Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8733692 | Critical Reviews in Oncology/Hematology | 2018 | 13 Pages |
Abstract
In this review we will describe the molecular alterations underlying each of these EGFR TKIs resistance mechanisms, focusing on the currently available and future therapeutic strategies to overcome these phenomena.
Keywords
STAT3FDAPI3KCAGCNJanus Kinase 2Tgf-αTKIDCRHGFSFKbHLHISHJAK2HDACmTOREGFRHER2EMAORRIn situ hybridizationSrc family kinasesMAPKPFsALKEuropean Medicines agencybasic helix–loop–helixImmunohistochemistryIHCProgression free survivaloverall survivalSCLCtransforming growth factor-αEMTDORTargeted therapyCNSFood and Drug AdministrationSmall-cell lung cancerNon-small cell lung cancercentral nervous systemGene copy numberHepatocyte growth factorphosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alphafluorescence in situ hybridizationAnaplastic lymphoma kinaseFishsignal transducer and activator of transcription 3duration of responseResistanceMETTyrosine kinase inhibitorTyrosine kinase inhibitorsoverall response rateDisease control ratehazard ratiomammalian target of rapamycinmitogen-activated protein kinaseepithelial-to-mesenchymal transitionHuman epidermal growth factor receptor 2Epidermal growth factor receptor
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Authors
Chiara Tomasello, Cinzia Baldessari, Martina Napolitano, Giulia Orsi, Giulia Grizzi, Federica Bertolini, Fausto Barbieri, Stefano Cascinu,