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dc.contributor.authorVyse, S
dc.contributor.authorHuang, PH
dc.date.accessioned2019-03-18T09:58:46Z
dc.date.issued2019-01
dc.identifier.citationSignal transduction and targeted therapy, 2019, 4 pp. 5 - ?
dc.identifier.issn2095-9907
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/3154
dc.identifier.eissn2059-3635
dc.identifier.doi10.1038/s41392-019-0038-9
dc.description.abstractInframe insertions of three or more base pairs in exon 20 of the epidermal growth factor receptor ( EGFR) gene were among the first EGFR mutations to be identified as oncogenic drivers in non-small cell lung cancer (NSCLC). However, unlike the classical EGFR L858R point mutation or exon 19 deletions, which represent the majority of EGFR mutations in NSCLC, low frequency EGFR exon 20 insertion mutations are associated with de novo resistance to targeted EGFR inhibitors and correlate with a poor patient prognosis. Here, we review the developments over the last 5 years in which pre-clinical studies, including elucidation of the crystal structure of an EGFR exon 20 insertion mutant kinase, have revealed a unique mechanism of kinase activation and steric conformation that define the lack of response of these EGFR mutations to clinically approved EGFR inhibitors. The recent development of several novel small molecule compounds that selectively inhibit EGFR exon 20 insertions holds promise for future therapeutic options that will be effective for patients with this molecular subtype of NSCLC.
dc.formatElectronic-eCollection
dc.format.extent5 - ?
dc.languageeng
dc.language.isoeng
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titleTargeting <i>EGFR</i> exon 20 insertion mutations in non-small cell lung cancer.
dc.typeJournal Article
dcterms.dateAccepted2019-02-13
rioxxterms.versionofrecord10.1038/s41392-019-0038-9
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0
rioxxterms.licenseref.startdate2019-01
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfSignal transduction and targeted therapy
pubs.notesNo embargo
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology/Protein Networks
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology/Molecular and Systems Oncology
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology/Protein Networks
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology/Molecular and Systems Oncology
pubs.publication-statusPublished
pubs.volume4
pubs.embargo.termsNo embargo
icr.researchteamProtein Networksen_US
icr.researchteamMolecular and Systems Oncologyen_US
dc.contributor.icrauthorVyse, Simonen
dc.contributor.icrauthorHuang, Paulen


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