Promises from Trametinib in RAF Active Tumors
Progression of human cancer occurs through genetic changes in cancer cells that activate biochemical pathways governing hallmarks of cancer, including proliferation and tumor-cell survival, 1 among others. Tumor growth factor receptors activate RAS oncoproteins, which subsequently activate a kinase...
Gespeichert in:
| Veröffentlicht in: | The New England journal of medicine 2012-07, Vol.367 (2), p.171-172 |
|---|---|
| 1. Verfasser: | |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 172 |
|---|---|
| container_issue | 2 |
| container_start_page | 171 |
| container_title | The New England journal of medicine |
| container_volume | 367 |
| creator | Sausville, Edward A |
| description | Progression of human cancer occurs through genetic changes in cancer cells that activate biochemical pathways governing hallmarks of cancer, including proliferation and tumor-cell survival,
1
among others. Tumor growth factor receptors activate RAS oncoproteins, which subsequently activate a kinase cascade that includes RAF, MEK, and ERK kinases. This pathway is mutated to promote tumor growth in at least 20% of cancers.
2
The RAS–MEK–ERK pathway is thus a focus of intense interest for the development of cancer drugs. First fruits from this quest have yielded drugs directed against growth factor receptors, including the monoclonal antibody trastuzumab and the small molecules erlotinib and . . . |
| doi_str_mv | 10.1056/NEJMe1205654 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1024937932</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1024937932</sourcerecordid><originalsourceid>FETCH-LOGICAL-c348t-a850bc815d7dc81683045e092224f64ab8370154029086211c2feb35b2382d1e3</originalsourceid><addsrcrecordid>eNpt0MtLw0AQBvBFFFurN88S0IMHo7Ozu8nmWErrg_pA6jnkMYGUblJ3E8H_3tVWEXEvM4cfH7MfY8ccLjmo6OphendPHP2q5A4bciVEKCVEu2wIgDqUcSIG7MC5JfjHZbLPBohRJIDjkIVPtjW1IxdUfgkWNjPU1U2dB3UTPI9nwbjo6jcKFr1prTtke1W2cnS0nSP2MpsuJjfh_PH6djKeh4WQugszrSAvNFdlXPoRaQFSESSIKKtIZrkWMXAlARPQEXJeYEW5UDkKjSUnMWLnm9y1bV97cl3qbyxotcoaanuXckCZCP8x9PT0D122vW38dV8qFlJi7NXFRhW2dc5Sla5tbTL77lH6WWP6u0bPT7ahfW6o_MHfvXlwtgHGuLShpfk_5wOevXNa</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1024734427</pqid></control><display><type>article</type><title>Promises from Trametinib in RAF Active Tumors</title><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>ProQuest Central UK/Ireland</source><source>New England Journal of Medicine</source><creator>Sausville, Edward A</creator><creatorcontrib>Sausville, Edward A</creatorcontrib><description>Progression of human cancer occurs through genetic changes in cancer cells that activate biochemical pathways governing hallmarks of cancer, including proliferation and tumor-cell survival,
1
among others. Tumor growth factor receptors activate RAS oncoproteins, which subsequently activate a kinase cascade that includes RAF, MEK, and ERK kinases. This pathway is mutated to promote tumor growth in at least 20% of cancers.
2
The RAS–MEK–ERK pathway is thus a focus of intense interest for the development of cancer drugs. First fruits from this quest have yielded drugs directed against growth factor receptors, including the monoclonal antibody trastuzumab and the small molecules erlotinib and . . .</description><identifier>ISSN: 0028-4793</identifier><identifier>EISSN: 1533-4406</identifier><identifier>DOI: 10.1056/NEJMe1205654</identifier><identifier>PMID: 22663012</identifier><language>eng</language><publisher>United States: Massachusetts Medical Society</publisher><subject>Antineoplastic Agents - therapeutic use ; Cancer ; Cell proliferation ; Cell survival ; Drug development ; Extracellular signal-regulated kinase ; Female ; Growth factor receptors ; Humans ; Kinases ; Male ; MAP Kinase Kinase 1 - antagonists & inhibitors ; MAP Kinase Kinase 2 - antagonists & inhibitors ; Melanoma - drug therapy ; Monoclonal antibodies ; Mutation ; Protein Kinase Inhibitors - therapeutic use ; Proteins ; Proto-Oncogene Proteins B-raf - genetics ; Pyridones - therapeutic use ; Pyrimidinones - therapeutic use ; Raf protein ; Targeted cancer therapy ; Trastuzumab ; Tumors</subject><ispartof>The New England journal of medicine, 2012-07, Vol.367 (2), p.171-172</ispartof><rights>Copyright © 2012 Massachusetts Medical Society. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c348t-a850bc815d7dc81683045e092224f64ab8370154029086211c2feb35b2382d1e3</citedby><cites>FETCH-LOGICAL-c348t-a850bc815d7dc81683045e092224f64ab8370154029086211c2feb35b2382d1e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.nejm.org/doi/pdf/10.1056/NEJMe1205654$$EPDF$$P50$$Gmms$$H</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1024734427?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,780,784,2759,2760,26103,27924,27925,52382,54064,64385,64387,64389,72469</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22663012$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sausville, Edward A</creatorcontrib><title>Promises from Trametinib in RAF Active Tumors</title><title>The New England journal of medicine</title><addtitle>N Engl J Med</addtitle><description>Progression of human cancer occurs through genetic changes in cancer cells that activate biochemical pathways governing hallmarks of cancer, including proliferation and tumor-cell survival,
1
among others. Tumor growth factor receptors activate RAS oncoproteins, which subsequently activate a kinase cascade that includes RAF, MEK, and ERK kinases. This pathway is mutated to promote tumor growth in at least 20% of cancers.
2
The RAS–MEK–ERK pathway is thus a focus of intense interest for the development of cancer drugs. First fruits from this quest have yielded drugs directed against growth factor receptors, including the monoclonal antibody trastuzumab and the small molecules erlotinib and . . .</description><subject>Antineoplastic Agents - therapeutic use</subject><subject>Cancer</subject><subject>Cell proliferation</subject><subject>Cell survival</subject><subject>Drug development</subject><subject>Extracellular signal-regulated kinase</subject><subject>Female</subject><subject>Growth factor receptors</subject><subject>Humans</subject><subject>Kinases</subject><subject>Male</subject><subject>MAP Kinase Kinase 1 - antagonists & inhibitors</subject><subject>MAP Kinase Kinase 2 - antagonists & inhibitors</subject><subject>Melanoma - drug therapy</subject><subject>Monoclonal antibodies</subject><subject>Mutation</subject><subject>Protein Kinase Inhibitors - therapeutic use</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins B-raf - genetics</subject><subject>Pyridones - therapeutic use</subject><subject>Pyrimidinones - therapeutic use</subject><subject>Raf protein</subject><subject>Targeted cancer therapy</subject><subject>Trastuzumab</subject><subject>Tumors</subject><issn>0028-4793</issn><issn>1533-4406</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpt0MtLw0AQBvBFFFurN88S0IMHo7Ozu8nmWErrg_pA6jnkMYGUblJ3E8H_3tVWEXEvM4cfH7MfY8ccLjmo6OphendPHP2q5A4bciVEKCVEu2wIgDqUcSIG7MC5JfjHZbLPBohRJIDjkIVPtjW1IxdUfgkWNjPU1U2dB3UTPI9nwbjo6jcKFr1prTtke1W2cnS0nSP2MpsuJjfh_PH6djKeh4WQugszrSAvNFdlXPoRaQFSESSIKKtIZrkWMXAlARPQEXJeYEW5UDkKjSUnMWLnm9y1bV97cl3qbyxotcoaanuXckCZCP8x9PT0D122vW38dV8qFlJi7NXFRhW2dc5Sla5tbTL77lH6WWP6u0bPT7ahfW6o_MHfvXlwtgHGuLShpfk_5wOevXNa</recordid><startdate>20120712</startdate><enddate>20120712</enddate><creator>Sausville, Edward A</creator><general>Massachusetts Medical Society</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>0TZ</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K0Y</scope><scope>LK8</scope><scope>M0R</scope><scope>M0T</scope><scope>M1P</scope><scope>M2M</scope><scope>M2O</scope><scope>M2P</scope><scope>M7P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20120712</creationdate><title>Promises from Trametinib in RAF Active Tumors</title><author>Sausville, Edward A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c348t-a850bc815d7dc81683045e092224f64ab8370154029086211c2feb35b2382d1e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Antineoplastic Agents - therapeutic use</topic><topic>Cancer</topic><topic>Cell proliferation</topic><topic>Cell survival</topic><topic>Drug development</topic><topic>Extracellular signal-regulated kinase</topic><topic>Female</topic><topic>Growth factor receptors</topic><topic>Humans</topic><topic>Kinases</topic><topic>Male</topic><topic>MAP Kinase Kinase 1 - antagonists & inhibitors</topic><topic>MAP Kinase Kinase 2 - antagonists & inhibitors</topic><topic>Melanoma - drug therapy</topic><topic>Monoclonal antibodies</topic><topic>Mutation</topic><topic>Protein Kinase Inhibitors - therapeutic use</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins B-raf - genetics</topic><topic>Pyridones - therapeutic use</topic><topic>Pyrimidinones - therapeutic use</topic><topic>Raf protein</topic><topic>Targeted cancer therapy</topic><topic>Trastuzumab</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sausville, Edward A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Pharma and Biotech Premium PRO</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>eLibrary</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</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>SciTech Premium Collection</collection><collection>New England Journal of Medicine</collection><collection>ProQuest Biological Science Collection</collection><collection>Consumer Health Database</collection><collection>Healthcare Administration Database</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Research Library</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</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 One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>The New England journal of medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sausville, Edward A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Promises from Trametinib in RAF Active Tumors</atitle><jtitle>The New England journal of medicine</jtitle><addtitle>N Engl J Med</addtitle><date>2012-07-12</date><risdate>2012</risdate><volume>367</volume><issue>2</issue><spage>171</spage><epage>172</epage><pages>171-172</pages><issn>0028-4793</issn><eissn>1533-4406</eissn><abstract>Progression of human cancer occurs through genetic changes in cancer cells that activate biochemical pathways governing hallmarks of cancer, including proliferation and tumor-cell survival,
1
among others. Tumor growth factor receptors activate RAS oncoproteins, which subsequently activate a kinase cascade that includes RAF, MEK, and ERK kinases. This pathway is mutated to promote tumor growth in at least 20% of cancers.
2
The RAS–MEK–ERK pathway is thus a focus of intense interest for the development of cancer drugs. First fruits from this quest have yielded drugs directed against growth factor receptors, including the monoclonal antibody trastuzumab and the small molecules erlotinib and . . .</abstract><cop>United States</cop><pub>Massachusetts Medical Society</pub><pmid>22663012</pmid><doi>10.1056/NEJMe1205654</doi><tpages>2</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0028-4793 |
| ispartof | The New England journal of medicine, 2012-07, Vol.367 (2), p.171-172 |
| issn | 0028-4793 1533-4406 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1024937932 |
| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; ProQuest Central UK/Ireland; New England Journal of Medicine |
| subjects | Antineoplastic Agents - therapeutic use Cancer Cell proliferation Cell survival Drug development Extracellular signal-regulated kinase Female Growth factor receptors Humans Kinases Male MAP Kinase Kinase 1 - antagonists & inhibitors MAP Kinase Kinase 2 - antagonists & inhibitors Melanoma - drug therapy Monoclonal antibodies Mutation Protein Kinase Inhibitors - therapeutic use Proteins Proto-Oncogene Proteins B-raf - genetics Pyridones - therapeutic use Pyrimidinones - therapeutic use Raf protein Targeted cancer therapy Trastuzumab Tumors |
| title | Promises from Trametinib in RAF Active Tumors |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-26T09%3A08%3A44IST&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=Promises%20from%20Trametinib%20in%20RAF%20Active%20Tumors&rft.jtitle=The%20New%20England%20journal%20of%20medicine&rft.au=Sausville,%20Edward%20A&rft.date=2012-07-12&rft.volume=367&rft.issue=2&rft.spage=171&rft.epage=172&rft.pages=171-172&rft.issn=0028-4793&rft.eissn=1533-4406&rft_id=info:doi/10.1056/NEJMe1205654&rft_dat=%3Cproquest_cross%3E1024937932%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=1024734427&rft_id=info:pmid/22663012&rfr_iscdi=true |