FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1963558982> ?p ?o ?g. }

• W1963558982 endingPage "471" @default.
• W1963558982 startingPage "458" @default.
• W1963558982 abstract "Abstract Activation of the epidermal growth factor receptor (EGFR) in glioblastoma (GBM) occurs through mutations or deletions in the extracellular (EC) domain. Unlike lung cancers with EGFR kinase domain (KD) mutations, GBMs respond poorly to the EGFR inhibitor erlotinib. Using RNAi, we show that GBM cells carrying EGFR EC mutations display EGFR addiction. In contrast to KD mutants found in lung cancer, glioma-specific EGFR EC mutants are poorly inhibited by EGFR inhibitors that target the active kinase conformation (e.g., erlotinib). Inhibitors that bind to the inactive EGFR conformation, however, potently inhibit EGFR EC mutants and induce cell death in EGFR-mutant GBM cells. Our results provide first evidence for single kinase addiction in GBM and suggest that the disappointing clinical activity of first-generation EGFR inhibitors in GBM versus lung cancer may be attributed to the different conformational requirements of mutant EGFR in these 2 cancer types. Significance: Approximately 40% of human glioblastomas harbor oncogenic EGFR alterations, but attempts to therapeutically target EGFR with first-generation EGFR kinase inhibitors have failed. Here, we demonstrate selective sensitivity of glioma-specific EGFR mutants to ATP-site competitive EGFR kinase inhibitors that target the inactive conformation of the catalytic domain. Cancer Discov; 2(5); 458–71. ©2012 AACR. Read the Commentary on this article by Park and Lemmon, p. 398. This article is highlighted in the In This Issue feature, p. 377." @default.
• W1963558982 created "2016-06-24" @default.
• W1963558982 creator A5000192581 @default.
• W1963558982 creator A5000808700 @default.
• W1963558982 creator A5003825991 @default.
• W1963558982 creator A5003871933 @default.
• W1963558982 creator A5008761191 @default.
• W1963558982 creator A5010356745 @default.
• W1963558982 creator A5013653329 @default.
• W1963558982 creator A5014264452 @default.
• W1963558982 creator A5016190247 @default.
• W1963558982 creator A5020324479 @default.
• W1963558982 creator A5021656597 @default.
• W1963558982 creator A5022266886 @default.
• W1963558982 creator A5025018584 @default.
• W1963558982 creator A5027150108 @default.
• W1963558982 creator A5028543570 @default.
• W1963558982 creator A5038569402 @default.
• W1963558982 creator A5039648429 @default.
• W1963558982 creator A5042065032 @default.
• W1963558982 creator A5044704795 @default.
• W1963558982 creator A5045925835 @default.
• W1963558982 creator A5046264008 @default.
• W1963558982 creator A5046338327 @default.
• W1963558982 creator A5049264826 @default.
• W1963558982 creator A5051168746 @default.
• W1963558982 creator A5053361713 @default.
• W1963558982 creator A5056561926 @default.
• W1963558982 creator A5057541817 @default.
• W1963558982 creator A5058375360 @default.
• W1963558982 creator A5059965175 @default.
• W1963558982 creator A5061018141 @default.
• W1963558982 creator A5063511816 @default.
• W1963558982 creator A5063590669 @default.
• W1963558982 creator A5064627876 @default.
• W1963558982 creator A5070190752 @default.
• W1963558982 creator A5075492015 @default.
• W1963558982 creator A5078400193 @default.
• W1963558982 creator A5079465721 @default.
• W1963558982 creator A5087562855 @default.
• W1963558982 creator A5091053515 @default.
• W1963558982 date "2012-05-01" @default.
• W1963558982 modified "2023-10-09" @default.
• W1963558982 title "Differential Sensitivity of Glioma- versus Lung Cancer–Specific EGFR Mutations to EGFR Kinase Inhibitors" @default.
• W1963558982 cites W1964321121 @default.
• W1963558982 cites W1966803171 @default.
• W1963558982 cites W1967394241 @default.
• W1963558982 cites W1971947883 @default.
• W1963558982 cites W1974024530 @default.
• W1963558982 cites W1992784105 @default.
• W1963558982 cites W1999851814 @default.
• W1963558982 cites W2006315580 @default.
• W1963558982 cites W2013138515 @default.
• W1963558982 cites W2021087717 @default.
• W1963558982 cites W2025183726 @default.
• W1963558982 cites W2028415754 @default.
• W1963558982 cites W2036044314 @default.
• W1963558982 cites W2037873277 @default.
• W1963558982 cites W2040176056 @default.
• W1963558982 cites W2040827479 @default.
• W1963558982 cites W2043696829 @default.
• W1963558982 cites W2045156702 @default.
• W1963558982 cites W2053655323 @default.
• W1963558982 cites W2069876014 @default.
• W1963558982 cites W2088388211 @default.
• W1963558982 cites W2090029719 @default.
• W1963558982 cites W2093616162 @default.
• W1963558982 cites W2094882473 @default.
• W1963558982 cites W2100772783 @default.
• W1963558982 cites W2101057168 @default.
• W1963558982 cites W2102626211 @default.
• W1963558982 cites W2103704392 @default.
• W1963558982 cites W2114195503 @default.
• W1963558982 cites W2116398087 @default.
• W1963558982 cites W2117521607 @default.
• W1963558982 cites W2123185010 @default.
• W1963558982 cites W2126818181 @default.
• W1963558982 cites W2128307445 @default.
• W1963558982 cites W2133051701 @default.
• W1963558982 cites W2137018685 @default.
• W1963558982 cites W2139203226 @default.
• W1963558982 cites W2139236349 @default.
• W1963558982 cites W2145497412 @default.
• W1963558982 cites W2149051154 @default.
• W1963558982 cites W2150059798 @default.
• W1963558982 cites W2151335185 @default.
• W1963558982 cites W2154670277 @default.
• W1963558982 cites W2157824687 @default.
• W1963558982 cites W2159013299 @default.
• W1963558982 cites W2161821474 @default.
• W1963558982 doi "https://doi.org/10.1158/2159-8290.cd-11-0284" @default.
• W1963558982 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3354723" @default.
• W1963558982 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22588883" @default.
• W1963558982 hasPublicationYear "2012" @default.
• W1963558982 type Work @default.
• W1963558982 sameAs 1963558982 @default.
• W1963558982 citedByCount "281" @default.
• W1963558982 countsByYear W19635589822012 @default.

• next