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• W1685156615 endingPage "42732" @default.
• W1685156615 startingPage "42717" @default.
• W1685156615 abstract "The clinical efficacy of EGFR tyrosine kinase inhibitors (TKIs) in non-small cell lung cancer (NSCLC) harbouring activating EGFR mutations is limited by the emergence of acquired resistance, mostly ascribed to the secondary EGFR-T790M mutation. Selective EGFR-T790M inhibitors have been proposed as a new, extremely relevant therapeutic approach. Here, we demonstrate that the novel irreversible EGFR-TKI CNX-2006, a structural analog of CO-1686, currently tested in a phase-1/2 trial, is active against in vitro and in vivo NSCLC models expressing mutant EGFR, with minimal effect on the wild-type receptor. By integration of genetic and functional analyses in isogenic cell pairs we provide evidence of the crucial role played by NF-κB1 in driving CNX-2006 acquired resistance and show that NF-κB activation may replace the oncogenic EGFR signaling in NSCLC when effective and persistent inhibition of the target is achieved in the presence of the T790M mutation. In this context, we demonstrate that the sole, either genetic or pharmacologic, inhibition of NF-κB is sufficient to reduce the viability of cells that adapted to EGFR-TKIs. Overall, our findings support the rational inhibition of members of the NF-κB pathway as a promising therapeutic option for patients who progress after treatment with novel mutant-selective EGFR-TKIs." @default.
• W1685156615 created "2016-06-24" @default.
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• W1685156615 date "2015-04-29" @default.
• W1685156615 modified "2023-09-30" @default.
• W1685156615 title "NF-κB drives acquired resistance to a novel mutant-selective EGFR inhibitor" @default.
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• W1685156615 doi "https://doi.org/10.18632/oncotarget.3956" @default.
• W1685156615 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4767465" @default.
• W1685156615 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26015408" @default.
• W1685156615 hasPublicationYear "2015" @default.
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