A Ras destabilizer KYA1797K overcomes the resistance of EGFR tyrosine kinase inhibitor in KRAS-mutated non-small cell lung cancer
The epidermal growth factor receptor (EGFR) inhibitors such as erlotinib and gefitinib are widely used for treatment of non-small cell lung cancer (NSCLC), but they have shown limited efficacy in an unselected population of patients. The KRAS mutations, which are identified in approximately 20% of N...
Gespeichert in:
| Veröffentlicht in: | Scientific reports 2019-01, Vol.9 (1), p.648-648, Article 648 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 648 |
|---|---|
| container_issue | 1 |
| container_start_page | 648 |
| container_title | Scientific reports |
| container_volume | 9 |
| creator | Park, Jieun Cho, Yong-Hee Shin, Wook-Jin Lee, Sang-Kyu Lee, JaeHeon Kim, Taehyung Cha, Pu-Hyeon Yang, Jee Sun Cho, Jaebeom Min, Do Sik Han, Gyoonhee Lee, Ho-Young Choi, Kang-Yell |
| description | The epidermal growth factor receptor (EGFR) inhibitors such as erlotinib and gefitinib are widely used for treatment of non-small cell lung cancer (NSCLC), but they have shown limited efficacy in an unselected population of patients. The
KRAS
mutations, which are identified in approximately 20% of NSCLC patients, have shown to be associated with the resistance to the EGFR tyrosine kinase inhibitors (TKIs). Currently, there is no clinically available targeted therapy which can effectively inhibit NSCLC tumors harboring
KRAS
mutations. This study aims to show the effectiveness of KYA1797K, a small molecule which revealed anti-cancer effect in colorectal cancer by destabilizing Ras via inhibiting the Wnt/β-catenin pathway, for the treatment of
KRAS
-mutated NSCLC. While erlotinib fail to have anti-transforming effect in NSCLC cell lines harboring
KRAS
mutations, KYA1797K effectively inhibited the Ras-ERK pathway in
KRAS
-mutant NSCLC cell lines. As a result, KYA1797K treatment suppressed the growth and transformation of
KRAS
mutant NSCLC cells and also induced apoptosis. Furthermore, KYA1797K effectively inhibited
Kras
-driven tumorigenesis in the
Kras
LA2
mouse model by suppressing the Ras-ERK pathway. The destabilization of Ras via inhibition of the Wnt/β-catenin pathway is a potential therapeutic strategy for
KRAS
-mutated NSCLC that is resistant to EGFR TKI. |
| doi_str_mv | 10.1038/s41598-018-37059-8 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6345925</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2344211384</sourcerecordid><originalsourceid>FETCH-LOGICAL-c474t-21823badfa9ab467f0fc6efd3850c83d5e49a1cd4affc034afd339ea213aa5a3</originalsourceid><addsrcrecordid>eNp9kU1v1DAQhiMEolXpH-CALHHhEurPJL4graq2VFsJadsLJ2viTHZdErvYSaVy45_jZfsFh_rgGWkev-OZtyjeM_qZUdEcJcmUbkrKmlLUVOmyeVXscypVyQXnr5_le8VhStc0H8W1ZPptsSdoVeuK0_3i94KsIJEO0wStG9wvjGT5fcFqXS9JuMVow4iJTBskEZPLlLdIQk9Ozk5XZLqLITmP5IfzkJA4v3Gtm0LMGVmuFpflOE8wYUd88GUaYRiIxXwNs18Tu9WK74o3PQwJD-_jQXF1enJ1_LW8-HZ2fry4KK2s5VRy1nDRQteDhlZWdU97W2HfiUZR24hOodTAbCeh7y0VOXRCaATOBIACcVB82cnezO2InUU_RRjMTXQjxDsTwJl_K95tzDrcmkpIpbnKAp_uBWL4Oed9mdGl7TDgMczJ8LwzyWtVNxn9-B96Hebo83SGCyk5Y6KRmeI7yuYlpoj942cYNVuPzc5jkz02fz02W-kPz8d4fPLgaAbEDki55NcYn3q_IPsHFvezmw</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2344211384</pqid></control><display><type>article</type><title>A Ras destabilizer KYA1797K overcomes the resistance of EGFR tyrosine kinase inhibitor in KRAS-mutated non-small cell lung cancer</title><source>Nature Free</source><source>DOAJ Directory of Open Access Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><source>Free Full-Text Journals in Chemistry</source><source>Springer Nature OA Free Journals</source><creator>Park, Jieun ; Cho, Yong-Hee ; Shin, Wook-Jin ; Lee, Sang-Kyu ; Lee, JaeHeon ; Kim, Taehyung ; Cha, Pu-Hyeon ; Yang, Jee Sun ; Cho, Jaebeom ; Min, Do Sik ; Han, Gyoonhee ; Lee, Ho-Young ; Choi, Kang-Yell</creator><creatorcontrib>Park, Jieun ; Cho, Yong-Hee ; Shin, Wook-Jin ; Lee, Sang-Kyu ; Lee, JaeHeon ; Kim, Taehyung ; Cha, Pu-Hyeon ; Yang, Jee Sun ; Cho, Jaebeom ; Min, Do Sik ; Han, Gyoonhee ; Lee, Ho-Young ; Choi, Kang-Yell</creatorcontrib><description>The epidermal growth factor receptor (EGFR) inhibitors such as erlotinib and gefitinib are widely used for treatment of non-small cell lung cancer (NSCLC), but they have shown limited efficacy in an unselected population of patients. The
KRAS
mutations, which are identified in approximately 20% of NSCLC patients, have shown to be associated with the resistance to the EGFR tyrosine kinase inhibitors (TKIs). Currently, there is no clinically available targeted therapy which can effectively inhibit NSCLC tumors harboring
KRAS
mutations. This study aims to show the effectiveness of KYA1797K, a small molecule which revealed anti-cancer effect in colorectal cancer by destabilizing Ras via inhibiting the Wnt/β-catenin pathway, for the treatment of
KRAS
-mutated NSCLC. While erlotinib fail to have anti-transforming effect in NSCLC cell lines harboring
KRAS
mutations, KYA1797K effectively inhibited the Ras-ERK pathway in
KRAS
-mutant NSCLC cell lines. As a result, KYA1797K treatment suppressed the growth and transformation of
KRAS
mutant NSCLC cells and also induced apoptosis. Furthermore, KYA1797K effectively inhibited
Kras
-driven tumorigenesis in the
Kras
LA2
mouse model by suppressing the Ras-ERK pathway. The destabilization of Ras via inhibition of the Wnt/β-catenin pathway is a potential therapeutic strategy for
KRAS
-mutated NSCLC that is resistant to EGFR TKI.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-018-37059-8</identifier><identifier>PMID: 30679620</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13 ; 13/31 ; 13/51 ; 14 ; 14/1 ; 14/5 ; 631/67/1059/602 ; 631/67/2195 ; 82 ; 82/80 ; 96 ; Apoptosis ; Colorectal cancer ; Colorectal carcinoma ; Enzyme inhibitors ; Epidermal growth factor ; Epidermal growth factor receptors ; Extracellular signal-regulated kinase ; Gefitinib ; Humanities and Social Sciences ; K-Ras protein ; Lung cancer ; Metabolic pathways ; multidisciplinary ; Mutants ; Mutation ; Non-small cell lung carcinoma ; Science ; Science (multidisciplinary) ; Small cell lung carcinoma ; Tumorigenesis ; Tyrosine kinase inhibitors ; Wnt protein ; β-Catenin</subject><ispartof>Scientific reports, 2019-01, Vol.9 (1), p.648-648, Article 648</ispartof><rights>The Author(s) 2019</rights><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><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-21823badfa9ab467f0fc6efd3850c83d5e49a1cd4affc034afd339ea213aa5a3</citedby><cites>FETCH-LOGICAL-c474t-21823badfa9ab467f0fc6efd3850c83d5e49a1cd4affc034afd339ea213aa5a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6345925/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6345925/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30679620$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Park, Jieun</creatorcontrib><creatorcontrib>Cho, Yong-Hee</creatorcontrib><creatorcontrib>Shin, Wook-Jin</creatorcontrib><creatorcontrib>Lee, Sang-Kyu</creatorcontrib><creatorcontrib>Lee, JaeHeon</creatorcontrib><creatorcontrib>Kim, Taehyung</creatorcontrib><creatorcontrib>Cha, Pu-Hyeon</creatorcontrib><creatorcontrib>Yang, Jee Sun</creatorcontrib><creatorcontrib>Cho, Jaebeom</creatorcontrib><creatorcontrib>Min, Do Sik</creatorcontrib><creatorcontrib>Han, Gyoonhee</creatorcontrib><creatorcontrib>Lee, Ho-Young</creatorcontrib><creatorcontrib>Choi, Kang-Yell</creatorcontrib><title>A Ras destabilizer KYA1797K overcomes the resistance of EGFR tyrosine kinase inhibitor in KRAS-mutated non-small cell lung cancer</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>The epidermal growth factor receptor (EGFR) inhibitors such as erlotinib and gefitinib are widely used for treatment of non-small cell lung cancer (NSCLC), but they have shown limited efficacy in an unselected population of patients. The
KRAS
mutations, which are identified in approximately 20% of NSCLC patients, have shown to be associated with the resistance to the EGFR tyrosine kinase inhibitors (TKIs). Currently, there is no clinically available targeted therapy which can effectively inhibit NSCLC tumors harboring
KRAS
mutations. This study aims to show the effectiveness of KYA1797K, a small molecule which revealed anti-cancer effect in colorectal cancer by destabilizing Ras via inhibiting the Wnt/β-catenin pathway, for the treatment of
KRAS
-mutated NSCLC. While erlotinib fail to have anti-transforming effect in NSCLC cell lines harboring
KRAS
mutations, KYA1797K effectively inhibited the Ras-ERK pathway in
KRAS
-mutant NSCLC cell lines. As a result, KYA1797K treatment suppressed the growth and transformation of
KRAS
mutant NSCLC cells and also induced apoptosis. Furthermore, KYA1797K effectively inhibited
Kras
-driven tumorigenesis in the
Kras
LA2
mouse model by suppressing the Ras-ERK pathway. The destabilization of Ras via inhibition of the Wnt/β-catenin pathway is a potential therapeutic strategy for
KRAS
-mutated NSCLC that is resistant to EGFR TKI.</description><subject>13</subject><subject>13/31</subject><subject>13/51</subject><subject>14</subject><subject>14/1</subject><subject>14/5</subject><subject>631/67/1059/602</subject><subject>631/67/2195</subject><subject>82</subject><subject>82/80</subject><subject>96</subject><subject>Apoptosis</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Enzyme inhibitors</subject><subject>Epidermal growth factor</subject><subject>Epidermal growth factor receptors</subject><subject>Extracellular signal-regulated kinase</subject><subject>Gefitinib</subject><subject>Humanities and Social Sciences</subject><subject>K-Ras protein</subject><subject>Lung cancer</subject><subject>Metabolic pathways</subject><subject>multidisciplinary</subject><subject>Mutants</subject><subject>Mutation</subject><subject>Non-small cell lung carcinoma</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Small cell lung carcinoma</subject><subject>Tumorigenesis</subject><subject>Tyrosine kinase inhibitors</subject><subject>Wnt protein</subject><subject>β-Catenin</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kU1v1DAQhiMEolXpH-CALHHhEurPJL4graq2VFsJadsLJ2viTHZdErvYSaVy45_jZfsFh_rgGWkev-OZtyjeM_qZUdEcJcmUbkrKmlLUVOmyeVXscypVyQXnr5_le8VhStc0H8W1ZPptsSdoVeuK0_3i94KsIJEO0wStG9wvjGT5fcFqXS9JuMVow4iJTBskEZPLlLdIQk9Ozk5XZLqLITmP5IfzkJA4v3Gtm0LMGVmuFpflOE8wYUd88GUaYRiIxXwNs18Tu9WK74o3PQwJD-_jQXF1enJ1_LW8-HZ2fry4KK2s5VRy1nDRQteDhlZWdU97W2HfiUZR24hOodTAbCeh7y0VOXRCaATOBIACcVB82cnezO2InUU_RRjMTXQjxDsTwJl_K95tzDrcmkpIpbnKAp_uBWL4Oed9mdGl7TDgMczJ8LwzyWtVNxn9-B96Hebo83SGCyk5Y6KRmeI7yuYlpoj942cYNVuPzc5jkz02fz02W-kPz8d4fPLgaAbEDki55NcYn3q_IPsHFvezmw</recordid><startdate>20190124</startdate><enddate>20190124</enddate><creator>Park, Jieun</creator><creator>Cho, Yong-Hee</creator><creator>Shin, Wook-Jin</creator><creator>Lee, Sang-Kyu</creator><creator>Lee, JaeHeon</creator><creator>Kim, Taehyung</creator><creator>Cha, Pu-Hyeon</creator><creator>Yang, Jee Sun</creator><creator>Cho, Jaebeom</creator><creator>Min, Do Sik</creator><creator>Han, Gyoonhee</creator><creator>Lee, Ho-Young</creator><creator>Choi, Kang-Yell</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</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>AEUYN</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20190124</creationdate><title>A Ras destabilizer KYA1797K overcomes the resistance of EGFR tyrosine kinase inhibitor in KRAS-mutated non-small cell lung cancer</title><author>Park, Jieun ; Cho, Yong-Hee ; Shin, Wook-Jin ; Lee, Sang-Kyu ; Lee, JaeHeon ; Kim, Taehyung ; Cha, Pu-Hyeon ; Yang, Jee Sun ; Cho, Jaebeom ; Min, Do Sik ; Han, Gyoonhee ; Lee, Ho-Young ; Choi, Kang-Yell</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-21823badfa9ab467f0fc6efd3850c83d5e49a1cd4affc034afd339ea213aa5a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>13</topic><topic>13/31</topic><topic>13/51</topic><topic>14</topic><topic>14/1</topic><topic>14/5</topic><topic>631/67/1059/602</topic><topic>631/67/2195</topic><topic>82</topic><topic>82/80</topic><topic>96</topic><topic>Apoptosis</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Enzyme inhibitors</topic><topic>Epidermal growth factor</topic><topic>Epidermal growth factor receptors</topic><topic>Extracellular signal-regulated kinase</topic><topic>Gefitinib</topic><topic>Humanities and Social Sciences</topic><topic>K-Ras protein</topic><topic>Lung cancer</topic><topic>Metabolic pathways</topic><topic>multidisciplinary</topic><topic>Mutants</topic><topic>Mutation</topic><topic>Non-small cell lung carcinoma</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Small cell lung carcinoma</topic><topic>Tumorigenesis</topic><topic>Tyrosine kinase inhibitors</topic><topic>Wnt protein</topic><topic>β-Catenin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Park, Jieun</creatorcontrib><creatorcontrib>Cho, Yong-Hee</creatorcontrib><creatorcontrib>Shin, Wook-Jin</creatorcontrib><creatorcontrib>Lee, Sang-Kyu</creatorcontrib><creatorcontrib>Lee, JaeHeon</creatorcontrib><creatorcontrib>Kim, Taehyung</creatorcontrib><creatorcontrib>Cha, Pu-Hyeon</creatorcontrib><creatorcontrib>Yang, Jee Sun</creatorcontrib><creatorcontrib>Cho, Jaebeom</creatorcontrib><creatorcontrib>Min, Do Sik</creatorcontrib><creatorcontrib>Han, Gyoonhee</creatorcontrib><creatorcontrib>Lee, Ho-Young</creatorcontrib><creatorcontrib>Choi, Kang-Yell</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</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>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 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>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>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>Science Database</collection><collection>Biological Science Database</collection><collection>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>MEDLINE - Academic</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>Park, Jieun</au><au>Cho, Yong-Hee</au><au>Shin, Wook-Jin</au><au>Lee, Sang-Kyu</au><au>Lee, JaeHeon</au><au>Kim, Taehyung</au><au>Cha, Pu-Hyeon</au><au>Yang, Jee Sun</au><au>Cho, Jaebeom</au><au>Min, Do Sik</au><au>Han, Gyoonhee</au><au>Lee, Ho-Young</au><au>Choi, Kang-Yell</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A Ras destabilizer KYA1797K overcomes the resistance of EGFR tyrosine kinase inhibitor in KRAS-mutated non-small cell lung cancer</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2019-01-24</date><risdate>2019</risdate><volume>9</volume><issue>1</issue><spage>648</spage><epage>648</epage><pages>648-648</pages><artnum>648</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>The epidermal growth factor receptor (EGFR) inhibitors such as erlotinib and gefitinib are widely used for treatment of non-small cell lung cancer (NSCLC), but they have shown limited efficacy in an unselected population of patients. The
KRAS
mutations, which are identified in approximately 20% of NSCLC patients, have shown to be associated with the resistance to the EGFR tyrosine kinase inhibitors (TKIs). Currently, there is no clinically available targeted therapy which can effectively inhibit NSCLC tumors harboring
KRAS
mutations. This study aims to show the effectiveness of KYA1797K, a small molecule which revealed anti-cancer effect in colorectal cancer by destabilizing Ras via inhibiting the Wnt/β-catenin pathway, for the treatment of
KRAS
-mutated NSCLC. While erlotinib fail to have anti-transforming effect in NSCLC cell lines harboring
KRAS
mutations, KYA1797K effectively inhibited the Ras-ERK pathway in
KRAS
-mutant NSCLC cell lines. As a result, KYA1797K treatment suppressed the growth and transformation of
KRAS
mutant NSCLC cells and also induced apoptosis. Furthermore, KYA1797K effectively inhibited
Kras
-driven tumorigenesis in the
Kras
LA2
mouse model by suppressing the Ras-ERK pathway. The destabilization of Ras via inhibition of the Wnt/β-catenin pathway is a potential therapeutic strategy for
KRAS
-mutated NSCLC that is resistant to EGFR TKI.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>30679620</pmid><doi>10.1038/s41598-018-37059-8</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 2045-2322 |
| ispartof | Scientific reports, 2019-01, Vol.9 (1), p.648-648, Article 648 |
| issn | 2045-2322 2045-2322 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6345925 |
| source | Nature Free; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection; Free Full-Text Journals in Chemistry; Springer Nature OA Free Journals |
| subjects | 13 13/31 13/51 14 14/1 14/5 631/67/1059/602 631/67/2195 82 82/80 96 Apoptosis Colorectal cancer Colorectal carcinoma Enzyme inhibitors Epidermal growth factor Epidermal growth factor receptors Extracellular signal-regulated kinase Gefitinib Humanities and Social Sciences K-Ras protein Lung cancer Metabolic pathways multidisciplinary Mutants Mutation Non-small cell lung carcinoma Science Science (multidisciplinary) Small cell lung carcinoma Tumorigenesis Tyrosine kinase inhibitors Wnt protein β-Catenin |
| title | A Ras destabilizer KYA1797K overcomes the resistance of EGFR tyrosine kinase inhibitor in KRAS-mutated non-small cell lung cancer |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-07T20%3A16%3A19IST&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=A%20Ras%20destabilizer%20KYA1797K%20overcomes%20the%20resistance%20of%20EGFR%20tyrosine%20kinase%20inhibitor%20in%20KRAS-mutated%20non-small%20cell%20lung%20cancer&rft.jtitle=Scientific%20reports&rft.au=Park,%20Jieun&rft.date=2019-01-24&rft.volume=9&rft.issue=1&rft.spage=648&rft.epage=648&rft.pages=648-648&rft.artnum=648&rft.issn=2045-2322&rft.eissn=2045-2322&rft_id=info:doi/10.1038/s41598-018-37059-8&rft_dat=%3Cproquest_pubme%3E2344211384%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2344211384&rft_id=info:pmid/30679620&rfr_iscdi=true |