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• W2890752806 abstract "Nearly all patients with BRAF-mutant melanoma will progress on BRAF inhibitor monotherapy and combination BRAF/MEK inhibitor therapy within the first year of therapy. In the vast majority of progressing melanomas, resistance occurs via the re-activation of MAPK signalling, commonly via alterations in BRAF, NRAS and MEK1/2. A small proportion of resistant melanomas rely on the activation of the compensatory PI3K/AKT signalling cascade, although activation of this pathway does not preclude patient responses to BRAF/MEK inhibition. We now show, that PI3K/AKT signalling via potent oncogenic PIK3CA and AKT3 mutants, is not sufficient to overcome proliferative arrest induced by BRAF/MEK inhibition, but rather enables the survival of a dormant population of MAPK-inhibited melanoma cells. The evolution of resistance in these surviving tumour cells was associated with MAPK re-activation and no longer depended on the initial PI3K/AKT-activating oncogene. This dynamic form of resistance alters signalling dependence and may lead to the evolution of tumour subclones highly resistant to multiple targeted therapies." @default.
• W2890752806 created "2018-09-27" @default.
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• W2890752806 date "2018-09-20" @default.
• W2890752806 modified "2023-10-17" @default.
• W2890752806 title "Oncogenic PI3K/AKT promotes the step-wise evolution of combination BRAF/MEK inhibitor resistance in melanoma" @default.
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• W2890752806 doi "https://doi.org/10.1038/s41389-018-0081-3" @default.
• W2890752806 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6148266" @default.
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• W2890752806 hasPublicationYear "2018" @default.
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