Epidermal growth factor receptor and K-Ras mutations and resistance of lung cancer to insulin-like growth factor 1 receptor tyrosine kinase inhibitors
DC Field | Value | Language |
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dc.contributor.author | Kim, Woo-Young | - |
dc.contributor.author | Prudkin, Ludmila | - |
dc.contributor.author | Feng, Lei | - |
dc.contributor.author | Kim, Edward S. | - |
dc.contributor.author | Hennessy, Bryan | - |
dc.contributor.author | Lee, Ju-Seog | - |
dc.contributor.author | Lee, J. Jack | - |
dc.contributor.author | Glisson, Bonnie | - |
dc.contributor.author | Lippman, Scott M. | - |
dc.contributor.author | Wistuba, Ignacio I. | - |
dc.contributor.author | Hong, Waun Ki | - |
dc.contributor.author | Lee, Ho-Young | - |
dc.date.available | 2021-02-22T13:03:34Z | - |
dc.date.issued | 2012-08 | - |
dc.identifier.issn | 0008-543X | - |
dc.identifier.issn | 1097-0142 | - |
dc.identifier.uri | https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/12392 | - |
dc.description.abstract | BACKGROUND: Most patients with nonsmall cell lung cancer (NSCLC) have responded poorly to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs). The authors investigated the involvement of insulinlike growth factor 1 receptor (IGF-1R) signaling in primary resistance to EGFR TKIs and the molecular determinants of resistance to IGF-1R TKIs. METHODS: Phosphorylated IGF-1R/insulin receptor (pIGF-1R/IR) was immunohistochemically evaluated in an NSCLC tissue microarray. The authors analyzed the antitumor effects of an IGF-1R TKI (PQIP or OSI-906), either alone or in combination with a small-molecular inhibitor (PD98059 or U0126) or with siRNA targeting K-Ras or mitogen-activated protein kinase/extracellular signal-regulated kinase kinase (MEK), in vitro and in vivo in NSCLC cells with variable histologic features and EGFR or K-Ras mutations. RESULTS: pIGF-1R/IR expression in NSCLC specimens was associated with a history of tobacco smoking, squamous cell carcinoma histology, mutant K-Ras, and wild-type (WT) EGFR, all of which have been strongly associated with poor response to EGFR TKIs. IGF-1R TKIs exhibited significant antitumor activity in NSCLC cells with WT EGFR and WT K-Ras but not in those with mutations in these genes. Introduction of mutant K-Ras attenuated the effects of IGF-1R TKIs on NSCLC cells expressing WT K-Ras. Conversely, inactivation of MEK restored sensitivity to IGF-TKIs in cells carrying mutant K-Ras. CONCLUSIONS: The mutation status of both EGFR and K-Ras could be a predictive marker of response to IGF-1R TKIs. Also, MEK antagonism can abrogate primary resistance of NSCLC cells to IGF-1R TKIs. Cancer 2012. © 2012 American Cancer Society. This study provides evidence for the first time that the mutation status of both epidermal growth factor receptor (EGFR) and K-Ras could be a predictive marker for response to insulinlike growth factor 1 receptor (IGF-1R) tyrosine kinase inhibitors (TKIs). Also, mitogen-activated protein kinase/extracellular signal-regulated kinase kinase antagonism can abrogate primary resistance of nonsmall cell lung cancer to IGF-1R TKIs. Copyright © 2012 American Cancer Society. | - |
dc.format.extent | 11 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | John Wiley and Sons Inc. | - |
dc.title | Epidermal growth factor receptor and K-Ras mutations and resistance of lung cancer to insulin-like growth factor 1 receptor tyrosine kinase inhibitors | - |
dc.type | Article | - |
dc.publisher.location | 미국 | - |
dc.identifier.doi | 10.1002/cncr.26656 | - |
dc.identifier.scopusid | 2-s2.0-84864692068 | - |
dc.identifier.wosid | 000307116900018 | - |
dc.identifier.bibliographicCitation | Cancer, v.118, no.16, pp 3993 - 4003 | - |
dc.citation.title | Cancer | - |
dc.citation.volume | 118 | - |
dc.citation.number | 16 | - |
dc.citation.startPage | 3993 | - |
dc.citation.endPage | 4003 | - |
dc.type.docType | Article | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | sci | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.subject.keywordPlus | 1,4 diamino 1,4 bis(2 aminophenylthio) 2,3 dicyanobutadiene | - |
dc.subject.keywordPlus | 2 (2 amino 3 methoxyphenyl)chromone | - |
dc.subject.keywordPlus | 3 [3 (4 methyl piperazin 1 yl)cyclobutyl] 1 (2 phenyl quinolin 7 yl) imidazo[1,5 a]pyrazin 8 ylamine | - |
dc.subject.keywordPlus | epidermal growth factor receptor | - |
dc.subject.keywordPlus | K ras protein | - |
dc.subject.keywordPlus | linsitinib | - |
dc.subject.keywordPlus | mitogen activated protein kinase | - |
dc.subject.keywordPlus | protein tyrosine kinase inhibitor | - |
dc.subject.keywordPlus | small interfering RNA | - |
dc.subject.keywordPlus | somatomedin C receptor | - |
dc.subject.keywordPlus | unclassified drug | - |
dc.subject.keywordPlus | animal experiment | - |
dc.subject.keywordPlus | animal model | - |
dc.subject.keywordPlus | antineoplastic activity | - |
dc.subject.keywordPlus | article | - |
dc.subject.keywordPlus | cancer cell culture | - |
dc.subject.keywordPlus | cancer resistance | - |
dc.subject.keywordPlus | cancer size | - |
dc.subject.keywordPlus | controlled study | - |
dc.subject.keywordPlus | drug potentiation | - |
dc.subject.keywordPlus | drug sensitivity | - |
dc.subject.keywordPlus | enzyme inactivation | - |
dc.subject.keywordPlus | gene mutation | - |
dc.subject.keywordPlus | gene targeting | - |
dc.subject.keywordPlus | histopathology | - |
dc.subject.keywordPlus | human | - |
dc.subject.keywordPlus | human cell | - |
dc.subject.keywordPlus | human tissue | - |
dc.subject.keywordPlus | immunohistochemistry | - |
dc.subject.keywordPlus | in vitro study | - |
dc.subject.keywordPlus | in vivo study | - |
dc.subject.keywordPlus | lung non small cell cancer | - |
dc.subject.keywordPlus | lung squamous cell carcinoma | - |
dc.subject.keywordPlus | major clinical study | - |
dc.subject.keywordPlus | mouse | - |
dc.subject.keywordPlus | nonhuman | - |
dc.subject.keywordPlus | pharmacogenetics | - |
dc.subject.keywordPlus | priority journal | - |
dc.subject.keywordPlus | protein expression | - |
dc.subject.keywordPlus | protein phosphorylation | - |
dc.subject.keywordPlus | RNA interference | - |
dc.subject.keywordPlus | smoking | - |
dc.subject.keywordPlus | tissue microarray | - |
dc.subject.keywordPlus | treatment response | - |
dc.subject.keywordPlus | wild type | - |
dc.subject.keywordAuthor | epidermal growth factor receptor | - |
dc.subject.keywordAuthor | insulinlike growth factor 1 receptor | - |
dc.subject.keywordAuthor | K-Ras | - |
dc.subject.keywordAuthor | lung cancer | - |
dc.subject.keywordAuthor | tyrosine kinase inhibitors | - |
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