8674</issn><eissn>1097-4172</eissn><coden>CELLB5</coden><abstract>Expression of an activated human c-H-
ras oncogene under control of rat elastase I regulating elements leads to neoplasia of the fetal exocrine pancreas. In most transgenic mice bearing this gene construct, massive tumors involving all the pancreatic acinar cells develop within a few days of pancreatic differentiation. Expression of the normal c-H-
ras proto-oncogene in acinar cells leads to more subtle anomalies, but no tumors develop. Thus modest amounts of the mutant
ras proteins are sufficient, in an otherwise normal genetic background, to lead to neoplastic transformation of differentiating pancreatic acinar cells. In contrast, a comparable elastase-
myc construct produces no pancreatic tumors in transgenic mice.</abstract><cop>Cambridge, MA</cop><pub>Elsevier Inc</pub><pmid>3470144</pmid><doi>10.1016/0092-8674(87)90710-0</doi><tpages>12</tpages></addata></record> |
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subjects | Animals Biological and medical sciences Cell Differentiation Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Cell Transformation, Neoplastic Fetus Flow Cytometry Fundamental and applied biological sciences. Psychology Genetic Engineering Mice Molecular and cellular biology Pancreas - cytology Pancreas - embryology Pancreas - pathology Pancreatic Neoplasms - genetics Pancreatic Neoplasms - pathology Proto-Oncogenes |
title | Pancreatic neoplasia induced by ras expression in acinar cells of transgenic mice |
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