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Title[redir]:
Activation of the AXL kinase causes resistance to EGFR-targeted therapy in lung cancer | Nature Genetics
Description:
Trever Bivona and colleagues identify the upregulation of the AXL kinase in human non–small cell lung cancer with acquired resistance to erlotinib. Inhibition of AXL restores sensitivity to erlotinib in in vitro and in vivo tumor models. The authors suggest AXL as a potential therapeutic target that may prevent or overcome acquired resistance in patients with EGFR-mutant lung cancer. Human non–small cell lung cancers (NSCLCs) with activating mutations in EGFR frequently respond to treatment with EGFR-targeted tyrosine kinase inhibitors (TKIs), such as erlotinib, but responses are not durable, as tumors acquire resistance. Secondary mutations in EGFR (such as T790M) or upregulation of the MET kinase are found in over 50% of resistant tumors. Here, we report increased activation of AXL and evidence for epithelial-to-mesenchymal transition (EMT) in multiple in vitro and in vivo EGFR-mutant lung cancer models with acquired resistance to erlotinib in the absence of the EGFR p.Thr790Met alteration or MET activation. Genetic or pharmacological inhibition of AXL restored sensitivity to erlotinib in these tumor models. Increased expression of AXL and, in some cases, of its ligand GAS6 was found in EGFR-mutant lung cancers obtained from individuals with acquired resistance to TKIs. These data identify AXL as a promising therapeutic target whose inhibition could prevent or overcome acquired resistance to EGFR TKIs in individuals with EGFR-mutant lung cancer.
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Keywords {🔍}
cancer, article, lung, scholar, google, cas, resistance, center, nature, egfr, university, axl, usa, kinase, erlotinib, acquired, medicine, case, research, lee, access, medical, content, mutations, tyrosine, inhibitors, york, data, cell, tumors, met, nonsmallcell, gefitinib, receptor, oncogene, tgb, department, cleveland, supplementary, cookies, zhang, authors, cancers, tumor, expression, gene, mutation, comprehensive, oncology, privacy,
Topics {✒️}
nature portfolio permissions reprints privacy policy advertising nature 471 nature small-cell lung cancer young soo park social media small-molecule kinase inhibitors oncology research se jin jang tumor cell growth egfr-mutant lung cancer mohamed abdel-rahman case genomics center dae ho lee data identify axl woo sung kim permissions tyrosine kinase inhibitors jung-shin lee springerlink instant access chang-min choi analyzed clinical data promising therapeutic target jin kyung rho governing axl expression lung cancer patients asan medical center astrocytoma cells leads stem cell traits yun jung choi ireland cancer center yale university school gefitinib-sensitizing egfr mutations egfr-targeted therapy vivo data privacy multiple anticancer therapies critical downstream target personal data jae cheol lee egfr mutant nsclc tumor-derived exosomes tumor microenvironment modulation egfr kinase domain activating erbb3 signaling comprehensive immunohistochemical study competing financial interests
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headline:Activation of the AXL kinase causes resistance to EGFR-targeted therapy in lung cancer
description:Trever Bivona and colleagues identify the upregulation of the AXL kinase in human nonâsmall cell lung cancer with acquired resistance to erlotinib. Inhibition of AXL restores sensitivity to erlotinib in in vitro and in vivo tumor models. The authors suggest AXL as a potential therapeutic target that may prevent or overcome acquired resistance in patients with EGFR-mutant lung cancer. Human nonâsmall cell lung cancers (NSCLCs) with activating mutations in EGFR frequently respond to treatment with EGFR-targeted tyrosine kinase inhibitors (TKIs), such as erlotinib, but responses are not durable, as tumors acquire resistance. Secondary mutations in EGFR (such as T790M) or upregulation of the MET kinase are found in over 50% of resistant tumors. Here, we report increased activation of AXL and evidence for epithelial-to-mesenchymal transition (EMT) in multiple in vitro and in vivo EGFR-mutant lung cancer models with acquired resistance to erlotinib in the absence of the EGFR p.Thr790Met alteration or MET activation. Genetic or pharmacological inhibition of AXL restored sensitivity to erlotinib in these tumor models. Increased expression of AXL and, in some cases, of its ligand GAS6 was found in EGFR-mutant lung cancers obtained from individuals with acquired resistance to TKIs. These data identify AXL as a promising therapeutic target whose inhibition could prevent or overcome acquired resistance to EGFR TKIs in individuals with EGFR-mutant lung cancer.
datePublished:2012-07-01T00:00:00Z
dateModified:2012-07-01T00:00:00Z
pageStart:852
pageEnd:860
sameAs:https://doi.org/10.1038/ng.2330
keywords:
Cancer genomics
Cancer therapeutic resistance
Gene therapy
Non-small-cell lung cancer
Biomedicine
general
Human Genetics
Cancer Research
Agriculture
Gene Function
Animal Genetics and Genomics
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headline:Activation of the AXL kinase causes resistance to EGFR-targeted therapy in lung cancer
description:Trever Bivona and colleagues identify the upregulation of the AXL kinase in human nonâsmall cell lung cancer with acquired resistance to erlotinib. Inhibition of AXL restores sensitivity to erlotinib in in vitro and in vivo tumor models. The authors suggest AXL as a potential therapeutic target that may prevent or overcome acquired resistance in patients with EGFR-mutant lung cancer. Human nonâsmall cell lung cancers (NSCLCs) with activating mutations in EGFR frequently respond to treatment with EGFR-targeted tyrosine kinase inhibitors (TKIs), such as erlotinib, but responses are not durable, as tumors acquire resistance. Secondary mutations in EGFR (such as T790M) or upregulation of the MET kinase are found in over 50% of resistant tumors. Here, we report increased activation of AXL and evidence for epithelial-to-mesenchymal transition (EMT) in multiple in vitro and in vivo EGFR-mutant lung cancer models with acquired resistance to erlotinib in the absence of the EGFR p.Thr790Met alteration or MET activation. Genetic or pharmacological inhibition of AXL restored sensitivity to erlotinib in these tumor models. Increased expression of AXL and, in some cases, of its ligand GAS6 was found in EGFR-mutant lung cancers obtained from individuals with acquired resistance to TKIs. These data identify AXL as a promising therapeutic target whose inhibition could prevent or overcome acquired resistance to EGFR TKIs in individuals with EGFR-mutant lung cancer.
datePublished:2012-07-01T00:00:00Z
dateModified:2012-07-01T00:00:00Z
pageStart:852
pageEnd:860
sameAs:https://doi.org/10.1038/ng.2330
keywords:
Cancer genomics
Cancer therapeutic resistance
Gene therapy
Non-small-cell lung cancer
Biomedicine
general
Human Genetics
Cancer Research
Agriculture
Gene Function
Animal Genetics and Genomics
image:
https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fng.2330/MediaObjects/41588_2012_Article_BFng2330_Fig1_HTML.jpg
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