{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1360021390573174784.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1172/jci.insight.173688"}},{"identifier":{"@type":"URI","@value":"https://insight.jci.org/articles/view/173688/files/pdf"}},{"identifier":{"@type":"PMID","@value":"37917191"}}],"resourceType":"学術雑誌論文(journal article)","dc:title":[{"@value":"MIG6 loss confers resistance to ALK/ROS1 inhibitors in NSCLC through EGFR activation by low-dose EGF"}],"description":[{"notation":[{"@value":"Although tyrosine kinase inhibitor (TKI) therapy shows marked clinical efficacy in patients with anaplastic lymphoma kinase (ALK) and ROS proto-oncogene 1 (ROS1)-positive non-small cell lung cancer (NSCLC), most of these patients eventually relapse with acquired resistance. Therefore, genome-wide CRISPR-Cas9 knockout screening was performed using an ALK-positive NSCLC cell line established from pleural effusion without ALK-TKI treatment. After 9 days of ALK-TKI therapy, sequencing analysis was performed, which identified several tumor-suppressor genes, such as NF2 or MED12, and multiple new candidate genes. Among them this study focused on ERRFI1, which is known as MIG6 and negatively regulates EGFR signaling. Interestingly MIG6 loss induced the resistance to ALK-TKIs by treatment with quite a low dose of EGF, which is equivalent to plasma concentration through the upregulation of MAPK and PI3K/Akt/mTOR pathways. Combination therapy with ALK-TKIs and anti-EGFR antibodies could overcome the acquired resistance in both in vivo and in vitro models. In addition, this confirmed that MIG6 loss induces resistance to ROS1-TKIs in ROS1-positive cell lines. This study found a novel factor that plays a role in ALK and ROS1-TKI resistance by activating the EGFR pathway with low-dose ligands."}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1380021390573174658","@type":"Researcher","foaf:name":[{"@value":"Nobuyuki Kondo"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021390573174786","@type":"Researcher","foaf:name":[{"@value":"Takahiro Utsumi"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021390573174656","@type":"Researcher","foaf:name":[{"@value":"Yuki Shimizu"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021390573174657","@type":"Researcher","foaf:name":[{"@value":"Ai Takemoto"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021390573174660","@type":"Researcher","foaf:name":[{"@value":"Tomoko Oh-hara"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021390573174661","@type":"Researcher","foaf:name":[{"@value":"Ken Uchibori"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021390573174785","@type":"Researcher","foaf:name":[{"@value":"Sophia Subat-Motoshi"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021390573174787","@type":"Researcher","foaf:name":[{"@value":"Hironori Ninomiya"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021390573174663","@type":"Researcher","foaf:name":[{"@value":"Kengo Takeuchi"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021390573174659","@type":"Researcher","foaf:name":[{"@value":"Makoto Nishio"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021390573174664","@type":"Researcher","foaf:name":[{"@value":"Yasunari Miyazaki"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021390573174662","@type":"Researcher","foaf:name":[{"@value":"Ryohei Katayama"}]}],"publication":{"publicationIdentifier":[{"@type":"EISSN","@value":"23793708"}],"prism:publicationName":[{"@value":"JCI Insight"}],"dc:publisher":[{"@value":"American Society for Clinical Investigation"}],"prism:publicationDate":"2023-12-22","prism:volume":"8","prism:number":"24"},"reviewed":"false","dcterms:accessRights":"http://purl.org/coar/access_right/c_abf2","dc:rights":["http://creativecommons.org/licenses/by/4.0/"],"url":[{"@id":"https://insight.jci.org/articles/view/173688/files/pdf"}],"createdAt":"2023-11-02","modifiedAt":"2023-12-21","foaf:topic":[{"@id":"https://cir.nii.ac.jp/all?q=Research%20Article","dc:title":"Research Article"}],"project":[{"@id":"https://cir.nii.ac.jp/crid/1040011231199652608","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"22K18383"},{"@type":"JGN","@value":"JP22K18383"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-22K18383/"}],"notation":[{"@language":"ja","@value":"動くタンパク質構造辞典構築を介した疾患関連分子の新規標的部位探索"},{"@language":"en","@value":"Searching druggable target sites by developing refined molecular dynamic simulations"}]},{"@id":"https://cir.nii.ac.jp/crid/1040573407559904768","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"22H04922"},{"@type":"JGN","@value":"JP22H04922"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-22H04922/"}],"notation":[{"@language":"ja","@value":"先端モデル動物支援プラットフォーム"}]}],"relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1050001335843648768","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Brigatinib combined with anti-EGFR antibody overcomes osimertinib resistance in EGFR-mutated non-small-cell lung cancer"},{"@value":"Brigatinib combined with anti-EGFR antibody overcomes osimertinib resistant in EGFR-mutated non-small-cell lung cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1050846637961560448","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@language":"en","@value":"YAP1 mediates survival of ALK-rearranged lung cancer cells treated with alectinib via pro-apoptotic protein regulation"}]},{"@id":"https://cir.nii.ac.jp/crid/1360002218684881664","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Activation of HER Family Signaling as a Mechanism of Acquired Resistance to ALK Inhibitors in EML4-ALK–Positive Non–Small Cell Lung Cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1360002220792257408","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Activated MET acts as a salvage signal after treatment with alectinib, a selective ALK inhibitor, in ALK-positive non-small cell lung cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1360004236369052288","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Paracrine Receptor Activation by Microenvironment Triggers Bypass Survival Signals and ALK Inhibitor Resistance in EML4-ALK Lung Cancer Cells"}]},{"@id":"https://cir.nii.ac.jp/crid/1360009142645234176","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Gilteritinib overcomes lorlatinib resistance in ALK-rearranged cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1360011143518087296","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Drug Resistance via Feedback Activation of Stat3 in Oncogene-Addicted Cancer Cells"}]},{"@id":"https://cir.nii.ac.jp/crid/1360011144509949824","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Metabolism and Effects of Epidermal Growth Factor and Related Growth Factors in Mammals*"}]},{"@id":"https://cir.nii.ac.jp/crid/1360011145536221824","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Stat3 is required for ALK-mediated lymphomagenesis and provides a possible therapeutic target"}]},{"@id":"https://cir.nii.ac.jp/crid/1360011145928230400","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Association of Patient Characteristics and Tumor Genomics With Clinical Outcomes Among Patients With Non–Small Cell Lung Cancer Using a Clinicogenomic Database"}]},{"@id":"https://cir.nii.ac.jp/crid/1360021396149532672","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"<scp><i>MET</i></scp> gene amplification is a mechanism of resistance to entrectinib in <scp>ROS1</scp>+ <scp>NSCLC</scp>"}]},{"@id":"https://cir.nii.ac.jp/crid/1360283692012944000","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Resensitization to Crizotinib by the Lorlatinib<i>ALK</i>Resistance Mutation L1198F"}]},{"@id":"https://cir.nii.ac.jp/crid/1360285706978893824","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"3D culture system containing gellan gum restores oncogene dependence in ROS1 rearrangements non-small cell lung cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1360285708415295360","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Rationale for co-targeting IGF-1R and ALK in ALK fusion–positive lung cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1360292619071816576","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"MED12 Controls the Response to Multiple Cancer Drugs through Regulation of TGF-β Receptor Signaling"}]},{"@id":"https://cir.nii.ac.jp/crid/1360292620642528896","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"The anaplastic lymphoma kinase in the pathogenesis of cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1360292620648253312","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Sequential ALK Inhibitors Can Select for Lorlatinib-Resistant Compound\n                    <i>ALK</i>\n                    Mutations in ALK-Positive Lung Cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1360302868772402560","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Molecular and clinicopathological characteristics of <i>ROS1</i>‐rearranged non‐small‐cell lung cancers identified by next‐generation sequencing"}]},{"@id":"https://cir.nii.ac.jp/crid/1360302868772845824","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Kinetics of RTK activation determine ERK reactivation and resistance to dual BRAF/MEK inhibition in melanoma"}]},{"@id":"https://cir.nii.ac.jp/crid/1360302868773506432","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Screening for anaplastic lymphoma kinase (<i>ALK</i>) gene rearrangements in non‐small‐cell lung cancer in New Zealand"}]},{"@id":"https://cir.nii.ac.jp/crid/1360302868773671552","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Identification of genes inducing resistance to ionizing radiation in human rectal cancer cell lines: re-sensitization of radio-resistant rectal cancer cells through down regulating NDRG1"}]},{"@id":"https://cir.nii.ac.jp/crid/1360302868774067968","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Normalized Serum EGF Levels as a Potential Biomarker in Non-Small Cell Lung Cancer: The Role of Platelets"}]},{"@id":"https://cir.nii.ac.jp/crid/1360302869449169664","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Genome‐scale CRISPR screening identifies cell cycle and protein ubiquitination processes as druggable targets for erlotinib‐resistant lung cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1360302869449611520","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Crizotinib resistance conferred by BRAF V600E mutation in non–small cell lung cancer harboring an oncogenic ROS1 fusion"}]},{"@id":"https://cir.nii.ac.jp/crid/1360302869450617728","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Case Report: Durable Response to the Combination of Brigatinib and Cetuximab Plus Icotinib in a NSCLC Patient Harboring EGFR L858R-T790M-cis-G796S and L718Q Resistance Mutations Following Progression With Osimertinib"}]},{"@id":"https://cir.nii.ac.jp/crid/1360306905618319360","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"MIG6 loss increased RET inhibitor tolerant persister cells in RET-rearranged non-small cell lung cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1360565165802985216","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"PF-06463922, an ALK/ROS1 Inhibitor, Overcomes Resistance to First and Second Generation ALK Inhibitors in Preclinical Models"}]},{"@id":"https://cir.nii.ac.jp/crid/1360565165847181056","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"P-glycoprotein Mediates Ceritinib Resistance in Anaplastic Lymphoma Kinase-rearranged Non-small Cell Lung Cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1360565168392415744","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Patient-derived models of acquired resistance can identify effective drug combinations for cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1360567183420668288","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Notch3-dependent β-catenin signaling mediates EGFR TKI drug persistence in EGFR mutant NSCLC"}]},{"@id":"https://cir.nii.ac.jp/crid/1360567186323310592","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Activation of EGFR Bypass Signaling by TGFα Overexpression Induces Acquired Resistance to Alectinib in\n                    <i>ALK</i>\n                    -Translocated Lung Cancer Cells"}]},{"@id":"https://cir.nii.ac.jp/crid/1360568468304993024","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"The new-generation selective ROS1/NTRK inhibitor DS-6051b overcomes crizotinib resistant ROS1-G2032R mutation in preclinical models"}]},{"@id":"https://cir.nii.ac.jp/crid/1360574093479739776","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Diverse Resistance Mechanisms to the Third-Generation ALK Inhibitor Lorlatinib in ALK-Rearranged Lung Cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1360574094456963328","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"<i>ALK</i> in Lung Cancer: Past, Present, and Future"}]},{"@id":"https://cir.nii.ac.jp/crid/1360574094844439168","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Evidence that MIG-6 is a tumor-suppressor gene"}]},{"@id":"https://cir.nii.ac.jp/crid/1360574095170536832","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Lorlatinib in non-small-cell lung cancer with ALK or ROS1 rearrangement: an international, multicentre, open-label, single-arm first-in-man phase 1 trial"}]},{"@id":"https://cir.nii.ac.jp/crid/1360579814653895168","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"GSK3 inhibition circumvents and overcomes acquired lorlatinib resistance in ALK-rearranged non-small-cell lung cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1360580236999768320","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Cancer Incidence, Mortality, Years of Life Lost, Years Lived With Disability, and Disability-Adjusted Life Years for 29 Cancer Groups From 2010 to 2019"}]},{"@id":"https://cir.nii.ac.jp/crid/1360584345436437120","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Epidermal growth factor and its influencing variables in healthy children and adults"}]},{"@id":"https://cir.nii.ac.jp/crid/1360584345436453120","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"MIG‐6 is essential for promoting glucose metabolic reprogramming and tumor growth in triple‐negative breast cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1360584345436626432","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Resistance to Targeted Agents Used to Treat Paediatric ALK-Positive ALCL"}]},{"@id":"https://cir.nii.ac.jp/crid/1360584345436722048","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Genome-wide CRISPR screening reveals genetic modifiers of mutant EGFR dependence in human NSCLC"}]},{"@id":"https://cir.nii.ac.jp/crid/1360846643620432128","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Molecular Mechanisms of Resistance to First- and Second-Generation ALK Inhibitors in\n                    <i>ALK</i>\n                    -Rearranged Lung Cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1360848658398357376","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"AXL confers intrinsic resistance to osimertinib and advances the emergence of tolerant cells"}]},{"@id":"https://cir.nii.ac.jp/crid/1360855567864132480","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Multiplex Genome Engineering Using CRISPR/Cas Systems"}]},{"@id":"https://cir.nii.ac.jp/crid/1360855568840506368","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Transformation to SCLC after Treatment with the ALK Inhibitor Alectinib"}]},{"@id":"https://cir.nii.ac.jp/crid/1360855569146712448","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"<i>ROS1</i> Rearrangements Define a Unique Molecular Class of Lung Cancers"}]},{"@id":"https://cir.nii.ac.jp/crid/1360855569156078848","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Pretreatment levels of the serum biomarkers CEA, CYFRA 21–1, SCC and the soluble EGFR and its ligands EGF, TGF-alpha, HB-EGF in the prediction of outcome in erlotinib treated non-small-cell lung cancer patients"}]},{"@id":"https://cir.nii.ac.jp/crid/1360855569269650304","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Widespread potential for growth-factor-driven resistance to anticancer kinase inhibitors"}]},{"@id":"https://cir.nii.ac.jp/crid/1360857593654700288","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"HER3 activation contributes toward the emergence of ALK inhibitor-tolerant cells in ALK-rearranged lung cancer with mesenchymal features"}]},{"@id":"https://cir.nii.ac.jp/crid/1360861704764973312","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Adaptive resistance to lorlatinib via EGFR signaling in ALK-rearranged lung cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1360861711792573568","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Mechanism of Drug Tolerant Persister Cancer Cells: The Landscape and Clinical Implication for Therapy"}]},{"@id":"https://cir.nii.ac.jp/crid/1360865819403888000","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Suppression of Mig-6 overcomes the acquired EGFR-TKI resistance of lung adenocarcinoma"}]},{"@id":"https://cir.nii.ac.jp/crid/1360865820410657792","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Effective Treatment of Lung Adenocarcinoma Harboring EGFR-Activating Mutation, T790M, and cis-C797S Triple Mutations by Brigatinib and Cetuximab Combination Therapy"}]},{"@id":"https://cir.nii.ac.jp/crid/1360865821079742592","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Nuclear Gene 33/Mig6 regulates the DNA damage response through an ATM serine/threonine kinase–dependent mechanism"}]},{"@id":"https://cir.nii.ac.jp/crid/1360865821080658048","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Expression of VEGF, EGF and HGF in early‑ and late‑stage colorectal cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1361418518722454784","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"First-Line Lorlatinib or Crizotinib in Advanced\n            <i>ALK</i>\n            -Positive Lung Cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1361418519941130880","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Genome-Scale CRISPR-Cas9 Knockout Screening in Human Cells"}]},{"@id":"https://cir.nii.ac.jp/crid/1361418520483923328","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Tumor cells can follow distinct evolutionary paths to become resistant to epidermal growth factor receptor inhibition"}]},{"@id":"https://cir.nii.ac.jp/crid/1361699995052967040","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Mechanisms of Acquired Crizotinib Resistance in ALK-Rearranged Lung Cancers"}]},{"@id":"https://cir.nii.ac.jp/crid/1361699995535763584","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Optimizing the Detection of Lung Cancer Patients Harboring Anaplastic Lymphoma Kinase (<i>ALK</i>) Gene Rearrangements Potentially Suitable for ALK Inhibitor Treatment"}]},{"@id":"https://cir.nii.ac.jp/crid/1361699996208067840","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Epidermal Growth Factor (Urogastrone) in Human Tissues*"}]},{"@id":"https://cir.nii.ac.jp/crid/1361699996471698432","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"A Novel ALK Secondary Mutation and EGFR Signaling Cause Resistance to ALK Kinase Inhibitors"}]},{"@id":"https://cir.nii.ac.jp/crid/1361981468331303680","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Crizotinib in ROS1-rearranged advanced non-small-cell lung cancer (NSCLC): updated results, including overall survival, from PROFILE 1001"}]},{"@id":"https://cir.nii.ac.jp/crid/1362262944396279808","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"MAGeCK enables robust identification of essential genes from genome-scale CRISPR/Cas9 knockout screens"}]},{"@id":"https://cir.nii.ac.jp/crid/1362262944747435008","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Inhibition of the EGF receptor by binding of MIG6 to an activating kinase domain interface"}]},{"@id":"https://cir.nii.ac.jp/crid/1362262946058371072","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Drug-tolerant persister cancer cells are vulnerable to GPX4 inhibition"}]},{"@id":"https://cir.nii.ac.jp/crid/1362544418528191488","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Aurora kinase A drives the evolution of resistance to third-generation EGFR inhibitors in lung cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1362544419407557376","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Mig-6 deficiency cooperates with oncogenic Kras to promote mouse lung tumorigenesis"}]},{"@id":"https://cir.nii.ac.jp/crid/1362544419877281024","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Leptin Mediates Tumor–Stromal Interactions That Promote the Invasive Growth of Breast Cancer Cells"}]},{"@id":"https://cir.nii.ac.jp/crid/1362544420331592320","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Loss of MIG6 Accelerates Initiation and Progression of Mutant Epidermal Growth Factor Receptor–Driven Lung Adenocarcinoma"}]},{"@id":"https://cir.nii.ac.jp/crid/1362544421089632640","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Resistance Mechanisms to Targeted Therapies in\n                    <i>ROS1</i>\n                    + and\n                    <i>ALK</i>\n                    + Non–small Cell Lung Cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1362825893457501184","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Targeting FGFR overcomes EMT-mediated resistance in EGFR mutant non-small cell lung cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1362825895434997248","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Structure and mechanism of activity-based inhibition of the EGF receptor by Mig6"}]},{"@id":"https://cir.nii.ac.jp/crid/1363107368701760768","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"RAS-MAPK dependence underlies a rational polytherapy strategy in EML4-ALK–positive lung cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1363107369507421440","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Phase II Study of Crizotinib in East Asian Patients With ROS1-Positive Advanced Non–Small-Cell Lung Cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1363107370147801728","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Prevalence of ROS1 fusion in Chinese patients with non‐small cell lung cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1363388845660416128","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Lorlatinib in advanced ROS1-positive non-small-cell lung cancer: a multicentre, open-label, single-arm, phase 1–2 trial"}]},{"@id":"https://cir.nii.ac.jp/crid/1363670319544933376","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Combined BRAF, EGFR, and MEK Inhibition in Patients with\n                    <i>BRAF</i>\n                    V600E-Mutant Colorectal Cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1363951794171905408","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Mig-6 controls EGFR trafficking and suppresses gliomagenesis"}]},{"@id":"https://cir.nii.ac.jp/crid/1364233268514574080","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Resistance to ROS1 Inhibition Mediated by EGFR Pathway Activation in Non-Small Cell Lung Cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1364233269706764032","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Genome-scale CRISPR-Cas9 knockout and transcriptional activation screening"}]},{"@id":"https://cir.nii.ac.jp/crid/1364233270580459904","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Updated overall survival and final progression-free survival data for patients with treatment-naive advanced ALK-positive non-small-cell lung cancer in the ALEX study"}]},{"@id":"https://cir.nii.ac.jp/crid/1370021390573174707","@type":"Product","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Patterns of metastatic spread and mechanisms of resistance to crizotinib in ROS1-positive non-small-cell lung cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1570572701522922752","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@language":"en","@value":"A chromatin-mediated reversible drug-tolerant state in cancer cell subpopulations"}]},{"@id":"https://cir.nii.ac.jp/crid/1572824501197000960","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer"},{"@value":"Identification of the transforming EML4-ALK fusion gene in non-small lung cancer"}]}],"dataSourceIdentifier":[{"@type":"CROSSREF","@value":"10.1172/jci.insight.173688"},{"@type":"KAKEN","@value":"PRODUCT-25183476"},{"@type":"KAKEN","@value":"PRODUCT-25323676"},{"@type":"OPENAIRE","@value":"doi_dedup___::57faa7d6b8f15747bac5a8a26bf654f7"},{"@type":"CROSSREF","@value":"10.1016/j.canlet.2024.217220_references_DOI_5SATR9hv1drbszLNHYjthMSagbo"}]}