RESEARCH HIGHLIGHTS
OB Drivers of colorectal cancers the design of targeted therapeutics for human colorectal cancers (crc) is dependent on the ability to distinguish alterations that are causal in tumor formation and progression from those that have little or no effect on tumor growth. to identify novel drivers of crc...
Gespeichert in:
| Veröffentlicht in: | Nature genetics 2009-04, Vol.41 (4), p.390 |
|---|---|
| Hauptverfasser: | , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | |
|---|---|
| container_issue | 4 |
| container_start_page | 390 |
| container_title | Nature genetics |
| container_volume | 41 |
| creator | Axton, Myles Bahcall, Orli Khidr, Lily Vogan, Kyle |
| description | OB Drivers of colorectal cancers the design of targeted therapeutics for human colorectal cancers (crc) is dependent on the ability to distinguish alterations that are causal in tumor formation and progression from those that have little or no effect on tumor growth. to identify novel drivers of crc, David largaespada and colleagues (Science published online, doi:10.1126/science.1163040; 26 February 2009) catalogued genes with common insertion sites (cis) generated in tumors harvested from a gastrointestinal (gi) tract-specific transgenic mouse model that exploits the transposition of a mutagen catalyzed by sleeping Beauty (sB) transposase. comparison of mouse cis genes with human genes that are mutated, amplified, deleted or aberrantly expressed in crc, listed in the catalog of somatic Mutations in cancer database (cOsMic), or known cancer genes identified by the cancer genome Project, revealed a significant overlap of mouse candidate genes and human genes that are altered in cancer. the authors identified 15 cis genes that are most likely to cause crc by virtue of being classified in at least three out of the five aforementioned categories. |
| format | Article |
| fullrecord | <record><control><sourceid>proquest</sourceid><recordid>TN_cdi_proquest_journals_222691585</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1675586581</sourcerecordid><originalsourceid>FETCH-proquest_journals_2226915853</originalsourceid><addsrcrecordid>eNpjYuA0NDUx0zU0N7RgAbINzAx1TQyMzTgYuIqLswwMDE1MDCw4GYSDXINdHYOcPRQ8PN09fIA4JJiHgTUtMac4lRdKczMoubmGOHvoFhTlF5amFpfEZ-WXFuUBpeKNjIzMLA1NLUyNiVIEABD4JxU</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>222691585</pqid></control><display><type>article</type><title>RESEARCH HIGHLIGHTS</title><source>Nature</source><source>SpringerLink Journals - AutoHoldings</source><creator>Axton, Myles ; Bahcall, Orli ; Khidr, Lily ; Vogan, Kyle</creator><creatorcontrib>Axton, Myles ; Bahcall, Orli ; Khidr, Lily ; Vogan, Kyle</creatorcontrib><description>OB Drivers of colorectal cancers the design of targeted therapeutics for human colorectal cancers (crc) is dependent on the ability to distinguish alterations that are causal in tumor formation and progression from those that have little or no effect on tumor growth. to identify novel drivers of crc, David largaespada and colleagues (Science published online, doi:10.1126/science.1163040; 26 February 2009) catalogued genes with common insertion sites (cis) generated in tumors harvested from a gastrointestinal (gi) tract-specific transgenic mouse model that exploits the transposition of a mutagen catalyzed by sleeping Beauty (sB) transposase. comparison of mouse cis genes with human genes that are mutated, amplified, deleted or aberrantly expressed in crc, listed in the catalog of somatic Mutations in cancer database (cOsMic), or known cancer genes identified by the cancer genome Project, revealed a significant overlap of mouse candidate genes and human genes that are altered in cancer. the authors identified 15 cis genes that are most likely to cause crc by virtue of being classified in at least three out of the five aforementioned categories.</description><identifier>ISSN: 1061-4036</identifier><identifier>EISSN: 1546-1718</identifier><language>eng</language><publisher>New York: Nature Publishing Group</publisher><subject>Apoptosis ; Colorectal cancer ; Genes ; Genetic testing ; Studies</subject><ispartof>Nature genetics, 2009-04, Vol.41 (4), p.390</ispartof><rights>Copyright Nature Publishing Group Apr 2009</rights><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></links><search><creatorcontrib>Axton, Myles</creatorcontrib><creatorcontrib>Bahcall, Orli</creatorcontrib><creatorcontrib>Khidr, Lily</creatorcontrib><creatorcontrib>Vogan, Kyle</creatorcontrib><title>RESEARCH HIGHLIGHTS</title><title>Nature genetics</title><description>OB Drivers of colorectal cancers the design of targeted therapeutics for human colorectal cancers (crc) is dependent on the ability to distinguish alterations that are causal in tumor formation and progression from those that have little or no effect on tumor growth. to identify novel drivers of crc, David largaespada and colleagues (Science published online, doi:10.1126/science.1163040; 26 February 2009) catalogued genes with common insertion sites (cis) generated in tumors harvested from a gastrointestinal (gi) tract-specific transgenic mouse model that exploits the transposition of a mutagen catalyzed by sleeping Beauty (sB) transposase. comparison of mouse cis genes with human genes that are mutated, amplified, deleted or aberrantly expressed in crc, listed in the catalog of somatic Mutations in cancer database (cOsMic), or known cancer genes identified by the cancer genome Project, revealed a significant overlap of mouse candidate genes and human genes that are altered in cancer. the authors identified 15 cis genes that are most likely to cause crc by virtue of being classified in at least three out of the five aforementioned categories.</description><subject>Apoptosis</subject><subject>Colorectal cancer</subject><subject>Genes</subject><subject>Genetic testing</subject><subject>Studies</subject><issn>1061-4036</issn><issn>1546-1718</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpjYuA0NDUx0zU0N7RgAbINzAx1TQyMzTgYuIqLswwMDE1MDCw4GYSDXINdHYOcPRQ8PN09fIA4JJiHgTUtMac4lRdKczMoubmGOHvoFhTlF5amFpfEZ-WXFuUBpeKNjIzMLA1NLUyNiVIEABD4JxU</recordid><startdate>20090401</startdate><enddate>20090401</enddate><creator>Axton, Myles</creator><creator>Bahcall, Orli</creator><creator>Khidr, Lily</creator><creator>Vogan, Kyle</creator><general>Nature Publishing Group</general><scope>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SS</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</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>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</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>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope></search><sort><creationdate>20090401</creationdate><title>RESEARCH HIGHLIGHTS</title><author>Axton, Myles ; Bahcall, Orli ; Khidr, Lily ; Vogan, Kyle</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-proquest_journals_2226915853</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Apoptosis</topic><topic>Colorectal cancer</topic><topic>Genes</topic><topic>Genetic testing</topic><topic>Studies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Axton, Myles</creatorcontrib><creatorcontrib>Bahcall, Orli</creatorcontrib><creatorcontrib>Khidr, Lily</creatorcontrib><creatorcontrib>Vogan, Kyle</creatorcontrib><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>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>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</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>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</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 Basic</collection><collection>Genetics Abstracts</collection><jtitle>Nature genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Axton, Myles</au><au>Bahcall, Orli</au><au>Khidr, Lily</au><au>Vogan, Kyle</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>RESEARCH HIGHLIGHTS</atitle><jtitle>Nature genetics</jtitle><date>2009-04-01</date><risdate>2009</risdate><volume>41</volume><issue>4</issue><spage>390</spage><pages>390-</pages><issn>1061-4036</issn><eissn>1546-1718</eissn><abstract>OB Drivers of colorectal cancers the design of targeted therapeutics for human colorectal cancers (crc) is dependent on the ability to distinguish alterations that are causal in tumor formation and progression from those that have little or no effect on tumor growth. to identify novel drivers of crc, David largaespada and colleagues (Science published online, doi:10.1126/science.1163040; 26 February 2009) catalogued genes with common insertion sites (cis) generated in tumors harvested from a gastrointestinal (gi) tract-specific transgenic mouse model that exploits the transposition of a mutagen catalyzed by sleeping Beauty (sB) transposase. comparison of mouse cis genes with human genes that are mutated, amplified, deleted or aberrantly expressed in crc, listed in the catalog of somatic Mutations in cancer database (cOsMic), or known cancer genes identified by the cancer genome Project, revealed a significant overlap of mouse candidate genes and human genes that are altered in cancer. the authors identified 15 cis genes that are most likely to cause crc by virtue of being classified in at least three out of the five aforementioned categories.</abstract><cop>New York</cop><pub>Nature Publishing Group</pub></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1061-4036 |
| ispartof | Nature genetics, 2009-04, Vol.41 (4), p.390 |
| issn | 1061-4036 1546-1718 |
| language | eng |
| recordid | cdi_proquest_journals_222691585 |
| source | Nature; SpringerLink Journals - AutoHoldings |
| subjects | Apoptosis Colorectal cancer Genes Genetic testing Studies |
| title | RESEARCH HIGHLIGHTS |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-11T22%3A59%3A09IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=RESEARCH%20HIGHLIGHTS&rft.jtitle=Nature%20genetics&rft.au=Axton,%20Myles&rft.date=2009-04-01&rft.volume=41&rft.issue=4&rft.spage=390&rft.pages=390-&rft.issn=1061-4036&rft.eissn=1546-1718&rft_id=info:doi/&rft_dat=%3Cproquest%3E1675586581%3C/proquest%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=222691585&rft_id=info:pmid/&rfr_iscdi=true |