The extracellular signal-regulated kinase (ERK) is a component of the mitogen-activated protein (MAP) cascade. ERK activation is a key signal step for the regulation of several biological responses like cell proliferation, cell differentiation and cell death. MAPK pathway is often mutated in cancer thus the efficient inhibition of ERK function may be the key to overcome previously described resistance to upstream kinases inhibitors. This is the case of BRAF and MEK inhibitors that lead to ERK re-activation and tumor recurrence.
Our goal is to study the mechanism of action and resistance of ERK inhibitors in lymphoma and to explore potential synergies between novel and already established inhibitors of cross-talking signaling networks.