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dc.contributor.authorPacini, L
dc.contributor.authorJenks, AD
dc.contributor.authorLima, NC
dc.contributor.authorHuang, PH
dc.date.accessioned2021-05-11T10:59:40Z
dc.date.available2021-05-11T10:59:40Z
dc.identifier.citationCells, 10 (5), pp. 1154 - 1154
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/4545
dc.identifier.eissn2073-4409
dc.identifier.eissn2073-4409en_US
dc.identifier.doi10.3390/cells10051154
dc.identifier.doi10.3390/cells10051154en_US
dc.description.abstract<jats:p>Lung cancer is the most common cause of cancer-related deaths globally. Genetic alterations, such as amplifications, mutations and translocations in the fibroblast growth factor receptor (FGFR) family have been found in non-small cell lung cancer (NSCLC) where they have a role in cancer initiation and progression. FGFR aberrations have also been identified as key compensatory bypass mechanisms of resistance to targeted therapy against mutant epidermal growth factor receptor (EGFR) and mutant Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) in lung cancer. Targeting FGFR is, therefore, of clinical relevance for this cancer type, and several selective and nonselective FGFR inhibitors have been developed in recent years. Despite promising preclinical data, clinical trials have largely shown low efficacy of these agents in lung cancer patients with FGFR alterations. Preclinical studies have highlighted the emergence of multiple intrinsic and acquired resistance mechanisms to FGFR tyrosine kinase inhibitors, which include on-target FGFR gatekeeper mutations and activation of bypass signalling pathways and alternative receptor tyrosine kinases. Here, we review the landscape of FGFR aberrations in lung cancer and the array of targeted therapies under clinical evaluation. We also discuss the current understanding of the mechanisms of resistance to FGFR-targeting compounds and therapeutic strategies to circumvent resistance. Finally, we highlight our perspectives on the development of new biomarkers for stratification and prediction of FGFR inhibitor response to enable personalisation of treatment in patients with lung cancer.</jats:p>
dc.format.extent1154 - 1154
dc.languageeng
dc.language.isoeng
dc.publisherMDPI AG
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.titleTargeting the Fibroblast Growth Factor Receptor (FGFR) Family in Lung Cancer
dc.typeJournal Article
dcterms.dateAccepted2021-05-07
rioxxterms.versionVoR
rioxxterms.versionofrecord10.3390/cells10051154
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfCells
pubs.issue5
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/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/Molecular Pathology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology/Molecular and Systems Oncology
pubs.publication-statusPublished online
pubs.volume10en_US
pubs.embargo.termsNo embargo
icr.researchteamMolecular and Systems Oncology
icr.researchteamMolecular and Systems Oncologyen_US
dc.contributor.icrauthorHuang, Paulen


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