Oncogenic mutations in NRAS and BRAF, which constitutively activate the ERK pathway, drive the aggressive growth of malignant melanoma. ERK signalling is therefore a primary therapeutic target. BRAF and MEK inhibitors can slow the progression of melanoma; however, resistance often develops. New treatment options are therefore needed.
A completely new approach has been proposed based on the finding that not only the inhibition of the ERK pathway, but also its excessive activation, is incompatible with the growth and survival of melanoma cells. However, this new concept, known as the ‘MAPK optimum’, has not yet been characterised in detail, nor has its general applicability to different subtypes of melanoma been confirmed.
We have recently discovered new functional interactions between the ERK pathway in melanoma and the eIF4F and AMPK signalling pathways, which significantly disrupt optimal ERK signalling and could serve as tools for its characterisation. This project aims to understand the mechanisms controlling ERK pathway activity at the level of these newly discovered interactions and to characterise the MAPK optimum in melanoma cells as a potential therapeutic target.

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