Co-targeting KRAS G12C and EGFR reduces both mutant and wild-type RAS-GTP

Abstract The combination of KRAS G12C inhibitors with EGFR inhibitors has reproducibly been shown to be beneficial. Here, we identify another benefit of this combination: it effectively inhibits both wild-type and mutant RAS. We believe that targeting both mutant and wild-type RAS helps explain why...

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Bibliografski detalji
Glavni autori: Thomas McFall, Michael Trogdon, Anita C. Guizar, John F. Langenheim, Laura Sisk-Hackworth, Edward C. Stites
Format: Članak
Jezik:English
Izdano: Nature Portfolio 2022-11-01
Serija:npj Precision Oncology
Online pristup:https://doi.org/10.1038/s41698-022-00329-w
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author Thomas McFall
Michael Trogdon
Anita C. Guizar
John F. Langenheim
Laura Sisk-Hackworth
Edward C. Stites
author_facet Thomas McFall
Michael Trogdon
Anita C. Guizar
John F. Langenheim
Laura Sisk-Hackworth
Edward C. Stites
author_sort Thomas McFall
collection DOAJ
description Abstract The combination of KRAS G12C inhibitors with EGFR inhibitors has reproducibly been shown to be beneficial. Here, we identify another benefit of this combination: it effectively inhibits both wild-type and mutant RAS. We believe that targeting both mutant and wild-type RAS helps explain why this combination of inhibitors is effective.
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spelling doaj.art-d2a834aeeb10413aae877a20897f77b62023-12-03T04:15:14ZengNature Portfolionpj Precision Oncology2397-768X2022-11-01611710.1038/s41698-022-00329-wCo-targeting KRAS G12C and EGFR reduces both mutant and wild-type RAS-GTPThomas McFall0Michael Trogdon1Anita C. Guizar2John F. Langenheim3Laura Sisk-Hackworth4Edward C. Stites5Department of Biochemistry and MCW Cancer Center, Medical College of WisconsinIntegrative Biology Laboratory, Salk Institute for Biological StudiesDepartment of Biochemistry and MCW Cancer Center, Medical College of WisconsinDepartment of Pathology, Medical College of WisconsinIntegrative Biology Laboratory, Salk Institute for Biological StudiesIntegrative Biology Laboratory, Salk Institute for Biological StudiesAbstract The combination of KRAS G12C inhibitors with EGFR inhibitors has reproducibly been shown to be beneficial. Here, we identify another benefit of this combination: it effectively inhibits both wild-type and mutant RAS. We believe that targeting both mutant and wild-type RAS helps explain why this combination of inhibitors is effective.https://doi.org/10.1038/s41698-022-00329-w
spellingShingle Thomas McFall
Michael Trogdon
Anita C. Guizar
John F. Langenheim
Laura Sisk-Hackworth
Edward C. Stites
Co-targeting KRAS G12C and EGFR reduces both mutant and wild-type RAS-GTP
npj Precision Oncology
title Co-targeting KRAS G12C and EGFR reduces both mutant and wild-type RAS-GTP
title_full Co-targeting KRAS G12C and EGFR reduces both mutant and wild-type RAS-GTP
title_fullStr Co-targeting KRAS G12C and EGFR reduces both mutant and wild-type RAS-GTP
title_full_unstemmed Co-targeting KRAS G12C and EGFR reduces both mutant and wild-type RAS-GTP
title_short Co-targeting KRAS G12C and EGFR reduces both mutant and wild-type RAS-GTP
title_sort co targeting kras g12c and egfr reduces both mutant and wild type ras gtp
url https://doi.org/10.1038/s41698-022-00329-w
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