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dc.contributor.authorDunnett-Kane, Victoria
dc.contributor.authorNicola, Pantelis
dc.contributor.authorBlackhall, Fiona H
dc.contributor.authorLindsay, Colin R
dc.date.accessioned2021-03-08T06:18:41Z
dc.date.available2021-03-08T06:18:41Z
dc.date.issued2021en
dc.identifier.citationDunnett-Kane V, Nicola P, Blackhall F, Lindsay C. Mechanisms of Resistance to KRAS(G12C) Inhibitors. Cancers (Basel). 2021;13(1).en
dc.identifier.pmid33466360en
dc.identifier.doi10.3390/cancers13010151en
dc.identifier.urihttp://hdl.handle.net/10541/623757
dc.description.abstractKRAS is one of the most common human oncogenes, but concerted efforts to produce direct inhibitors have largely failed, earning KRAS the title of "undruggable". Recent efforts to produce subtype specific inhibitors have been more successful, and several KRASG12C inhibitors have reached clinical trials, including adagrasib and sotorasib, which have shown early evidence of efficacy in patients. Lessons from other inhibitors of the RAS pathway suggest that the effect of these drugs will be limited in vivo by the development of drug resistance, and pre-clinical studies of G12C inhibitors have identified evidence of this. In this review we discuss the current evidence for G12C inhibitors, the mechanisms of resistance to G12C inhibitors and potential approaches to overcome them. We discuss possible targets of combination therapy, including SHP2, receptor tyrosine kinases, downstream effectors and PD1/PDL1, and review the ongoing clinical trials investigating these inhibitors.en
dc.language.isoenen
dc.relation.urlhttps://dx.doi.org/10.3390/cancers13010151en
dc.titleMechanisms of resistance to KRAS(G12C)iInhibitorsen
dc.typeArticleen
dc.contributor.departmentWythenshawe Hospital, Manchester University NHS Foundation Trust, Manchester M23 9Len
dc.identifier.journalCancersen
dc.description.noteen]
refterms.dateFOA2021-03-08T12:45:05Z


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