MEK1/2 inhibitor withdrawal reverses acquired resistance driven by BRAF amplification whereas KRAS amplification promotes EMT-chemoresistance (Q64071499)

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scientific article published on 02 May 2019

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English	MEK1/2 inhibitor withdrawal reverses acquired resistance driven by BRAF amplification whereas KRAS amplification promotes EMT-chemoresistance	scientific article published on 02 May 2019

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24 April 2020

MEK1/2 inhibitor withdrawal reverses acquired resistance driven by BRAFV600E amplification whereas KRASG13D amplification promotes EMT-chemoresistance (English)

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Julio Saez-Rodriguez

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Matthew J Sale

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Kathryn Balmanno

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Jayeta Saxena

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Katarzyna Wojdyla

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Rebecca E McIntyre

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Rebecca Gilley

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Anna Woroniuk

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Karen D Howarth

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Gareth Hughes

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Jonathan R Dry

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Pilar Caro

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David Oxley

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Susan Ashton

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David J Adams

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Nature Communications

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Europe PubMed Central

11 June 2022

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22 June 2022

https://europepmc.org/article/PMC/6497655

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Targeting RAF kinases for cancer therapy: BRAF-mutated melanoma and beyond

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Melanoma whole-exome sequencing identifies (V600E)B-RAF amplification-mediated acquired B-RAF inhibitor resistance

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Identification of the MEK1(F129L) activating mutation as a potential mechanism of acquired resistance to MEK inhibition in human cancers carrying the B-RafV600E mutation

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ERK inhibition overcomes acquired resistance to MEK inhibitors.

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Concurrent MEK2 mutation and BRAF amplification confer resistance to BRAF and MEK inhibitors in melanoma

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BRAF gene amplification can promote acquired resistance to MEK inhibitors in cancer cells harboring the BRAF V600E mutation

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High-intensity Raf signal causes cell cycle arrest mediated by p21Cip1.

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Raf-induced proliferation or cell cycle arrest is determined by the level of Raf activity with arrest mediated by p21Cip1.

1 reference

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Senescence of human fibroblasts induced by oncogenic Raf.

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Sequential activation of the MEK-extracellular signal-regulated kinase and MKK3/6-p38 mitogen-activated protein kinase pathways mediates oncogenic ras-induced premature senescence

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Activation of forkhead box O transcription factors by oncogenic BRAF promotes p21cip1-dependent senescence.

1 reference

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1 reference

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1 reference

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2019NatCo..10.2030S

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