Loading…
Insertional mutagenesis using the Sleeping Beauty transposon system identifies drivers of erythroleukemia in mice
Insertional mutagenesis is a powerful means of identifying cancer drivers in animal models. We used the Sleeping Beauty (SB) transposon/transposase system to identify activated oncogenes in hematologic cancers in wild-type mice and mice that express a stabilized cyclin E protein (termed cyclin ET74A...
Saved in:
| Published in: | Scientific reports 2019-04, Vol.9 (1), p.5488, Article 5488 |
|---|---|
| Main Authors: | , , , , , , , , , |
| Format: | Article |
| Language: | English |
| Subjects: | |
| Citations: | Items that this one cites Items that cite this one |
| Online Access: | Get full text |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| cited_by | cdi_FETCH-LOGICAL-c430t-8f87c5c8cd7a2e034d93b7d324049fede53f73dcc01de8321984859b0f84e2b33 |
|---|---|
| cites | cdi_FETCH-LOGICAL-c430t-8f87c5c8cd7a2e034d93b7d324049fede53f73dcc01de8321984859b0f84e2b33 |
| container_end_page | |
| container_issue | 1 |
| container_start_page | 5488 |
| container_title | Scientific reports |
| container_volume | 9 |
| creator | Loeb, Keith R Hughes, Bridget T Fissel, Brian M Osteen, Nyka J Knoblaugh, Sue E Grim, Jonathan E Drury, Luke J Sarver, Aaron Dupuy, Adam J Clurman, Bruce E |
| description | Insertional mutagenesis is a powerful means of identifying cancer drivers in animal models. We used the Sleeping Beauty (SB) transposon/transposase system to identify activated oncogenes in hematologic cancers in wild-type mice and mice that express a stabilized cyclin E protein (termed cyclin ET74AT393A). Cyclin E governs cell division and is misregulated in human cancers. Cyclin ET74AT393A mice develop ineffective erythropoiesis that resembles early-stage human myelodysplastic syndrome, and we sought to identify oncogenes that might cooperate with cyclin E hyperactivity in leukemogenesis. SB activation in hematopoietic precursors caused T-cell leukemia/lymphomas (T-ALL) and pure red blood cell erythroleukemias (EL). Analysis of >12,000 SB integration sites revealed markedly different oncogene activations in EL and T-ALL: Notch1 and Ikaros were most common in T-ALL, whereas ETS transcription factors (Erg and Ets1) were targeted in most ELs. Cyclin E status did not impact leukemogenesis or oncogene activations. Whereas most SB insertions were lost during culture of EL cell lines, Erg insertions were retained, indicating Erg's key role in these neoplasms. Surprisingly, cyclin ET74AT393A conferred growth factor independence and altered Erg-dependent differentiation in EL cell lines. These studies provide new molecular insights into erythroid leukemia and suggest potential therapeutic targets for human leukemia. |
| doi_str_mv | 10.1038/s41598-019-41805-x |
| format | article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6445099</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2202210226</sourcerecordid><originalsourceid>FETCH-LOGICAL-c430t-8f87c5c8cd7a2e034d93b7d324049fede53f73dcc01de8321984859b0f84e2b33</originalsourceid><addsrcrecordid>eNpVkd9LJDEMx8vhcYr6D9yDFO55zv6a3fZF8ERPQfDBu-fSbTO71Zl2bTri_veOrooGQhqSfBvyIeQnZ785k_oYFW-Nbhg3jeKatc3TN7InmGobIYXY-fTeJYeId2yyVhjFzQ-yK5lRTKvZHnm4SgilxpxcT4exuiUkwIh0xJiWtK6A3vYA65fkD7ixbmgtLuE6Y04UN1hhoDFAqrGLgDSU-AgFae4olE1dldzDeA9DdDQmOkQPB-R753qEw7e4T_5fnP87u2yub_5enZ1eN15JVhvd6blvvfZh7gQwqYKRi3mQQjFlOgjQym4ug_eMB9BScKOVbs2CdVqBWEi5T062uutxMUDw04rF9XZd4uDKxmYX7ddKiiu7zI92plTLjJkEfr0JlPwwAlZ7l8cy3QmtEEwIPvls6hLbLl8yYoHu4wfO7AspuyVlJ1L2lZR9moaOPu_2MfLORT4DUJCSyw</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2202210226</pqid></control><display><type>article</type><title>Insertional mutagenesis using the Sleeping Beauty transposon system identifies drivers of erythroleukemia in mice</title><source>Open Access: PubMed Central</source><source>Nature Open Access</source><source>ProQuest - Publicly Available Content Database</source><source>Free Full-Text Journals in Chemistry</source><creator>Loeb, Keith R ; Hughes, Bridget T ; Fissel, Brian M ; Osteen, Nyka J ; Knoblaugh, Sue E ; Grim, Jonathan E ; Drury, Luke J ; Sarver, Aaron ; Dupuy, Adam J ; Clurman, Bruce E</creator><creatorcontrib>Loeb, Keith R ; Hughes, Bridget T ; Fissel, Brian M ; Osteen, Nyka J ; Knoblaugh, Sue E ; Grim, Jonathan E ; Drury, Luke J ; Sarver, Aaron ; Dupuy, Adam J ; Clurman, Bruce E</creatorcontrib><description>Insertional mutagenesis is a powerful means of identifying cancer drivers in animal models. We used the Sleeping Beauty (SB) transposon/transposase system to identify activated oncogenes in hematologic cancers in wild-type mice and mice that express a stabilized cyclin E protein (termed cyclin ET74AT393A). Cyclin E governs cell division and is misregulated in human cancers. Cyclin ET74AT393A mice develop ineffective erythropoiesis that resembles early-stage human myelodysplastic syndrome, and we sought to identify oncogenes that might cooperate with cyclin E hyperactivity in leukemogenesis. SB activation in hematopoietic precursors caused T-cell leukemia/lymphomas (T-ALL) and pure red blood cell erythroleukemias (EL). Analysis of >12,000 SB integration sites revealed markedly different oncogene activations in EL and T-ALL: Notch1 and Ikaros were most common in T-ALL, whereas ETS transcription factors (Erg and Ets1) were targeted in most ELs. Cyclin E status did not impact leukemogenesis or oncogene activations. Whereas most SB insertions were lost during culture of EL cell lines, Erg insertions were retained, indicating Erg's key role in these neoplasms. Surprisingly, cyclin ET74AT393A conferred growth factor independence and altered Erg-dependent differentiation in EL cell lines. These studies provide new molecular insights into erythroid leukemia and suggest potential therapeutic targets for human leukemia.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-019-41805-x</identifier><identifier>PMID: 30940846</identifier><language>eng</language><publisher>England: Nature Publishing Group</publisher><subject>Acute lymphoblastic leukemia ; Animal models ; Animals ; Cancer ; Cell culture ; Cell Culture Techniques ; Cell division ; Cyclin E ; Cyclin E - genetics ; Disease Models, Animal ; DNA Transposable Elements ; E protein ; Erythrocytes ; Erythroleukemia ; Erythropoiesis ; Ets-1 protein ; Genetic Predisposition to Disease ; Hemopoiesis ; Hyperactivity ; Ikaros protein ; Insertional mutagenesis ; Leukemia ; Leukemia, Erythroblastic, Acute - genetics ; Leukemogenesis ; Lymphocytes T ; Lymphoma ; Mice ; Mutagenesis ; Mutagenesis, Insertional ; Myelodysplastic syndrome ; Neoplasia ; Notch1 protein ; Oncogene Proteins - genetics ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - genetics ; Rodents ; Therapeutic applications ; Transcription factors ; Transcriptional Regulator ERG - genetics ; Transposase ; Transposases - genetics ; Transposons</subject><ispartof>Scientific reports, 2019-04, Vol.9 (1), p.5488, Article 5488</ispartof><rights>This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s) 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c430t-8f87c5c8cd7a2e034d93b7d324049fede53f73dcc01de8321984859b0f84e2b33</citedby><cites>FETCH-LOGICAL-c430t-8f87c5c8cd7a2e034d93b7d324049fede53f73dcc01de8321984859b0f84e2b33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2202210226/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2202210226?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,315,733,786,790,891,25783,27957,27958,37047,44625,53827,53829,75483</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30940846$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Loeb, Keith R</creatorcontrib><creatorcontrib>Hughes, Bridget T</creatorcontrib><creatorcontrib>Fissel, Brian M</creatorcontrib><creatorcontrib>Osteen, Nyka J</creatorcontrib><creatorcontrib>Knoblaugh, Sue E</creatorcontrib><creatorcontrib>Grim, Jonathan E</creatorcontrib><creatorcontrib>Drury, Luke J</creatorcontrib><creatorcontrib>Sarver, Aaron</creatorcontrib><creatorcontrib>Dupuy, Adam J</creatorcontrib><creatorcontrib>Clurman, Bruce E</creatorcontrib><title>Insertional mutagenesis using the Sleeping Beauty transposon system identifies drivers of erythroleukemia in mice</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><description>Insertional mutagenesis is a powerful means of identifying cancer drivers in animal models. We used the Sleeping Beauty (SB) transposon/transposase system to identify activated oncogenes in hematologic cancers in wild-type mice and mice that express a stabilized cyclin E protein (termed cyclin ET74AT393A). Cyclin E governs cell division and is misregulated in human cancers. Cyclin ET74AT393A mice develop ineffective erythropoiesis that resembles early-stage human myelodysplastic syndrome, and we sought to identify oncogenes that might cooperate with cyclin E hyperactivity in leukemogenesis. SB activation in hematopoietic precursors caused T-cell leukemia/lymphomas (T-ALL) and pure red blood cell erythroleukemias (EL). Analysis of >12,000 SB integration sites revealed markedly different oncogene activations in EL and T-ALL: Notch1 and Ikaros were most common in T-ALL, whereas ETS transcription factors (Erg and Ets1) were targeted in most ELs. Cyclin E status did not impact leukemogenesis or oncogene activations. Whereas most SB insertions were lost during culture of EL cell lines, Erg insertions were retained, indicating Erg's key role in these neoplasms. Surprisingly, cyclin ET74AT393A conferred growth factor independence and altered Erg-dependent differentiation in EL cell lines. These studies provide new molecular insights into erythroid leukemia and suggest potential therapeutic targets for human leukemia.</description><subject>Acute lymphoblastic leukemia</subject><subject>Animal models</subject><subject>Animals</subject><subject>Cancer</subject><subject>Cell culture</subject><subject>Cell Culture Techniques</subject><subject>Cell division</subject><subject>Cyclin E</subject><subject>Cyclin E - genetics</subject><subject>Disease Models, Animal</subject><subject>DNA Transposable Elements</subject><subject>E protein</subject><subject>Erythrocytes</subject><subject>Erythroleukemia</subject><subject>Erythropoiesis</subject><subject>Ets-1 protein</subject><subject>Genetic Predisposition to Disease</subject><subject>Hemopoiesis</subject><subject>Hyperactivity</subject><subject>Ikaros protein</subject><subject>Insertional mutagenesis</subject><subject>Leukemia</subject><subject>Leukemia, Erythroblastic, Acute - genetics</subject><subject>Leukemogenesis</subject><subject>Lymphocytes T</subject><subject>Lymphoma</subject><subject>Mice</subject><subject>Mutagenesis</subject><subject>Mutagenesis, Insertional</subject><subject>Myelodysplastic syndrome</subject><subject>Neoplasia</subject><subject>Notch1 protein</subject><subject>Oncogene Proteins - genetics</subject><subject>Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - genetics</subject><subject>Rodents</subject><subject>Therapeutic applications</subject><subject>Transcription factors</subject><subject>Transcriptional Regulator ERG - genetics</subject><subject>Transposase</subject><subject>Transposases - genetics</subject><subject>Transposons</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNpVkd9LJDEMx8vhcYr6D9yDFO55zv6a3fZF8ERPQfDBu-fSbTO71Zl2bTri_veOrooGQhqSfBvyIeQnZ785k_oYFW-Nbhg3jeKatc3TN7InmGobIYXY-fTeJYeId2yyVhjFzQ-yK5lRTKvZHnm4SgilxpxcT4exuiUkwIh0xJiWtK6A3vYA65fkD7ixbmgtLuE6Y04UN1hhoDFAqrGLgDSU-AgFae4olE1dldzDeA9DdDQmOkQPB-R753qEw7e4T_5fnP87u2yub_5enZ1eN15JVhvd6blvvfZh7gQwqYKRi3mQQjFlOgjQym4ug_eMB9BScKOVbs2CdVqBWEi5T062uutxMUDw04rF9XZd4uDKxmYX7ddKiiu7zI92plTLjJkEfr0JlPwwAlZ7l8cy3QmtEEwIPvls6hLbLl8yYoHu4wfO7AspuyVlJ1L2lZR9moaOPu_2MfLORT4DUJCSyw</recordid><startdate>20190402</startdate><enddate>20190402</enddate><creator>Loeb, Keith R</creator><creator>Hughes, Bridget T</creator><creator>Fissel, Brian M</creator><creator>Osteen, Nyka J</creator><creator>Knoblaugh, Sue E</creator><creator>Grim, Jonathan E</creator><creator>Drury, Luke J</creator><creator>Sarver, Aaron</creator><creator>Dupuy, Adam J</creator><creator>Clurman, Bruce E</creator><general>Nature Publishing Group</general><general>Nature Publishing Group UK</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>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</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>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>5PM</scope></search><sort><creationdate>20190402</creationdate><title>Insertional mutagenesis using the Sleeping Beauty transposon system identifies drivers of erythroleukemia in mice</title><author>Loeb, Keith R ; Hughes, Bridget T ; Fissel, Brian M ; Osteen, Nyka J ; Knoblaugh, Sue E ; Grim, Jonathan E ; Drury, Luke J ; Sarver, Aaron ; Dupuy, Adam J ; Clurman, Bruce E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c430t-8f87c5c8cd7a2e034d93b7d324049fede53f73dcc01de8321984859b0f84e2b33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Acute lymphoblastic leukemia</topic><topic>Animal models</topic><topic>Animals</topic><topic>Cancer</topic><topic>Cell culture</topic><topic>Cell Culture Techniques</topic><topic>Cell division</topic><topic>Cyclin E</topic><topic>Cyclin E - genetics</topic><topic>Disease Models, Animal</topic><topic>DNA Transposable Elements</topic><topic>E protein</topic><topic>Erythrocytes</topic><topic>Erythroleukemia</topic><topic>Erythropoiesis</topic><topic>Ets-1 protein</topic><topic>Genetic Predisposition to Disease</topic><topic>Hemopoiesis</topic><topic>Hyperactivity</topic><topic>Ikaros protein</topic><topic>Insertional mutagenesis</topic><topic>Leukemia</topic><topic>Leukemia, Erythroblastic, Acute - genetics</topic><topic>Leukemogenesis</topic><topic>Lymphocytes T</topic><topic>Lymphoma</topic><topic>Mice</topic><topic>Mutagenesis</topic><topic>Mutagenesis, Insertional</topic><topic>Myelodysplastic syndrome</topic><topic>Neoplasia</topic><topic>Notch1 protein</topic><topic>Oncogene Proteins - genetics</topic><topic>Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - genetics</topic><topic>Rodents</topic><topic>Therapeutic applications</topic><topic>Transcription factors</topic><topic>Transcriptional Regulator ERG - genetics</topic><topic>Transposase</topic><topic>Transposases - genetics</topic><topic>Transposons</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Loeb, Keith R</creatorcontrib><creatorcontrib>Hughes, Bridget T</creatorcontrib><creatorcontrib>Fissel, Brian M</creatorcontrib><creatorcontrib>Osteen, Nyka J</creatorcontrib><creatorcontrib>Knoblaugh, Sue E</creatorcontrib><creatorcontrib>Grim, Jonathan E</creatorcontrib><creatorcontrib>Drury, Luke J</creatorcontrib><creatorcontrib>Sarver, Aaron</creatorcontrib><creatorcontrib>Dupuy, Adam J</creatorcontrib><creatorcontrib>Clurman, Bruce E</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>ProQuest 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>Science Database (Alumni Edition)</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>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest Science Journals</collection><collection>Biological Science Database</collection><collection>ProQuest - Publicly Available Content Database</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>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Loeb, Keith R</au><au>Hughes, Bridget T</au><au>Fissel, Brian M</au><au>Osteen, Nyka J</au><au>Knoblaugh, Sue E</au><au>Grim, Jonathan E</au><au>Drury, Luke J</au><au>Sarver, Aaron</au><au>Dupuy, Adam J</au><au>Clurman, Bruce E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Insertional mutagenesis using the Sleeping Beauty transposon system identifies drivers of erythroleukemia in mice</atitle><jtitle>Scientific reports</jtitle><addtitle>Sci Rep</addtitle><date>2019-04-02</date><risdate>2019</risdate><volume>9</volume><issue>1</issue><spage>5488</spage><pages>5488-</pages><artnum>5488</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Insertional mutagenesis is a powerful means of identifying cancer drivers in animal models. We used the Sleeping Beauty (SB) transposon/transposase system to identify activated oncogenes in hematologic cancers in wild-type mice and mice that express a stabilized cyclin E protein (termed cyclin ET74AT393A). Cyclin E governs cell division and is misregulated in human cancers. Cyclin ET74AT393A mice develop ineffective erythropoiesis that resembles early-stage human myelodysplastic syndrome, and we sought to identify oncogenes that might cooperate with cyclin E hyperactivity in leukemogenesis. SB activation in hematopoietic precursors caused T-cell leukemia/lymphomas (T-ALL) and pure red blood cell erythroleukemias (EL). Analysis of >12,000 SB integration sites revealed markedly different oncogene activations in EL and T-ALL: Notch1 and Ikaros were most common in T-ALL, whereas ETS transcription factors (Erg and Ets1) were targeted in most ELs. Cyclin E status did not impact leukemogenesis or oncogene activations. Whereas most SB insertions were lost during culture of EL cell lines, Erg insertions were retained, indicating Erg's key role in these neoplasms. Surprisingly, cyclin ET74AT393A conferred growth factor independence and altered Erg-dependent differentiation in EL cell lines. These studies provide new molecular insights into erythroid leukemia and suggest potential therapeutic targets for human leukemia.</abstract><cop>England</cop><pub>Nature Publishing Group</pub><pmid>30940846</pmid><doi>10.1038/s41598-019-41805-x</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 2045-2322 |
| ispartof | Scientific reports, 2019-04, Vol.9 (1), p.5488, Article 5488 |
| issn | 2045-2322 2045-2322 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6445099 |
| source | Open Access: PubMed Central; Nature Open Access; ProQuest - Publicly Available Content Database; Free Full-Text Journals in Chemistry |
| subjects | Acute lymphoblastic leukemia Animal models Animals Cancer Cell culture Cell Culture Techniques Cell division Cyclin E Cyclin E - genetics Disease Models, Animal DNA Transposable Elements E protein Erythrocytes Erythroleukemia Erythropoiesis Ets-1 protein Genetic Predisposition to Disease Hemopoiesis Hyperactivity Ikaros protein Insertional mutagenesis Leukemia Leukemia, Erythroblastic, Acute - genetics Leukemogenesis Lymphocytes T Lymphoma Mice Mutagenesis Mutagenesis, Insertional Myelodysplastic syndrome Neoplasia Notch1 protein Oncogene Proteins - genetics Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - genetics Rodents Therapeutic applications Transcription factors Transcriptional Regulator ERG - genetics Transposase Transposases - genetics Transposons |
| title | Insertional mutagenesis using the Sleeping Beauty transposon system identifies drivers of erythroleukemia in mice |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-09-22T06%3A24%3A54IST&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=Insertional%20mutagenesis%20using%20the%20Sleeping%20Beauty%20transposon%20system%20identifies%20drivers%20of%20erythroleukemia%20in%20mice&rft.jtitle=Scientific%20reports&rft.au=Loeb,%20Keith%20R&rft.date=2019-04-02&rft.volume=9&rft.issue=1&rft.spage=5488&rft.pages=5488-&rft.artnum=5488&rft.issn=2045-2322&rft.eissn=2045-2322&rft_id=info:doi/10.1038/s41598-019-41805-x&rft_dat=%3Cproquest_pubme%3E2202210226%3C/proquest_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c430t-8f87c5c8cd7a2e034d93b7d324049fede53f73dcc01de8321984859b0f84e2b33%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2202210226&rft_id=info:pmid/30940846&rfr_iscdi=true |