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MEK1/2 inhibitor withdrawal reverses acquired resistance driven by BRAF^V600E amplification whereas KRAS^G13D amplification promotes EMT-chemoresistance

Colorectal cancer cells can acquire resistance to MEK inhibition due to BRAF or KRAS amplification. Here, the authors show that while MEK inhibitor withdrawal in BRAF mutant cells restores sensitivity to the inhibitor through the loss of BRAF amplification mediated by a p57-dependent mechanism, drug withdrawal from KRAS mutant cells does not restore sensitivity but results in EMT and chemoresistance.

Matthew J. Sale
Kathryn Balmanno
Simon J. Cook
ResearchOpen Access02 May 2019
Nature Communications

Volume: 10, P: 1-22
Targeting melanoma’s MCL1 bias unleashes the apoptotic potential of BRAF and ERK1/2 pathway inhibitors

BRAF or MEK1/2 inhibitors are cytostatic in melanoma and the surviving cells develop drug resistance. This study shows that the pro-survival pool is biased towards MCL1 in melanoma so that BRAF or MEK1/2 inhibitors are synthetic lethal with the MCL1 inhibitor AZD5991, improving tumour growth inhibition.

Matthew J. Sale
Emma Minihane
Simon J. Cook
ResearchOpen Access14 Nov 2019
Nature Communications

Volume: 10, P: 1-19
Differential requirement for dimerization partner DP between E2F-dependent activation of tumor suppressor and growth-related genes

Hideyuki Komori
Yasuko Goto
Kiyoshi Ohtani
ResearchOpen Access31 May 2018
Scientific Reports

Volume: 8, P: 1-12

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